pituitrin and Inappropriate-ADH-Syndrome

Topics: Churg-Strauss Syndrome; Cyclophosphamide; Granulomatosis with Polyangiitis; Humans; Immunoglobulins, Intravenous; Inappropriate ADH Syndrome; Male; Methylprednisolone; Middle Aged; Vasopressins

Hyponatremia and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) are associated with significant mortality and morbidity. The effectiveness and safety of oral urea for SIADH are still debated.. To evaluate the efficacy and safety of urea for the treatment of SIADH.. A systematic search of Medline and Embase was conducted for controlled and uncontrolled studies of urea for SIADH in adult patients. The primary outcome was serum sodium concentration after treatment. Secondary outcomes included the proportion of patients with osmotic demyelination syndrome (ODS), intracranial pressure, and resource use such as length of stay.. Twenty-three studies involving 537 patients with SIADH were included, of which 462 were treated with urea. The pooled mean baseline serum sodium was 125.0 mmol/L (95% CI, 122.6-127.5 mmol/L). The median treatment duration with oral urea was 5 days. Urea increased serum sodium concentration by a mean of 9.6 mmol/L (95% CI, 7.5-11.7 mmol/L). The mean increase in serum sodium after 24 hours was 4.9 mmol/L (95% CI, 0.5-9.3 mmol/L). Adverse events were few, mainly consisting of distaste or dysgeusia, and no case of ODS was reported. Resource use was too infrequently reported to be synthesized.. In this systematic review of the use of urea in SIADH and despite the lack of randomized clinical trials, lower-quality evidence was identified that suggests that urea may be an effective, safe, and inexpensive treatment modality that warrants further exploration.

Topics: Adult; Demyelinating Diseases; Humans; Inappropriate ADH Syndrome; Sodium; Urea; Vasopressins

Hyponatremia, especially if acute and severe, can be a life-threatening condition. Several conditions can trigger hyponatremia. In this review, we will discuss two conditions that can determine euvolemic hyponatremia: the cerebral/renal salt wasting (CRSW) syndrome and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), including the two subtypes: reset osmostat (RO) and nephrogenic syndrome of inappropriate antidiuresis (NSIAD) and their differential diagnoses. Despite the passage of over 70 years since its first description, to date, the true etiopathogenesis of CRSW syndrome, a rare cause of hypovolemic/euvolemic hyponatremia, is almost unknown. SIADH, including RO and NSIAD, is sometimes difficult to differentiate from CRSW syndrome; in its differential diagnosis, the clinical approach based on the evaluation of the extracellular volume (ECV) was proven insufficient. We therefore suggest a simple diagnostic algorithm based on the assessment of the degree of hyponatremia, urinary osmolality, and the assessment of the fraction of urate excretion (FEUa) in conditions of hyponatremia and after serum sodium correction, to be applied in children over 1 year of life.

Topics: Algorithms; Child; Diagnosis, Differential; Genetic Diseases, X-Linked; Humans; Hyponatremia; Inappropriate ADH Syndrome; Sodium; Uric Acid; Vasopressins

We report a mediastinal neuroblastoma in an octogenarian with paraneoplastic syndrome of inappropriate antidiuretic hormone secretion (SIADH). Neuroblastomas are very rare tumors in adults, with thoracic or mediastinal locations being especially uncommon. These neoplasms have been occasionally associated with the SIADH. Given the rarity of incidence and paucity of diagnostic and outcomes data, the significance of standard neuroblastoma prognostic characteristics is unclear, and no treatment paradigms exist for these patients. Further studies are needed to inform future clinical guidelines.

Topics: Adult; Aged, 80 and over; Humans; Inappropriate ADH Syndrome; Mediastinal Neoplasms; Neuroblastoma; Vasopressins

Hyponatremia is the most frequent electrolytic disorder in hospitalized patients, and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), the most frequent cause of hiponatremia with clinically normal extracellular volume. It consists of a disorder of the regulation of body water that obeys to different causes, mainly cancer, pulmonary illnesses, disorders of the central nervous system and diverse drugs. As in any hiponatremia it a physiological knowledge of the regulation of body water and sodium is essential as well as the application of precise diagnostic criteria in order to manage the problem with an effective treatment. The available data until the moment show that the clinical diagnosis of SIADH made by professionals is mainly not supported on the established criteria drawn by experts and this lack of accuracy probably hits in the therapeutic result. The basis of the treatment of the SIADH is to correct its cause, water restriction, solutes (sodium chloride) and the use of vaptans in case of failure of the previous measures.

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Sodium; Sodium Chloride; Vasopressins

Linezolid is a synthetic oxazolidinone antimicrobial drug with a broad spectrum and a unique mechanism of inhibiting resistant pathogenic strains, and it was approved by the Food and Drug Administration (FDA) in April 2000. Several different systemic side effects were reported after the use of this medication. In this article, we report a case in which a syndrome of inappropriate antidiuretic hormone (SIADH) was developed after linezolid treatment was started.. We present the case of a 79-year-old woman who developed severe hyponatremia during linezolid treatment (0.6 g i.v. q12 h) after undergoing hemiarthroplasty for left femoral neck fracture. The patient's baseline serum sodium upon admission (138 mmol/L) decreased to 118 mmol/L, urine sodium was 102 mmol/L, plasma osmolality was 248 mOsm/kg and urine osmolarity was 310 mOsm/kg at day 4, thus a diagnosis of SIADH was made. The patient was not taking any other medication known to cause SIADH, and she did not present a comorbidity that could explain her condition. Her serum sodium increased to 135 and 137 mmol/L, respectively, 11 and 12 days after cessation of linezolid, strongly suggesting that SIADH was the cause in this case.. This is the fourth case of linezolid-induced SIADH. A thorough workup was essential for the diagnosis to correctly differentiate between SIADH and other causes of hyponatremia, which helped us properly conducting follow-up treatments. SIADH is a rare but serious side effect of linezolid, and practicing physicians should be aware of this complication. It is necessary to periodically monitor the serum sodium.

Topics: Aged; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Linezolid; Sodium; Vasopressins

Arginine vasopressin (AVP)-mediated osmoregulatory disorders, such as diabetes insipidus (DI) and syndrome of inappropriate secretion of antidiuretic hormone (SIADH) are common in the differential diagnosis for children with hypo- and hypernatremia and require timely recognition and treatment. DI is caused by a failure to concentrate urine secondary to impaired production of or response to AVP, resulting in hypernatremia. Newer methods of diagnosing DI include measuring copeptin levels; copeptin is AVP's chaperone protein and serves as a surrogate biomarker of AVP secretion. Intraoperative copeptin levels may also help predict the risk for developing DI after neurosurgical procedures. Copeptin levels hold diagnostic promise in other pediatric conditions, too. Recently, expanded genotype and phenotype correlations in inherited DI disorders have been described and may better predict the clinical course in affected children and infants. Similarly, newer formulations of synthetic AVP may improve pediatric DI treatment. In contrast to DI, SIADH, characterized by inappropriate AVP secretion, commonly leads to severe hyponatremia. Contemporary methods aid clinicians in distinguishing SIADH from other hyponatremic conditions, particularly cerebral salt wasting. Further research on the efficacy of therapies for pediatric SIADH is needed, although some adult treatments hold promise for pediatrics. Lastly, expansion of home point-of-care sodium testing may transform management of SIADH and DI in children. In this article, we review recent developments in the understanding of pathophysiology, diagnostic workup, and treatment of better outcomes and quality of life for children with these challenging disorders.

Topics: Child; Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Neurophysins; Protein Precursors; Vasopressins

Nephrogenic syndrome of inappropriate antidiuresis (NSIAD), first described in 2005, is a rare genetic X-linked disease, presenting with hyponatremia, hyposmolarity, euvolemia, inappropriately concentrated urine, increased natriuresis, and undetectable or very low arginine-vasopressine (AVP) circulating levels. It can occur in neonates, infants, or later in life. NSIAD must be early recognized and treated to prevent severe hyponatremia, which can show a dangerous impact on neonatal outcome. In fact, it potentially leads to death or, in case of survival, neurologic sequelae. This review is an update of NSIAD 12 years after the first description, focusing on reported cases of neonatal and infantile onset. The different molecular patterns affecting the AVP receptor 2 (V2R) and determining its gain of function are reported in detail; moreover, we also provide a comparison between the different triggers involved in the development of hyponatremia, the evolution of the symptoms, and modality and efficacy of the different treatments available.

Topics: Age of Onset; Antidiuretic Hormone Receptor Antagonists; Clinical Trials as Topic; Diuretics, Osmotic; Drinking; Gain of Function Mutation; Genetic Diseases, X-Linked; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant; Infant, Newborn; Mutation, Missense; Receptors, Vasopressin; Renal Reabsorption; Signal Transduction; Sodium; Treatment Outcome; Urea; Vasopressins

Disorders of water balance are a disease commonly encountered in our clinical practice. Analysis of vasopressin receptor type II (V2R) is essential to understand the physiology of water balance and it is used as a biological prototype of G protein-coupled receptors (GPCRs). Nephrogenic syndrome of inappropriate antidiuresis (NSIAD) is a syndrome of inappropriate antidiuretic hormone secretion (SIADH) with low plasmatic vasopressin. The evidence on the role of V2 receptor and of aquaporin (AQP) in the mechanism of action for antidiuretic hormone (ADH) was based on the identification of protein gene mutations in patients with nephrogenic diabetes insipidus and NSIAD syndrome. V2R activating mutations were found in patients with NSIAD, contrasting with the numerous V2R inactivating mutations related to X-linked mutations described in patients with nephrogenic diabetes insipidus.

Topics: Aquaporins; Diabetes Insipidus, Nephrogenic; Genetic Diseases, X-Linked; Humans; Inappropriate ADH Syndrome; Mutation; Neurophysins; Protein Precursors; Receptors, Vasopressin; Vasopressins

Topics: Aquaporin 2; Biomarkers; Body Water; Diabetes Insipidus, Neurogenic; Education, Medical, Continuing; Humans; Inappropriate ADH Syndrome; Kidney; Polymers; Receptors, Vasopressin; Sodium; Vasopressins; Water-Electrolyte Imbalance

Disorders of body fluids are among the most commonly encountered problems in the practice of clinical medicine. This is in large part because many different disease states can potentially disrupt the finely balanced mechanisms that control the intake and output of water and solute. It therefore behooves clinicians treating such patients to have a good understanding of the pathophysiology, the differential diagnosis and the management of these disorders. Since body water is the primary determinant of the osmolality of the extracellular fluid (ECF), disorders of body water homeostasis can be divided into hypoosmolar disorders, in which there is an excess of body water relative to body solute, and hyperosmolar disorders, in which there is a deficiency of body water relative to body solute. The classical hyperosmolar disorder is diabetes insipidus (DI), and the classical hypoosmolar disorder is the syndrome of inappropriate antidiuretic hormone secretion (SIADH). This chapter first reviews the regulatory mechanisms underlying water and sodium metabolism, the two major determinants of body fluid homeostasis. The major disorders of water metabolism causing hyperosmolality and hypoosmolality, DI and SIADH, are then discussed in detail, including the pathogenesis, differential diagnosis and treatment of these disorders.

Topics: Animals; Diabetes Insipidus; Diagnosis, Differential; Humans; Hypernatremia; Inappropriate ADH Syndrome; Vasopressins; Water; Water-Electrolyte Imbalance

Dysnatremia is among the most common electrolyte disorders in clinical medicine and its improper management can have serious consequences associated with increased morbidity and mortality of patients. The aim of this study is to update the pathophysiology of dysnatremia and review some simple clinical and laboratory tools, easy to interpret, that allow us to make a quick and simple approach. Dysnatremia involves water balance disorders. Water balance is directly related to osmoregulation. There are mechanisms to maintain plasma osmolality control; which are triggered by 1-2% changes. Hypothalamic osmoreceptors detect changes in plasma osmolality, regulating the secretion of Antidiuretic Hormone (ADH), which travels to the kidneys resulting in more water being reabsorbed into the blood; therefore, the kidney is the main regulator of water balance. When a patient is suffering dysnatremia, it is important to assess how his ADH-renal axis is working. There are causes of this condition easy to identify, however, to differentiate a syndrome of inappropriate ADH secretion from cerebral salt-wasting syndrome is often more difficult. In the case of hypernatremia, to suspect insipidus diabetes and to differentiate its either central or nephrogenic origin is essential for its management. In conclusion, dysnatremia management requires pathophysiologic knowledge of its development in order to make an accurate diagnosis and appropriate treatment, avoiding errors that may endanger the health of our patients.

Topics: Child; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins; Water-Electrolyte Imbalance

Excessive secretion of vasopressin in the course of Syndrome of Inappropriate Antidiuretic Hormone Secretion is a common cause of hyponatremia in cancer patients. Clinical symptoms depend on the cause, rate of change of sodium level and their absolute values. Treatment options include fluid restrictions, intravenous administration of hypertonic sodium chloride solutions, loop diuretics and vaptans. The sodium level should not be adjusted too fast, because it may lead to irreversible brain damage. The article presents pathophysiology, diagnostics and recommendations of management of this oncological emergency.

Topics: Emergencies; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infusions, Intravenous; Neoplasms; Saline Solution, Hypertonic; Vasopressins

Water excretion is regulated in large part through the regulation of osmotic water permeability of the renal collecting duct epithelium. Water permeability is controlled by vasopressin through regulation of the water channel, aquaporin-2 (AQP2). Two processes contribute: (1) regulation of AQP2 trafficking to the apical plasma membrane; and (2) regulation of the total amount of the AQP2 protein in the cells. Regulation of AQP2 abundance is defective in several water-balance disorders, including many polyuric disorders and the syndrome of inappropriate antidiuresis. Here we review vasopressin signaling in the renal collecting duct that is relevant to the two modes of water permeability regulation.

Topics: Animals; Aquaporin 2; beta Catenin; Cyclic AMP; Cyclic AMP-Dependent Protein Kinases; Heart Failure; Humans; Inappropriate ADH Syndrome; Kidney Tubules, Collecting; Liver Cirrhosis; Mice; Myosin-Light-Chain Kinase; Nephrotic Syndrome; Permeability; Phosphoproteins; Phosphorylation; Polyuria; Proto-Oncogene Proteins c-akt; Proto-Oncogene Proteins c-jun; Rats; Signal Transduction; Transcription Factor AP-1; Transcription Factors; Vasopressins

Disturbances in sodium concentration are common in the critically ill patient and associated with increased mortality. The key principle in treatment and prevention is that plasma [Na+] (P-[Na+]) is determined by external water and cation balances. P-[Na+] determines plasma tonicity. An important exception is hyperglycaemia, where P-[Na+] may be reduced despite plasma hypertonicity. The patient is first treated to secure airway, breathing and circulation to diminish secondary organ damage. Symptoms are critical when handling a patient with hyponatraemia. Severe symptoms are treated with 2 ml/kg 3% NaCl bolus infusions irrespective of the supposed duration of hyponatraemia. The goal is to reduce cerebral symptoms. The bolus therapy ensures an immediate and controllable rise in P-[Na+]. A maximum of three boluses are given (increases P-[Na+] about 6 mmol/l). In all patients with hyponatraemia, correction above 10 mmol/l/day must be avoided to reduce the risk of osmotic demyelination. Practical measures for handling a rapid rise in P-[Na+] are discussed. The risk of overcorrection is associated with the mechanisms that cause hyponatraemia. Traditional classifications according to volume status are notoriously difficult to handle in clinical practice. Moreover, multiple combined mechanisms are common. More than one mechanism must therefore be considered for safe and lasting correction. Hypernatraemia is less common than hyponatraemia, but implies that the patient is more ill and has a worse prognosis. A practical approach includes treatment of the underlying diseases and restoration of the distorted water and salt balances. Multiple combined mechanisms are common and must be searched for. Importantly, hypernatraemia is not only a matter of water deficit, and treatment of the critically ill patient with an accumulated fluid balance of 20 litres and corresponding weight gain should not comprise more water, but measures to invoke a negative cation balance. Reduction of hypernatraemia/hypertonicity is critical, but should not exceed 12 mmol/l/day in order to reduce the risk of rebounding brain oedema.

Topics: Critical Illness; Decision Support Techniques; Diuresis; Diuretics; Humans; Hypernatremia; Hyponatremia; Hypothyroidism; Iatrogenic Disease; Inappropriate ADH Syndrome; Plasma Volume; Sodium Chloride Symporter Inhibitors; Vasopressins

Hyponatremia is the most common electrolyte disorder in the hospital setting and is defined as a serum sodium concentration less than 135 mmol/l. Most patients have mild hyponatremia (plasma sodium concentration 130-134 mmol/l) and few if any symptoms. Serum sodium concentrations between 120 and 129 mmol/l can be associated with lack of concentration, nausea, forgetfulness, apathy and loss of balance. Severe hyponatremia (<120 mmol/l) can cause coma or grand mal seizure. If hyponatremia occurs acutely (duration <48 h) it will cause more severe symptoms than are observed in chronic hyponatremia (>48 h). It is important to distinguish between different types of hyponatremia: euvolemic hyponatremia causing syndrome of inappropriate antidiuretic hormone secretion(SIADH) also known as Schwartz-Bartter syndrome, hypervolemic hyponatremia (cardiac failure and liver cirrhosis) and hypovolemic hyponatremia (diarrhoea, vomiting or other gastrointestinal fluid losses). Increased levels of ADH and continued fluid intake are the pathogenetic causes of all three types of hyponatremia; nonetheless, infusion of isotonic fluid is the therapy of choice for hypovolemic hyponatremia. In contrast, fluid restriction, lithium carbonate, urea, loop diuretics or demeclocycline have been used as therapeutic options to correct hyponatremia in euvolemic or hypervolemic hyponatremia but most of these therapies have proven to be cumbersome and inefficient. Recently a new class of pharmacological agents has become available, the vaptans, orally taken vasopressin antagonists. Clinical trials showed them to provide effective, specific and safe therapy of hyponatremia. In Europe tolvaptan, the only such agent on the market is now approved for the treatment of euvolemic hyponatremia.

Topics: Critical Care; Diagnosis, Differential; Emergency Service, Hospital; Humans; Hyponatremia; Inappropriate ADH Syndrome; Sodium Chloride; Vasopressins

The syndrome of inappropriate antidiuresis (SIAD; formerly the syndrome of inappropriate secretion of antidiuretic hormone) is the most frequent cause of hyponatremia. A strong association exists between mortality and hyponatremia, which reflects the severity of the underlying disease. In SIAD, hyponatremia is associated with normovolaemia but the assessment of extracellular volume can be difficult. Clinical features are mainly neurological and can lead to death but mechanisms of adaptation can limit cerebral oedema. The notion of mild asymptomatic hyponatremia was questioned by the observation of subclinical neurocognitive impairment, a greater risk of falls and fractures. Aetiologies are classified into six groups: neurologic disorders, infections mainly cerebral, meningeal and pulmonary, drugs in particular antidepressants, tumors, genetic causes, and idiopathic. Symptomatic acute hyponatremia is a therapeutic emergency that is not specific of SIAD. When hyponatremia is asymptomatic, fluid restriction with salt intake is generally sufficient but urea can be an alternative. In chronic SIAD, there is currently no recommendation. Fluid restriction is not always feasible; urea has proved its efficacy, its good tolerance and its long-term harmlessness. Vaptans have demonstrated their good tolerance and their efficacy on the correction of hyponatremia from SIAD in studies subgroups, for moderate hyponatremia and asymptomatic patients. In the only study having compared vaptans and urea, efficacy and tolerance were similar. Because of the cost difference between vaptans and urea and while waiting for follow-up studies, urea appears at present as the first-line treatment of hyponatremia in SIAD.

Topics: Diagnosis, Differential; Genetic Predisposition to Disease; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infections; Neoplasms; Neurophysins; Protein Precursors; Vasopressins; Water-Electrolyte Balance

The therapies of mood and anxiety disorders are not solved, because current antidepressants have delayed onset of therapeutic action and a significant number of patients are non-responsive. Research on the field was leaning towards neuropeptides as therapeutic targets. Vasopressin (VP) is a hot candidate, as beyond its peripheral actions VP is implicated in interneuronal communication and modulates the hypothalamo-pituitary-adrenal (HPA), the key stress axis, as well as behavioural functions. Affective disorders are stress related disorders and the most frequently occurring abnormality in depressed subjects is hyperactivity of the HPA. VP with nucleus paraventricularis hypothalami origin is a direct adrenocorticotrophin secretagogue through its V1b receptor. VP seems to have special importance under prolonged stress conditions, which are known to be strong predictive factor of depressive disorder and can induce depressive-like symptoms. Preclinical and clinical data summarized in this review underline the importance of VP in the development of anxiety- and depressive-like symptoms. Orally active nonpeptiderg V1b antagonists were developed and seemed to have effective anxiolytic and antidepressant profile in preclinical studies, which was not fully confirmed by clinical observations. It seems that V1a receptors on special brain areas could have same importance. Taken together current knowledge strongly implies an importance of vasopressinergic regulation in affective disorders and consider VP as endogenous anxiogenic/depressogenic substance. However, wide range of side effects could develop as a result of an intervention on the VP system; therefore there is a need for area-specific targeting of VP receptors (e.g. with modified nanoparticles).

Topics: Animals; Anti-Anxiety Agents; Antidepressive Agents; Antidiuretic Hormone Receptor Antagonists; Anxiety; Anxiety Disorders; Depression; Depressive Disorder; Diabetes Insipidus; Disease Models, Animal; Humans; Hypothalamo-Hypophyseal System; Inappropriate ADH Syndrome; Mice; Mice, Inbred BALB C; Mice, Knockout; Molecular Targeted Therapy; Mood Disorders; Pituitary-Adrenal System; Rats; Rats, Brattleboro; Rats, Mutant Strains; Receptors, Vasopressin; Stress, Psychological; Vasopressins

Hyponatremia is a marker of different underlying diseases and it can be a cause of morbidity itself; this implies the importance of a correct approach to the problem. The syndrome of inappropriate antidiuresis (SIAD) is one of the most common causes of hyponatremia: it is a disorder of sodium and water balance characterized by urinary dilution impairment and hypotonic hyponatremia, in the absence of renal disease or any identifiable non-osmotic stimulus able to induce antidiuretic hormone (ADH) release; according to its definition, it is diagnosed through an exclusion algorithm. SIAD is usually observed in hospitalized patients and its prevalence may be as high as 35%. The understanding of the syndrome has notably evolved over the last years, as reflected by the significant change in the name, once the syndrome of inappropriate secretion of ADH (SIADH), today SIAD. This review is up to date and it analyses the newest notions about pathophysiological mechanisms, classification, management and therapy of SIAD, including vaptans.

Topics: Animals; Benzazepines; Disease Management; Humans; Hyponatremia; Inappropriate ADH Syndrome; Neurophysins; Protein Precursors; Vasopressins; Water-Electrolyte Balance

Topics: Hormones, Ectopic; Humans; Inappropriate ADH Syndrome; Paraneoplastic Endocrine Syndromes; Vasopressins

Hyponatremia is the most prevalent electrolyte disorder in hospitalized patients. Vasopressin plays an important role in the pathogenesis of this disorder through its action on the vasopressin type 2 receptor (V(2)R), leading to electrolyte-free water reabsorption. Multiple vasopressin receptor antagonists have recently been developed that differ in their specificity for V(2)R and V(1)R. These agents have applications in diseases that can result in hypervolemic and euvolemic hyponatremia, such as the syndrome of inappropriate antidiuretic hormone secretion, congestive heart failure and cirrhosis. V(2)R antagonists have demonstrated promise in the short-term correction of hyponatremia, although the long-term survival benefits of these drugs are less clear. This review discusses the physiology of vasopressin in hyponatremia, the clinical implications of the disorder and examples of individual therapeutics used in treatment strategies.

Topics: Animals; Antidiuretic Agents; Antidiuretic Hormone Receptor Antagonists; Clinical Trials as Topic; Heart Failure; Humans; Hyponatremia; Inappropriate ADH Syndrome; Liver Cirrhosis; Receptors, Vasopressin; Vasopressins

The syndrome of inappropriate ADH secretion (SIADH), also recently referred to as the "syndrome of inappropriate antidiuresis", is an often underdiagnosed cause of hypotonic hyponatremia, resulting for instance from ectopic release of ADH in lung cancer or as a side-effect of various drugs. In SIADH, hyponatremia results from a pure disorder of water handling by the kidney, whereas external Na+ balance is usually well regulated. Despite increased total body water, only minor changes of urine output and modest edema are usually seen. Renal function and acid-base balance are often preserved, while neurological impairment may range from subclinical to life-threatening. Hypouricemia is a distinguishing feature. The major causes and clinical variants of SIADH are reviewed, with particular emphasis on iatrogenic complications and hospital-acquired hyponatremia. Effective treatment of SIADH with water restriction, aquaretics, or hypertonic saline + loop diuretics, as opposed to worsening of hyponatremia during parenteral isotonic fluid administration, underscores the importance of an early accurate diagnosis and careful follow-up of these patients.

Topics: Algorithms; Humans; Hyponatremia; Inappropriate ADH Syndrome; Models, Biological; Neurophysins; Osmolar Concentration; Protein Precursors; Vasopressins; Water-Electrolyte Balance

Hyponatremia is the most common electrolyte disorder in patients with cirrhosis. This disorder can be a result of substantial loss of extracellular fluid "hypotonic or hypovolemic hyponatremia" or develop in the context of an increase in extracellular fluid volume and in the absence of major sodium losses; this situation occurs in patients with advanced cirrhosis and is known as "dilutional or hypervolemic hyponatremia". In dilutional or hypervolemic hyponatremia, serum sodium concentration is reduced, plasma volume is increased (although the effective plasma volume is decreased due to marked arterial vasodilation in the splanchnic circulation) and extracellular fluid volume is increased, with ascites and edema in the absence of signs of dehydration. This is a result of the marked deterioration in renal excretion of solute-free water, leading to disproportionate water retention in relation to sodium retention. Hypotonic hyponatremia represents 10% of all hyponatremias in patients with cirrhosis. Since hypervolemic hyponatremia is by far the most frequent form of this disorder, the present chapter will concentrate specifically on hypervolemic hyponatremia in cirrhosis.

Topics: Antidiuretic Hormone Receptor Antagonists; Ascites; Blood Volume; Contraindications; Disease Progression; Diuresis; Extracellular Fluid; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Liver Cirrhosis; Liver Transplantation; Natriuresis; Prognosis; Saline Solution, Hypertonic; Splanchnic Circulation; Vasodilation; Vasopressins

The non-peptide vasopressin antagonists (VPA), called vaptans, were developed in the 1990s to antagonize both the pressor and antidiuretic effects of vasopressin. There are three subtypes of VPA receptors: V1a, V1b and V2. V1a receptors are widely distributed in the body, mainly the blood vessels and myocardium. The V1b receptors are located mainly in the anterior pituitary gland and play a role in ACTH release. V2 receptors are located in the collecting tubular renal cells. Both V1a and V1b receptors act through the intracellular phosphoinositol signalling pathway, Ca(++) being the second messenger. V2 receptors work through AMPc generation, which promotes aquaporin 2 (AQP2) trafficking and allows water to enter the cell. The vaptans act competitively at the AVP receptor. The most important are mozavaptan, lixivaptan, satavaptan and tolvaptan, all of which are selective V2 antagonists and are administered through the oral route. In contrast, conivaptan is a dual V1 and V2 antagonist administered through the endovenous route. The main characteristics of vaptans are their effect on free water elimination without affecting electrolyte excretion. There are several studies on the effects of these drugs in hypervolemic hyponatremia (heart failure, hepatic cirrhosis) as well as in normovolemic hyponatremia (inappropriate secretion of ADH [SIADH]). Current studies show that the vaptans are effective and well tolerated, although knowledge of these drugs remains limited. There are no studies of the use of vaptans in severe hyponatremia. Osmotic demyelination syndrome due to excessively rapid correction of hyponatremia has not been described.

Topics: Adult; Antidiuretic Hormone Receptor Antagonists; Aquaporin 2; Benzamides; Benzazepines; Calcium Signaling; Clinical Trials as Topic; Cyclic AMP; Double-Blind Method; Drug Therapy, Combination; Heart Failure; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney Tubules, Collecting; Liver Cirrhosis; Morpholines; Multicenter Studies as Topic; Neoplasms; Pituitary Gland, Anterior; Pyrroles; Randomized Controlled Trials as Topic; Receptors, Vasopressin; Second Messenger Systems; Spiro Compounds; Tolvaptan; Vasopressins

Intensive care patients often suffer from hypo- or hypernatremia. These dysnatremias reflect an antidiuretic-hormone (ADH)-related water imbalance and are the result of the underlying disease. However, they are often triggered by drug side effects and exacerbated by an intentional or unintentional sodium imbalance. Dysnatremias are also caused by artificial ventilation; however, the mechanisms behind this are beyond the scope of this article. Considerations regarding etiology, water and sodium balance and, in particular, the variable in urine dilution or concentration, take priority over a brisk normalization of sodium concentration. Therefore, the 3 most important factors are: 1) delivery of water and sodium to the collecting duct; 2) generation and maintenance of an osmotic pressure gradient exerted by solutes present in the renal medullary interstitium; 3) the regulated water permeability of collecting duct cells under the control of antidiuretic hormone. With these, most disorders can already be identified from patient history and simple factors such as body weight and serum and urine osmolality.

Topics: Critical Care; Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Sodium; Vasopressins; Water-Electrolyte Imbalance

The vasopressin system is complex and interacts with the central nervous, cardiovascular, renal, and hematological systems. Vasopressin plays an important role in the control of blood osmolarity and vascular tone, but is also involved in many other physiological events, which are mediated mainly via three types of vasopressin receptor: V1R, V2R, and V3R. V1R primarily mediate the vascular, and V2R the aquaretic, effects of vasopressin. Vasopressin may also interact with other receptors, like adrenergic and angiotensin-II receptors, or with distinct biological pathways, including those of nitric oxide and the K(ATP) channel. There are numerous clinical situations where vasopressin receptor modulators (agonists or antagonists) could be used. Currently, vasopressin and terlipressin are most commonly used to stimulate V1R in vasodilatory shock and cardiac arrest, while desmopressin, a synthetic analogue of vasopressin, acts on V2R; but new molecules are becoming available in the treatment of inappropriate antidiuretic hormone (ADH) secretion.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Brain Diseases; Cardiovascular Diseases; Clinical Trials as Topic; Drugs, Investigational; Hemorrhage; Humans; Inappropriate ADH Syndrome; Receptors, Vasopressin; Skin Diseases; Vasopressins

Hyponatremia, defined by a serum sodium concentration of less than 135 mmmol/l, is a complex clinical occurrence frequently manifested in newborns admitted to the neonatal intensive care unit. The pathogenetic mechanisms and clinical timing underlying the onset of hyponatremia have not been well established in the newborn. Aim of this review is to present a practical approach and management of hypotonic hyponatremia in newborns, with particular emphasis on nephrogenic syndrome of inappropriate antidiuresis, recently described by us for the first time in the literature in a newborn.

Topics: Administration, Oral; Diabetes Insipidus, Nephrogenic; Female; Fluid Therapy; Humans; Hyponatremia; Hypoxia-Ischemia, Brain; Inappropriate ADH Syndrome; Infant; Infant, Newborn; Male; Neurophysins; Polymorphism, Single Nucleotide; Protein Precursors; Syndrome; Urea; Vasopressins

Patients with thymoma are likely to present with associated autoimmunologic disorders. The occurrence of syndrome of inappropriate antidiuretic hormone (SIADH) attributable to thymoma is extremely rare. We herein present an extremely rare case of a 59-year-old man patient who was discovered to have malignant thymoma associated with myasthenia gravis, Graves' disease, and SIADH. He was admitted for evaluation and treatment of hyponatremia (Na 125 mEq/l). SIADH was diagnosed, and thymoma was identified as its cause. The patient was also found to have both Graves' disease and myasthenia gravis. The hyponatremia was normalized with water restriction and 3% saline therapy before thymectomy. The thymic tumor was a Masaoka stage III thymoma that resulted in direct invasion to the wall of the innominate vein, but there was no finding of invasion to other mediastinal organs. Complete thymectomy with innominate vein graft was performed. Microscopic histopathology findings corresponded to those of a mixed-type thymoma and type B2. However, immunohistochemical stain for antidiuretic hormone was negative in the tumor cells. Adjuvant radiation therapy was employed postoperatively, and the patient's postoperative recovery was uneventful. He subsequently reached a euthyroid state. And the reversal to normal sodium and osmolality levels was continued after the tumor removal without any further management for hyponatremia. The observation of this interesting case and a literature review provided us with the opportunity to explore the pathogenesis and clinical aspects of thymoma-related autoimmune and/or endocrine disorders which must be suspected in patients with thymoma.

Topics: Graves Disease; Humans; Immunohistochemistry; Inappropriate ADH Syndrome; Male; Middle Aged; Myasthenia Gravis; Thymectomy; Thymoma; Thymus Neoplasms; Vasopressins

Etiopathogenesis, diagnostics and therapy of hyponatremias are summarized for clinicians. Hyponatremia is the most common electrolyte abnormality. Mild to moderate hyponatremia and severe hyponatremia are found in 15-30% and 1-4% of hospitalized patients, respectively. Pathophysiologically, hyponatremias are classified into two groups: hyponatremia due to non-osmotic hypersecretion of vasopressin (hypovolemic, hypervolemic, euvolemic) and hyponatremia of non-hypervasopressinemic origin (pseudohyponatremia, water intoxication, cerebral salt wasting syndrome). Patients with mild hyponatremia are almost always asymptomatic. Severe hyponatremia is usually associated with central nervous system symptoms and can be life-threatening. Diagnostic evaluation of patients with hyponatremia is directed toward identifying the extracellular fluid volume status, the neurological symptoms and signs, the severity and duration of hyponatremia, the rate at which hyponatremia developed. The first step to determine the probable cause of hyponatremia is the differentiation of the hypervasopressinemic and non-hypervasopressinemic hyponatremias with measurement of plasma osmolality, glucose, lipids and proteins. For further differential diagnosis of hyponatremia, the determination of urine osmolality, the clinical assessment of extracellular fluid volume status and the measurement of urine sodium concentration provide important information. The most important representative of euvolemic hyponatremias is SIADH. The diagnosis of SIADH is based on the exclusion of other hyponatremic conditions; low plasma osmolality (<275 mosmol/kg) and inappropriate urine concentration (urine osmolality >100 mosmol/kg) are of pathognomic value. Acute (<48 hrs) severe hyponatremia (<120 mmol/l) necessitates emergency care with rapid restoration of normal osmotic milieu (1 mmol/l/hr increase rate of serum sodium). Patients with chronic symptomatic hyponatremia have a high risk of osmotic demyelination syndrome in brain if rapid correction of the plasma sodium occurs (maximal rate of correction of serum sodium should be 0.5 mmol/l/hr or less). The conventional treatments for chronic asymptomatic hyponatremia (except hypovolemic patients) include water restriction and/or the use of demeclocycline or lithium or furosemide and salt supplementation. Vasopressin receptor antagonists have opened a new forthcoming therapeutic era. V2 receptor antagonists, such as lixivaptan, tolvaptan, satavaptan and the V2+

Topics: Antidiuretic Hormone Receptor Antagonists; Azepines; Benzamides; Benzazepines; Blood Volume; Brain Diseases; Central Nervous System; Chronic Disease; Demeclocycline; Demyelinating Diseases; Diagnosis, Differential; Diuretics; Extracellular Fluid; Furosemide; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lithium Compounds; Morpholines; Osmolar Concentration; Osmosis; Pyrroles; Severity of Illness Index; Sodium; Spiro Compounds; Time Factors; Tolvaptan; Vasopressins

Causes of hyponatremia in children include the syndrome of appropriate antidiuretic hormone secretion, the syndrome of inappropriate antidiuretic hormone secretion and cerebral salt wasting. The purpose of this review is to distinguish these possibilities, focusing on cerebral salt wasting.. Most cases of hyponatremia in children are due to the syndrome of appropriate antidiuretic hormone secretion. The syndrome of inappropriate antidiuretic hormone secretion can be seen with neurological injury, pain and medication use. Recent studies suggest that cerebral salt wasting is a rare cause of hyponatremia. When cerebral salt wasting is diagnosed, it is often difficult to make a direct link with the central nervous system insult.. The clinical condition, assessment of extracellular fluid space volume status, measurement of urinary electrolytes and responses to infusion of saline solutions can distinguish between syndrome of appropriate antidiuretic hormone secretion, syndrome of inappropriate antidiuretic hormone secretion and cerebral salt wasting. The word 'cerebral' in 'cerebral salt wasting syndrome' can thus be inappropriate, conveying inaccurate causation.

Topics: Brain Injuries; Child; Diagnosis, Differential; Humans; Hyponatremia; Hypovolemia; Inappropriate ADH Syndrome; Sodium; Vasopressins

Total body water and tonicity is tightly regulated by renal action of antidiuretic hormone (ADH), reninangiotensin-aldosterone system, norepinephrine and by the thirst mechanism. Abnormalities in water balance are manifested as sodium disturbances--hyponatremia and hypernatremia. Hyponatremia ([Na+ < 136 meq/ l]) is a common abnormality in hospitalized patients and is associated with increased morbidity and mortality. A common cause of hyponatremia is impaired renal water excretion either due to low extracellular fluid volume or inappropriate secretion of ADH. Clinical assessment of total body water and urine studies help in determining cause and guiding treatment of hyponatremia. Acute and severe hyponatremia cause neurological symptoms necessitating rapid correction with hypertonic saline. Careful administration and monitoring of serum [Na+] is required to avoid overcorrection and complication of osmotic demyelination. Vasopressin receptor antagonists are being evaluated in management of euvolemic and hypervolemic hyponatremia. Hypematremia ([Na+] > 145 meq/l) is caused by primary water deficit (with or without Na+ loss) and commonly occurs from inadequate access to water or impaired thirst mechanism. Assessment of the clinical circumstances and urine studies help determine the etiology, while management of hypernatremia involves fluid resuscitation and avoiding neurological complications from hypernatremia or its correction. Frequent monitoring of [Na+] is of paramount importance in the treatment of sodium disorders that overcomes the limitations of prediction equations.

Topics: Antidiuretic Agents; Antidiuretic Hormone Receptor Antagonists; Fluid Therapy; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Sodium Chloride; Vasopressins; Water-Electrolyte Balance

Topics: Aquaporin 2; Body Water; Dehydration; Diabetes Insipidus; Edema; Humans; Inappropriate ADH Syndrome; Kidney Concentrating Ability; Mutation; Osmolar Concentration; Sodium; Vasopressins

Hyponatremia is a common clinical problem in hospitalized patients and nursing home residents. It also may occur in healthy athletes after endurance exercise. The majority of patients with hyponatremia are asymptomatic and do not require immediate correction of hyponatremia. Symptomatic hyponatremia is a medical emergency requiring rapid correction to prevent the worsening of brain edema. How fast we should increase the serum sodium levels depends on the onset of hyponatremia and still remains controversial. If the serum sodium levels are corrected too rapidly, patients may develop central pontine myelinolysis, but if they are corrected too slowly, patients may die of brain herniation. We review the epidemiology and mechanisms of hyponatremia, the sensitivity of women to hyponatremic injury, the adaptation and maladaptation of brain cells to hyponatremia and its correction, and the practical ways of managing hyponatremia. Because the majority of hyponatremia is caused by the non-osmotic release of vasopressin, the recent approval of the vasopressin receptor antagonist conivaptan for euvolemic hyponatremia may simplify hyponatremia management. However, physicians should be aware of the risk of rapid correction of hyponatremia, hypotension, and excessive fluid intake.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Brain; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Kidney Concentrating Ability; Kidney Tubules, Collecting; Male; Osmolar Concentration; Vasopressins

Topics: Cushing Syndrome; Edema; Humans; Hyperaldosteronism; Hypertension; Hypokalemia; Hyponatremia; Inappropriate ADH Syndrome; Mineralocorticoid Excess Syndrome, Apparent; Renin-Angiotensin System; Vasopressins

Topics: Aquaporin 2; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Humans; Hyponatremia; Hypothalamus; Inappropriate ADH Syndrome; Mutation; Receptors, Vasopressin; Vasopressins

Topics: Body Water; Diabetes Insipidus; Electrolytes; Humans; Hyperaldosteronism; Hypertension; Hypoaldosteronism; Inappropriate ADH Syndrome; Natriuretic Peptides; Renin-Angiotensin System; Vasopressins; Water-Electrolyte Imbalance

Topics: Arginine Vasopressin; Body Water; Diabetes Insipidus, Neurogenic; Diagnosis, Differential; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Kidney Tubules, Collecting; Osmolar Concentration; Vasopressins

Hyponatremia is the most frequent electrolyte disorder encountered in hospitalized patients. It is a state of relative water excess due to stimulated arginine vasopressin (AVP) and fluid intake greater than obligatory losses. This kind of hyponatremia occurs in the syndrome of inappropriate antidiuretic hormone secretion, congestive heart failure, and liver cirrhosis. Fluid restriction is the presently recommended treatment for hyponatremia. However, fluid restriction may be very difficult for patients to achieve, is slow to work, and does not allow a graded therapeutic approach. More efficient and specific treatments of hyponatremia are needed. In this respect, pharmacologic research has yielded a number of compounds exhibiting antagonistic qualities at the vasopressin V2 receptor. Among these agents, peptidic derivatives of AVP turned out to have intrinsic antidiuretic properties in vivo when given over days or weeks. The development of such agents for use in patients has not been pursued. However, several promising nonpeptide, vasopressin receptor antagonists have been described; these agents are VPA-985 (lixivaptan), YM-087 (conivaptan), OPC-41061 (tolvaptan), and SR-121463. Prospective, randomized, placebo-controlled trials performed with these agents found that they corrected hyponatremia efficiently and safely. Most of the studies were conducted over a 4- to 28-day period. Long-term studies will be needed in the future to address such issues as the eventual benefit to patients and the effects of vasopressin antagonists on morbidity and mortality of patients with hyponatremia.

Topics: Antidiuretic Hormone Receptor Antagonists; Azepines; Benzamides; Benzazepines; Humans; Hyponatremia; Inappropriate ADH Syndrome; Morpholines; Pyrroles; Randomized Controlled Trials as Topic; Spiro Compounds; Tolvaptan; Vasopressins

Charles Darwin, in his Origin of the Species, noted that different species of finches on the Galapagos Islands had adapted their beak size based on where they sought their food. Homer Smith, in his book From Fish to Philosopher, discussed the evolution of the nephron from a single conduit in salt water vertebrates, to nephrons with large glomerular capillaries and proximal and distal tubules in fresh water vertebrates, to smaller glomerular capillaries in amphibians, to nephrons with loops of Henle to allow for urinary concentration and dilution in mammals. The kidney with its million nephrons has emerged as the vital organ for regulating body fluid composition and volume. With the recent discovery of aquaporin water channels, our understanding of volume regulation has been greatly enhanced. This article reviews current knowledge regarding: 1) the unifying hypothesis of body fluid volume regulation; 2) brain aquaporins and their role in pathophysiologic states; and 3) function and regulation of renal aquaporins in the syndrome of inappropriate antidiuretic hormone secretion (SIADH).

Topics: Animals; Aquaporins; Body Water; Brain; Finches; Fishes; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Vasopressins; Water-Electrolyte Balance

Topics: Humans; Inappropriate ADH Syndrome; Liver Cirrhosis; Vasopressins

Vasopressin, or antidiuretic hormone, is a peptide hormone that is released from the posterior pituitary gland in response to changes in blood pressure and plasma osmolality. The main pathophysiological states associated with high plasma vasopressin concentrations are cirrhosis, cardiac failure and syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Pharmacological treatments for disorders of excess vasopressin secretion have been limited. However, oral bio-available selective and non-selective V(1) and V(2) receptor antagonists have recently become available for clinical use. Water retention in cirrhosis is a common problem, leading to ascites, peripheral oedema and hyponatraemia. Raised plasma vasopressin concentrations and decreased delivery of glomerular filtrate are believed to be the most important factors in the development of water retention. V(2) receptor antagonists are aquaretic agents that promote water excretion and improve hyponatraemia. Their potential role in cirrhosis has been examined in a number of recent studies that have shown increased free water clearance and serum sodium concentrations with few adverse effects. V(2) receptor antagonists represent a novel and promising new class of agent that may have major clinical utility in the treatment of patients with liver cirrhosis.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Azepines; Benzamides; Benzazepines; Controlled Clinical Trials as Topic; Diuretics; Heart Failure; Homeostasis; Humans; Inappropriate ADH Syndrome; Liver Cirrhosis; Models, Animal; Morpholines; Piperidines; Pyrroles; Quinolones; Rats; Spiro Compounds; Vasopressins

Topics: Azepines; Benzamides; Brain Diseases, Metabolic; Humans; Hyponatremia; Inappropriate ADH Syndrome; Liver Cirrhosis; Pyrroles; Vasopressins

In humans and most other mammals, the antidiuretic hormone (ADH) is a nonapeptide often referred to as arginine vasopressin (AVP). It is produced by large neurons that originate in the supraoptic and paraventricular nucleus of the hypothalamus and project through the pituitary stalk to terminate on capillary plexuses scattered throughout the posterior pituitary. These plexuses drain into the systemic circulation by way of the cavernous sinus and superior vena cava.

Topics: Arginine Vasopressin; Humans; Hypernatremia; Inappropriate ADH Syndrome; Vasopressins

The syndrome of inappropriate secretion of antidiuretic hormone (ADH) was recognized in a 68-year-old man with a poorly differentiated metastatic adenocarcinoma of the prostate. Elevated levels of ADH were found in the tissues of the primary tumor and lymph node metastasis. The patient's clinical course is detailed and the pathophysiology of this syndrome is discussed. To our knowledge, this case is the ninth reported case of syndrome of inappropriate secretion of ADH with adenocarcinoma of the prostate. Antidiuretic hormone activity was proven in only three cases including this case.

Topics: Adenocarcinoma; Aged; Diagnosis, Differential; Diethylstilbestrol; Humans; Inappropriate ADH Syndrome; Lymphatic Metastasis; Male; Prostate-Specific Antigen; Prostatic Neoplasms; Sodium; Vasopressins

Patients who drink more electrolyte-free water than they can excrete may develop hyponatremia. A subgroup of hyponatremic patients has a reduced excretion of electrolyte-free water and a low rate of excretion of solutes even though vasopressin is not detected in their plasma. Basal water permeability in the distal nephron, by permitting a limited volume of electrolyte-free water to be reabsorbed, offers a way to help explain these findings. Basal water permeability will also be considered from the perspective of integrative physiology in evolutionary and developmental biology settings. Its possible clinical importance will be explored in patients with chronic hyponatremia who have a low distal volume delivery. These patients may develop osmotic demyelination if a large solute load leads to a very rapid excretion of electrolyte-free water.

Topics: Capillary Permeability; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney Tubules, Collecting; Nephrons; Syndrome; Vasopressins; Water-Electrolyte Balance

Topics: Diabetes Insipidus; Diagnosis, Differential; Diuretics; Humans; Inappropriate ADH Syndrome; Vasopressins; Water-Electrolyte Imbalance

Disorders of the serum sodium concentration (hypo- and hypernatremia) are amongst the most frequent electrolyte disorders in clinical medicine. They are attributable to disturbance of to water metabolism. Hyponatremia is almost always a condition of water excess while hypernatremia is due water deficiency. Physiological normonatremia (normal plasma osmolality) is maintained by an integrated system involving regulated water intake via thirst and control of water excretion via antidiuretic hormone secretion. Therefore hypo- and hypernatremia should be analyzed in terms of dysregulated ADH secretion, fluid intake and renal water excretion. Hyponatremia is usually a disorder of vasopressin excess, due to 'non-osmotic' vasopressin release. The latter may occur in two different settings: (I) SIADH, (II) baroreceptor mediated vasopressin secretion (cardiac failure, liver cirrhosis). This entities are easy to distinguish in clinical practice. SIADH is associated with striking lower plasma concentrations of urate, creatinine and urea. In SIADH the blood pressure is normal and there is no edema. In contrast in the hyponatremia of liver cirrhosis and heart failure the plasma measurements indicated are usually slightly elevated, the blood pressure is low and there is edema. The typical patient with hypernatremia is old and has no thirst sensation. Hypo- or hypernatremia may cause major neurologic symptoms. These symptoms are more related to the rate of change in the serum sodium concentration than to the absolute level of a hypo- or hypernatremia reached. The traditional treatment for hyponatremia used to be water restriction. However V2-Vasopressin-Antagonists may provide a better treatment modality in the future. Hypernatremia is treated by slow rehydratation.

Topics: Diagnosis, Differential; Drinking; Fluid Therapy; Heart Failure; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Liver Cirrhosis; Vasopressins

An 88-year-old patient with a poorly differentiated adenocarcinoma of the prostate gland was found to have all cardinal findings of syndrome of inappropriate antidiuretic hormone secretion (SIADH). Elevated levels of antidiuretic hormone were found in the patient's serum and in the prostatic tumor and the cytoplasms of the tumor was positive for prostate specific antigen and was faintly positive for antidiuretic hormone (ADH). He responded well to combination therapy of androgen blockade with leuprorelin acetate and flutamide, and laboratory findings of SIADH and serum ADH level returned to normal. However, he died of sudden profuse bleeding caused by gastric ulcers 6 months after the therapy. Ten cases of SIADH caused by prostatic cancer have been reported including the present case.

Topics: Adenocarcinoma; Aged; Androgen Antagonists; Antineoplastic Agents, Hormonal; Flutamide; Humans; Inappropriate ADH Syndrome; Leuprolide; Male; Paraneoplastic Endocrine Syndromes; Prostatic Neoplasms; Treatment Outcome; Vasopressins

Topics: Diagnosis, Differential; Humans; Hyponatremia; Inappropriate ADH Syndrome; Neoplasms; Osmotic Pressure; Plasma Volume; Prognosis; Vasopressins; Water Deprivation

Topics: Animals; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Kidney Concentrating Ability; Vasopressins; Water-Electrolyte Balance

Hyponatremia in virtually all patients results from water retention due to an inability to excrete ingested water. In most cases, this defect represents the persistent secretion of ADH (such as in effective circulating volume depletion, and in the syndrome of inappropriate ADH secretion), although free water excretion can also be limited in disorders in which ADH levels may be appropriately suppressed (such as in advanced renal failure, and in primary polydipsia). The symptoms of hyponatremia primarily reflect neurologic dysfunction induced by cerebral edema and are related both to the severity and to the rapidity of reductions in the plasma sodium concentration. The degree of cerebral edema which occurs in acute hyponatremia is much less with chronic hyponatremia, because the brain cells lose solutes, leading to the osmotic movement of water out the cells and less brain swelling. In general, hyponatremia is corrected acutely by giving Na+ to patients who are volume-depleted and by restricting water intake in patients who are normovolemic or edematous. The optimal rate of correction should be defined to prevent the risk of central demyelinating lesions.

Topics: Adrenal Insufficiency; Adult; Brain Edema; Edema; Female; Humans; Hyponatremia; Hypothyroidism; Inappropriate ADH Syndrome; Kidney Failure, Chronic; Models, Biological; Osmolar Concentration; Potassium; Pregnancy; Syndrome; Vasopressins

Topics: Atrial Natriuretic Factor; Biomarkers; Humans; Hyperaldosteronism; Hypothyroidism; Inappropriate ADH Syndrome; Vasopressins; Water-Electrolyte Balance

Thirst and drinking are essential components of normal osmoregulation in healthy man. Abnormalities of thirst appreciation, in particular hypodipsia, have profound implications for water homeostasis. The combination of cranial diabetes insipidus and hypodipsia can have particularly serious consequences, with the potential for life-threatening hyponatraemia. Although the tools for measuring thirst are subjective and lack true specificity, their use in clinical research has contributed greatly to our understanding of the physiology of thirst appreciation and the abnormal control of thirst in osmoregulatory disorders. The precise neural control of thirst appreciation remains unknown, and perhaps as a result of this, satisfactory therapies for the treatment of disorders of thirst have not yet been developed; behavioural modification and retraining of drinking habits remain the rather limited cornerstones of management.

Topics: Adult; Aged; Aging; Brain Neoplasms; Diabetes Insipidus; Diabetes Mellitus; Drinking; Humans; Inappropriate ADH Syndrome; Middle Aged; Schizophrenia; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Diabetes Insipidus; Diagnosis, Differential; Humans; Inappropriate ADH Syndrome; Pituitary Function Tests; Pituitary Gland, Posterior; Polyuria; Vasopressins; Water; Water Deprivation

The aquaporins are a recently recognized family of water channels that mediate water transport in kidney and in other organs. Aquaporin-2, 'vasopressin-regulated water channel', is regulated by vasopressin in two ways to account for overall control of collecting duct water permeability. First, vasopressin has a short-term effect in triggering translocation of aquaporin-2-containing intracytoplasmic vesicles to the apical plasma membrane, thus increasing principal cell water permeability. Second, vasopressin has a long-term effect in increasing the abundance of aquaporin-2 in collecting duct principal cells, increasing the maximal attainable water permeability. Using animal models, defects in these control mechanisms have been shown to be associated with several disorders of water balance, including central diabetes insipidus, congenital nephrogenic diabetes insipidus, acquired diabetes insipidus, syndrome of inappropriate antidiuretic hormone secretion, and several extracellular fluid volume expanded states.

Topics: Animals; Aquaporin 2; Aquaporin 6; Aquaporins; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Drinking; Extracellular Space; Humans; Inappropriate ADH Syndrome; Ion Channels; Kidney Tubules, Collecting; Vasopressins; Water-Electrolyte Imbalance

Topics: Animals; Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Mutation; Vasopressins

Topics: Animals; Body Water; Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Vasopressins

Hyponatremia is the most frequent electrolyte disorder in clinical medicine. It is usually attributable to primary vasopressin excess, causing the syndrome of inappropriate antidiuresis (SIAD), or to secondary vasopressin stimulation, involving a baroreceptor mechanism. The latter is regularly found in the hyponatremia of liver cirrhosis, cardiac failure and volume contraction. In the first kind of setting the concentrations of creatinine, urea and urate in plasma will be low because of the associated volume expanded state. In the second type of setting they will be elevated because of the circulatory compromise of these patients. The hyponatremia of SIAD may be treated by water restriction, furosemide and substitution of the inadvertent sodium losses by giving 3% NaCl. Baroreceptor hyponatremia is best treated by fluid restriction together with judiciously administered saline. In correcting severe chronic hyponatremia, the rate of correction should not exceed 1 mM/l/h and the corrected serum sodium concentration should not be higher than 130 mM/l. In the foreseeable future oral non-peptide oral vasopressin antagonists will become available. They are expected to become new tools for the treatment of hyponatremia.

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Pressoreceptors; Vasopressins

The physiology of the release of antidiuretic hormone (ADH) from the posterior pituitary is briefly reviewed. The importance of both osmolar and non-osmolar stimuli is emphasised. Osmolar and non-osmolar factors usually reinforce each other; for example, hydropenia leads to hyperosmolality and hypovolaemia, both promoting ADH release, while hydration has the opposite effect. In disease, osmolar and non-osmolar factors may become dissociated leading to baroreceptor-mediated ADH release in the presence of hyponatraemia and hypo-osmolality. Examples include heart failure, glucocorticoid or thyroxine deficiency, hepatic cirrhosis and nephrotic syndrome with or without the superimposed effect of diuretics, i.e. conditions in which circulatory, and in particular effective arterial, volume is reduced. It is dangerous to label such conditions as 'inappropriate' secretion of ADH since the maintenance of circulating volume is at least as important a physiological requirement as the defence of tonicity. The syndrome of inappropriate secretion of ADH (SIADH) is uncommon in childhood and should only be diagnosed when physiological release of ADH in response to non-osmolar as well as osmolar factors has been excluded. Criteria for the correct identification of SIADH are discussed; the presence of continuing urinary sodium excretion in the presence of hyponatraemia and hypo-osmolality is essential to the diagnosis. SIADH in children is usually due to intracranial disease or injury. The mainstay of treatment is water restriction which reverses all the physiological abnormalities of the condition. Hypertonic saline is rarely indicated for the short-term control of neurological manifestations such as seizures. Drugs have little or no place in the treatment of SIADH in children.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Humans; Inappropriate ADH Syndrome; Osmolar Concentration; Pituitary Gland, Posterior; Vasopressins

Hyponatraemia is very common in AIDS patients. It is observed in about 40-50% of hospitalized patients. It may contribute to overall mortality in advanced disease. Vasopressin measurements in these patients basically present two distinct syndromes: hyponatraemia and 'normal' vasopressin levels (i.e. measurable vasopressin) and hyponatraemia with suppressed vasopressin. Hyponatraemia with suppressed vasopressin is very rare and has only been observed in AIDS patients with dementia and primary polydipsia. Hyponatraemia and measurable vasopressin can be also divided into two syndromes. In some patients vasopressin is 'appropriately' elevated, i.e. in those with body fluid losses (diarrhoea) or chronic hypovolaemia (adrenal failure); these patients also present with hyperuricaemia and other signs of low blood volume. In other patients vasopressin is 'inappropriately' elevated in those with no clinical evidence of hypovolaemia (typically characterized by low serum uric acid levels) such as in Pneumocystis carinii pneumonia and other opportunistic infections leading to SIADH. CSWS is a relatively frequent complication in some patients with cerebral infection or tumour. High-dose trimethoprim (for Pneumocystis carinii prevention) acts as an amiloride-like drug and induces a clinical state characterized by hyponatraemia and hyperkalaemia which is indistinguishable from hyporeninaemic hypoaldosteronism. The mechanism of the hyponatraemia caused by other drugs (miconazole, pentamidine, amphotericin, vidarabine) is not as yet known.

Topics: Acquired Immunodeficiency Syndrome; Adrenal Insufficiency; Humans; Hyponatremia; Inappropriate ADH Syndrome; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Biomarkers, Tumor; Carcinoma, Small Cell; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Neoplasms; Neurophysins; Oxytocin; RNA, Messenger; Vasopressins

Topics: Adult; Age Factors; Aged; Electrolytes; Female; Humans; Inappropriate ADH Syndrome; Japan; Male; Middle Aged; Sex Factors; Sodium; Vasopressins

Topics: Adrenocorticotropic Hormone; Aged; Aged, 80 and over; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Vasopressins

In tuberculous meningitis there is a disturbance of control involving hyponatraemia and increased urinary elimination of antidiuretic hormone resulting in hypersecretion of vasopressin. This inappropriate secretion of antidiuretic hormone should not be confused with the Schwartz-Bartter syndrome, which is reserved for paraneoplastic syndromes. The pathophysiology remains poorly understood but its recognition in cases of lymphocytic meningitis is improved as the correct diagnosis has precise therapeutic implications.

Topics: Aged; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Tuberculosis, Meningeal; Vasopressins

Topics: Adenocarcinoma; Aged; Female; Hormones, Ectopic; Humans; Inappropriate ADH Syndrome; Stomach Neoplasms; Vasopressins

A great deal of information has been accumulated on the synthesis and release of AVP, oxytocin, and their associated neurophysins under normal circumstances. In 1957, Schwartz and Bartter first described SIAD in patients with lung cancer and postulated that the clinical findings were the results of excessive vasopressin secretion. Tumors have been known since 1964 to produce vasopressin, and small cell (oat cell) carcinoma of the lung is by far the most frequent malignant cause of SIAD. The biosynthetic pathway for the synthesis of AVP and its associated neurophysin (and to a lesser extent, oxytocin and its neurophysin) is well described and is similar if not identical to the synthesis of these peptides in the hypothalamus. However, there is little reliable information on the control of peptide synthesis and release by these tumors. The clinical picture of SIAD is well described and occurs in 20% to 40% of patients with SCCL, although up to 88% of patients with extensive SCCL have elevated circulating levels of one or more neurohypophyseal peptides. This information has led to considerable interest in the use of these peptides as tumor markers for the diagnosis, evaluation, and assessment of therapy in these patients. With the recognition of the high incidence of secretion of neurohypophyseal peptides by SCCL, studies have been initiated to determine the value of radioactive vasopressin neurophysin antibodies in localizing tumors that synthesize these peptides. The studies provide potentially useful information in diagnosing and following patients with SCCL and also offer some promise that radiolabeled antineurophysins could eventually be used to treat these patients.

Topics: Biomarkers, Tumor; Fluid Therapy; Hormones, Ectopic; Humans; Hypothalamic Hormones; Hypothalamus; Inappropriate ADH Syndrome; Neurophysins; Oxytocin; Paraneoplastic Endocrine Syndromes; Sodium; Vasopressins

Disorders of water homeostasis are common in psychiatric patients and include compulsive water drinking, the syndrome of inappropriate antidiuretic hormone secretion (SIADH), and the syndrome of self-induced water intoxication (SIWI). Although water intoxication was recognized nearly 70 years ago, the physiological basis of these disorders of water metabolism still remains elusive. This review will provide a historical overview, critique current studies on compulsive water drinking and SIWI, discuss possible etiologies, and present current approaches to treatment of these disorders. Because of the complexity of the subject, a review of normal water homeostasis and the SIADH will be included.

Topics: Drinking; Humans; Hyponatremia; Inappropriate ADH Syndrome; Mental Disorders; Psychotropic Drugs; Thirst; Vasopressins; Water Intoxication

Topics: Blood Volume; Combined Modality Therapy; Heart Failure; Humans; Hyponatremia; Inappropriate ADH Syndrome; Liver Cirrhosis; Nephrotic Syndrome; Vasopressins

Topics: Diagnosis, Differential; Humans; Inappropriate ADH Syndrome; Vasopressins; Water-Electrolyte Imbalance

Topics: Adrenocorticotropic Hormone; Animals; Arachidonic Acids; Cattle; Diabetes Insipidus; Glycolysis; Humans; Inappropriate ADH Syndrome; Liver; Pituitary Diseases; Pituitary Gland, Posterior; Rats; Second Messenger Systems; Signal Transduction; Vasopressins

Topics: Animals; Body Water; Homeostasis; Humans; Hyponatremia; Inappropriate ADH Syndrome; Nutritional Physiological Phenomena; Sodium Chloride; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: ACTH Syndrome, Ectopic; Adrenocorticotropic Hormone; Aged; Chorionic Gonadotropin; Diagnosis, Differential; Female; Hormones, Ectopic; Humans; Hypercalcemia; Inappropriate ADH Syndrome; Male; Middle Aged; Paraneoplastic Endocrine Syndromes; Vasopressins

Topics: Body Water; Diuretics; Extracellular Space; Glucocorticoids; Humans; Hyperlipidemias; Hyponatremia; Inappropriate ADH Syndrome; Kidney Failure, Chronic; Lithium; Lithium Carbonate; Osmolar Concentration; Sodium; Vasodilator Agents; Vasopressins

Topics: Age Factors; Aged; Benzothiadiazines; Body Water; Body Weight; Diuretics; Female; Furosemide; Humans; Hyponatremia; Iatrogenic Disease; Inappropriate ADH Syndrome; Male; Middle Aged; Potassium; Prognosis; Risk; Sex Factors; Sodium; Sodium Chloride; Sodium Chloride Symporter Inhibitors; Vasopressins

Topics: Addison Disease; Aldosterone; Endocrine Glands; Glomerular Filtration Rate; Humans; Hydrocortisone; Inappropriate ADH Syndrome; Kidney; Parathyroid Hormone; Thyroid Hormones; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance; Wounds and Injuries

Topics: Adrenocorticotropic Hormone; Carcinoma, Small Cell; Chorionic Gonadotropin; Cushing Syndrome; Diagnosis, Differential; Gynecomastia; Hormones, Ectopic; Humans; Hypercalcemia; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Vasopressins

Topics: Adrenocorticotropic Hormone; Antigens, Neoplasm; Calcitonin; Calcium Metabolism Disorders; Carcinoembryonic Antigen; Carcinoma, Bronchogenic; Female; Growth Hormone; Hormones; Hormones, Ectopic; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Paraneoplastic Endocrine Syndromes; Pituitary Hormones, Anterior; Prognosis; Secretory Component; Vasopressins

Topics: Animals; Central Nervous System Diseases; Diagnosis, Differential; Humans; Hyponatremia; Hypothalamo-Hypophyseal System; Inappropriate ADH Syndrome; Neoplasms; Nephrons; Vasopressins; Water-Electrolyte Imbalance

Vasopressin is capable of being stimulated by several nonosmotic factors such as hypovolemia, hypotension, pharmacologic agents and stress. Vasopressin levels of only 1-2 pg/ml are capable of decreasing substantially renal water excretion. If water is ingested or given intravenously in this setting, positive water balance with hypotonicity and hyponatremia of extracellular fluid (ECF) occur. Such dilution of the ECF results in water movement into cells and potential central nervous system complications [3]. Many disorders (see Tab. 1) may be associated with nonosmotic stimulation of vasopressin release. In these clinical settings, judicious administration of free water and monitoring of serum sodium concentration is necessary. A knowledge of clinical conditions associated with vasopressin-mediated water retention may have therapeutic implications as well. Thus, in recent years it has become appreciated that selected pharmacologic agents such as lithium and demeclocycline can impair the water retaining property of vasopressin [26]. Although lithium appears too toxic for routine usage, demeclocycline has proved to be efficacious therapy in some patients with high vasopressin levels and hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone who are unable to limit their water intake [9]. More recently, other compounds that selectively antagonize the hydro-osmotic effect of vasopressin are being tested and soon may be available [13].

Topics: Adrenal Cortex Diseases; Blood Volume; Diuresis; Extracellular Space; Humans; Hyponatremia; Hypothyroidism; Inappropriate ADH Syndrome; Liver Cirrhosis; Osmosis; Respiratory Insufficiency; Vasopressins

The osmolality of body fluids is normally maintained within a narrow range. This constancy is achieved largely via hypothalamic osmo-receptors that regulate thirst and arginine vasopressin, the antidiuretic hormone (ADH). Anything that interferes with the full expression of either osmoregulatory function exposes the patient to the hazards of abnormal increases or decreases in plasma osmolality. Hyposmolality is almost always due to a defect in water excretion. Increased intake may contribute to the problem but is rarely, if ever, a sufficient cause. Impaired water excretion can be due to a primary defect in the osmoregulation of ADH (inappropriate antidiuresis) or secondary to nonosmotic stimuli like hypovolemia or nausea. The two types differ in clinical presentation and treatment. Resetting of the ADH osmostat is commonly associated with resetting of the thirst osmostat. Hyperosmolarity is almost always due to deficient water intake. Excessive excretion may contribute to the problem but is never a sufficient cause. Impaired water intake can result from a defect in either the osmoregulation of thirst of the necessary motor responses. Thirst may be deficient because of primary osmoreceptor damage as in the syndrome of adipsic hypernatremia or secondary to nonosmotic influences on the set of the system. They are distinguishable by the clinical presentation as well as the type of ADH defects with which they are associated. So-called essential hypernatremia due to primary resetting of the osmostat has been postulated, but unambiguous evidence for such an entity has not yet been reported.

Topics: Body Water; Hemodynamics; Humans; Inappropriate ADH Syndrome; Osmolar Concentration; Sodium; Thirst; Vasopressins; Water-Electrolyte Imbalance

Topics: Anti-Inflammatory Agents; Chlorpropamide; Diabetes Insipidus; Female; Furosemide; Humans; Inappropriate ADH Syndrome; Male; Polyuria; Vasopressins

Topics: Demeclocycline; Humans; Hypothyroidism; Inappropriate ADH Syndrome; Lithium; Neoplasms; Osmolar Concentration; Vasopressins

Topics: Diuresis; Humans; Inappropriate ADH Syndrome; Kidney; Osmolar Concentration; Polyuria; Vasopressins

Topics: Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Osmolar Concentration; Pituitary Function Tests; Vasopressins

Topics: Animals; Arginine Vasopressin; Chlorpropamide; Deamino Arginine Vasopressin; Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Lypressin; Vasopressins; Water-Electrolyte Imbalance

Arginine vasotocin, arginine vasopressin, and oxytocin play a critical role in the stimulation of labor and delivery and in salt and water homeostasis in the newborn infant. The authors present information on their chemistry, secretion, and metabolism, and discuss the clinical effects upon target organs of their presence or absence.

Topics: Animals; Arginine Vasopressin; Diabetes Insipidus; Female; Fetus; Humans; Inappropriate ADH Syndrome; Infant, Newborn; Infant, Newborn, Diseases; Oxytocin; Pituitary Gland; Pituitary Gland, Posterior; Pituitary Hormones, Posterior; Pregnancy; Vasopressins; Vasotocin

The purpose of this study was to determine the efficacy and safety of tolvaptan in Japanese patients with hyponatremia secondary to syndrome of inappropriate secretion of antidiuretic hormone (SIADH). This multicenter, open-label, dose-escalation, phase III study enrolled Japanese patients (20-85 years old) with hyponatremia secondary to SIADH who were unresponsive to fluid restriction. Oral tolvaptan was administered for up to 30 days, initially at 7.5 mg/day, but escalated daily as necessary, based on the serum sodium concentration and safety, over the first 10 days until the optimal maintenance dose was determined for each patient (maximum 60 mg/day). The primary endpoint was the proportion of patients with normalized serum sodium concentration on the day after the final tolvaptan dose. Secondary endpoints included the mean change in serum sodium concentration from baseline on the day after the final dose. Sixteen patients (male, 81.3%; mean ± standard deviation age 71.9 ± 6.1 years) received tolvaptan treatment and 11 patients completed the study with one patient re-administered tolvaptan in the treatment period. Serum sodium concentrations normalized in 13 of 16 (81.3%) patients on the day after the final tolvaptan dose. The mean change in serum sodium concentration from baseline on the day after the final dose was 11.0 ± 4.3 mEq/L. Adverse events considered related to tolvaptan (10 [62.5%] patients) were generally of mild to moderate severity. Oral tolvaptan corrects hyponatremia in Japanese patients with SIADH with a similar efficacy and safety profile as that noted in non-Japanese patients.

Topics: Administration, Oral; Adult; Aged; Aged, 80 and over; Dose-Response Relationship, Drug; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Japan; Male; Middle Aged; Tolvaptan; Treatment Outcome; Vasopressins; Young Adult

The approach to hyponatremia is in a state of flux, especially in differentiating syndrome of inappropriate antidiuretic hormone secretion (SIADH) from cerebral-renal salt wasting (RSW) because of diametrically opposite therapeutic goals. Considering RSW can occur without cerebral disease, we determined the prevalence of RSW in the general hospital wards.. To differentiate SIADH from RSW, we used an algorithm based on fractional excretion (FE) of urate and nonresponse to saline infusions in SIADH as compared to excretion of dilute urines and prompt increase in serum sodium in RSW.. Of 62 hyponatremic patients, (A) 17 patients (27%) had SIADH, 11 were nonresponsive to isotonic saline, and 5 normalized a previously high FEurate after correction of hyponatremia; (B) 19 patients (31%) had a reset osmostat based on normal FEurates and spontaneously excreted dilute urines; (C) 24 patients (38%) had RSW, 21 had no clinical evidence of cerebral disease, 19 had saline-induced dilute urines; 2 had undetectable plasma ADH levels when urine was dilute, 10 required 5% dextrose in water to prevent rapid increase in serum sodium, 11 had persistently increased FEurate after correction of hyponatremia and 10 had baseline urinary sodium < 20 mEq/L; (D) 1 patient had Addison disease with a low FEurate and (E) 1 patient (1.6%) had hyponatremia due to hydrochlorothiazide.. Of the 24 patients with RSW, 21 had no cerebral disease, supporting our proposal to change cerebral-renal salt wasting to renal salt wasting. Application of established pathophysiological standards and a new algorithm based on determination of FEurate were superior to the volume approach for determination of urinary sodium when identifying the cause of hyponatremia.

Topics: Aged; Aged, 80 and over; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Prevalence; Saline Solution; Uric Acid; Vasopressins

This study investigated the development of hyponatremia and its underlying mechanism in elderly patients prescribed paroxetine. Patients were 15 men and women (mean age, 75.7 +/- 5.3 years) who were participants in a treatment study of late-life depression and who were without medical illness or other medications known to cause hyponatremia or alter antidiuretic hormone (ADH) secretion. Blood samples for measurement of plasma sodium, ADH, blood urea nitrogen (BUN), creatinine, glucose, and osmolality were determined prior to initiation of paroxetine (week 0) and at 2, 4, 6, and 12 weeks of treatment with paroxetine. Hyponatremia (serum sodium < 135 mEq/L) was identified in 6 of 15 patients after 2 weeks of treatment with paroxetine. Despite low plasma osmolality, ADH levels were not suppressed appropriately. Data suggest hyponatremia is a common adverse event in elderly patients prescribed paroxetine and implicates inappropriate secretion of ADH as the potential mechanism.

Topics: Aged; Depressive Disorder, Major; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Osmolar Concentration; Paroxetine; Pilot Projects; Prospective Studies; Selective Serotonin Reuptake Inhibitors; Severity of Illness Index; Vasopressins

Vasopressin-neurophysin (hNpI), oxytocin-neurophysin (hNpII) and blood osmolality were assayed before any treatment in basal conditions in 35 patients suffering from lung carcinoma (20 oat cell, 6 undifferentiated and 9 well-differentiated epidermoid cell carcinomas). Plasma vasopressin (antidiuretic hormone, ADH) was also assayed in 7 of the 20 patients suffering from oat cell carcinoma. We found a close correlation (r = 0.98) between plasma ADH and hNpI levels in the 7 patients. Further, hNpI was elevated in 13 out of the 20 oat cell carcinoma patients and in none of the epidermoid-cell carcinoma group; however, searching for an abnormality of ADH secretion as reflected by a detectable plasma hNpI level together with subnormal plasma osmolality revealed 2 additional positive results in the oat cell carcinoma group, and 2 out of the 6 in the undifferentiated-cell carcinoma group. hNpII was increased together with an increase in hNpI in 6 oat cell carcinoma patients; it was specifically increased without hNpI increment in 2 additional oat cell carcinoma patients and in 2 patients of the undifferentiated-cell carcinoma group (different from the 2 positive for the hNpI-osmolality ratio). hNpI and hNpII were normal in the majority of undifferentiated and all of the differentiated epidermoid-cell carcinoma group. Hence, our results show that simultaneous measurements of hNpI, hNpII, and blood osmolality could detect abnormalities in 17 out of 20 oat cell carcinoma patients, in 4 of the 9 undifferentiated-cell carcinoma patients, but in none of the differentiated epidermoid-cell carcinoma patients, suggesting that the neurophysin assay can be used for the early detection of oat cell- and possibly other neuroendocrine-derived carcinomas.

Topics: Biomarkers, Tumor; Carcinoma, Small Cell; Carcinoma, Squamous Cell; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Neurophysins; Osmolar Concentration; Oxytocin; Vasopressins

Primary central nervous system lymphoma (PCNSL) rarely originates in the hypothalamus. Hypothalamic PCNSL can present with various symptoms specific to dysfunction of the hypothalamus, including consciousness disturbance, cognitive impairment, hypopituitarism, and diabetes insipidus (DI). However, it remains unclear whether syndrome of inappropriate secretion of antidiuretic hormone (SIADH) can present as an initial sign of hypothalamic PCNSL.. Ninety-nine patients with PCNSL were diagnosed between January 2006 and December 2020 at our institutes. The initial symptoms and signs, hypothalamic-pituitary functions, serum sodium (Na) value, Karnofsky Performance Status (KPS) score on admission, and duration from onset to diagnosis were retrospectively investigated from the medical charts.. Eight and 91 patients had hypothalamic PCNSL (hypothalamic group) and PCNSL located in other regions (control group), respectively. Patients' pathological diagnoses were diffuse large B-cell lymphoma (97 patients) and intravascular lymphoma (two patients). Six patients presented with hyponatremia derived from SIADH or suspected SIADH, and one presented with DI. Statistically significant differences between the hypothalamic and control groups were detected only in the preoperative serum Na values and KPS scores.. SIADH can be an initial presentation of hypothalamic PCNSL. Early detection of hypothalamic PCNSL from SIADH may lead to proper management and improved prognosis.

Topics: Diabetes Insipidus; Humans; Hyponatremia; Hypothalamus; Inappropriate ADH Syndrome; Retrospective Studies; Vasopressins

We report a case of the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) after total proctocolectomy followed with ileal pouch-anal anastomosis (TPC-IPAA) for ulcerative colitis (UC). The patient was a 46-year-old woman. She was diagnosed with UC of pancolitis in 2000. High grade dysplasia was detected in the transverse colon after a surveillance colonoscopy in 2021. She underwent laparoscopy-assisted TPC-IPAA. On the sixth postoperative day, she had a decreased level of consciousness that worsened on the following day. Her laboratory data showed a serum sodium level of 108 mEq/L and the plasma osmolality was 234 mOsm/kg. We did not find any other abnormalities in the laboratory examination that could cause hyponatremia. Computed tomography scan showed no central nervous system disturbances such as a pituitary tumor, antidiuretic hormone-producing tumors, or pulmonary diseases. The patient was diagnosed with Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) caused by surgical invasion. We started to administer 3% sodium chloride slowly to improve the hyponatremia. Her serum sodium level became normal and stable. Although it is rare for SIADH to be caused by abdominal surgery, if hyponatremia is observed after surgery, the possibility of postoperative SIADH should be considered.

Topics: Colitis, Ulcerative; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Middle Aged; Proctocolectomy, Restorative; Sodium; Vasopressins

Classic treatment for syndrome of inappropriate antidiuretic hormone (SIADH) is fluid restriction. However, this is not ideal for infants who need large fluid volumes to ensure adequate caloric intake for growth. The use of urea has not been thoroughly studied in children.. This infant had SIADH complicated by poor growth, solitary central incisor, and NF1. Following failed attempts to correct hyponatremia with fluid restriction and other therapeutics, urea normalized sodium levels and allowed liberalization of formula volumes, which resulted in improved weight gain.. Urea is a safe, cost-effective, long-term treatment for SIADH in infants who are unable to fluid restrict due to caloric goals.

Topics: Child; Humans; Hyponatremia; Inappropriate ADH Syndrome; Incisor; Infant; Neurofibromatosis 1; Urea; Vasopressins

Hyponatremia is the most frequent electrolytic disorder in clinical practice. In addition to neurological symptoms, hyponatremia, even when mild/moderate and chronic, has been related to other manifestations, such as bone demineralization and increased risk of fractures. To better elucidate tissue alterations associated with reduced serum sodium concentration [Na. Overall, these findings shed new light on the possible consequences of chronic hyponatremia and prompt a more thorough evaluation of hyponatremic patients.

Topics: Animals; Deamino Arginine Vasopressin; Hyponatremia; Inappropriate ADH Syndrome; Liver; Male; Mice; Sodium; Spermatogenesis; Vasopressins

A 31-year-old female presented to the emergency department with abdominal pain, vomiting and constipation. Serum sodium levels were recorded at 110 mmol/L on admission, dropping to 96 mmol/L despite fluid restriction. The patient developed hallucinations and required hypertonic saline administration in critical care. Urinary sodium was detected at 149 mmol/L, consistent with syndrome of inappropriate antidiuretic hormone secretion (SiADH). Urinary porphyrins were also raised, consistent with a diagnosis of acute intermittent porphyria with SiADH as a complication.

Topics: Abdominal Pain; Adult; Female; Humans; Inappropriate ADH Syndrome; Porphyria, Acute Intermittent; Sodium; Vasopressins

Fructose has recently been proposed to stimulate vasopressin secretion in humans. Fructose-induced vasopressin secretion is not only postulated to result from ingestion of fructose-containing drinks but may also occur from endogenous fructose production via activation of the polyol pathway. This raises the question of whether fructose might be involved in some cases of vasopressin-induced hyponatremia, especially in situations where the cause is not fully known such as in the syndrome of inappropriate secretion of diuretic hormone (SIADH) and exercise-associated hyponatremia, which has been observed in marathon runners. Here we discuss the new science of fructose and vasopressin, and how it may play a role in some of these conditions, as well as in the complications associated with rapid treatment (such as the osmotic demyelination syndrome). Studies to test the role of fructose could provide new pathophysiologic insights as well as novel potential treatment strategies for these common conditions.

Topics: Diuretics; Humans; Hyponatremia; Inappropriate ADH Syndrome; Running; Vasopressins

Hypothalamic hamartoma (HH) typically presents with gonadotrophin-dependent precocious puberty and/or seizures. Other endocrine disturbances are rare. We describe an infant with syndrome of inappropriate secretion of anti-diuretic hormone (SIADH) and a HH.. A 6-week-old infant presented with seizures and life-threatening hyponatremia. A HH was identified on magnetic resonance imaging. Clinical examination and biochemistry were consistent with SIADH, and serum copeptin was high during hyponatremia, further supporting this diagnosis. Tolvaptan was effective in normalizing plasma sodium and enabling liberalization of fluids to ensure sufficient nutritional intake and weight gain and manage hunger.. Hyponatremia due to SIADH is novel at presentation of a HH, and can be challenging to diagnose and manage. Successful management of hyponatremia in this case was achieved using tolvaptan.

Topics: Antidiuretic Hormone Receptor Antagonists; Benzazepines; Diuretics; Humans; Hyponatremia; Inappropriate ADH Syndrome; Seizures; Tolvaptan; Vasopressins

The syndrome of inappropriate ADH-secretion (SIADH) is a common cause of low sodium levels with diverse aetiology. Here, we report a case of a 41 years old male patient diagnosed with SIADH and a good response to Tolvaptan therapy. Of interest, as a potential unique cause, magnetic resonance imaging revealed a micronodular structure in the posterior pituitary, while no other common cause of SIADH could be identified. Hence, to the best of our knowledge, this is the first case of a Tolvaptan-responsive SIADH associated with a pituitary micronodular structure.

Topics: Adult; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Pituitary Gland, Posterior; Tolvaptan; Vasopressins

Hyperimmunoglobulin E syndrome (HIES) due to dedicator of cytokinesis8 (DOCK8) deficiency may present in infancy and childhood with different clinical features involving recurrent infections, allergic dysregulation, and autoimmunity.. In this report, we describe a patient who first presented with severe hypereosinophilia and went on to develop the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in the context of a severe herpes infection. Investigation revealed the presence of underlying DOCK8 deficiency presenting with atypical clinical features.. Distinct inflammatory features associated with infections may be seen in the course of primary immunodeficiency diseases, and early functional and molecular genetic tests will aid the proper management.

Topics: Child; Eosinophilia; Guanine Nucleotide Exchange Factors; Humans; Hypersensitivity; Inappropriate ADH Syndrome; Infant; Job Syndrome; Vasopressins

A 1-year-old spayed female Miniature Schnauzer had chronic hyponatremia, accompanied by polyuria and polydipsia. Blood tests and urinalysis revealed severe hyponatremia, low plasma osmolality with euvolemia, and increased sodium excretion in urine. Hypothyroidism and hypoadrenocorticism were ruled out as causes. These findings led to the diagnosis of syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Magnetic resonance imaging (MRI) showed dilation of the lateral ventricles, indicating severe hydrocephalus. Tolvaptan, a vasopressin V2 receptor antagonist commonly used in human SIADH, was administered along with water restriction. This treatment resulted in a consistent increase in plasma sodium levels without any adverse effects. This case report represents the first documented evidence of the therapeutic efficacy of tolvaptan in treating SIADH in a dog.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Dog Diseases; Dogs; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Sodium; Tolvaptan; Vasopressins

A macro pituitary tumour or giant pituitary tumour is regarded as a rare causal factor in syndrome of inappropriate antidiuretic hormone (SIADH) cases. Previous reports have presented findings showing that blood flow insufficiency related to stress caused by an obstructive mass may lead to inappropriate secretion of arginine vasopressin. On the other hand, prolactin is known to influence water metabolism, and several cases of a macroprolactinoma or giant prolactinoma (PRLoma) in patients with SIADH have been reported. Nevertheless, few studies have examined such a relationship with SIADH and discussion of pathophysiological factors has been limited. The present report provides details of an elderly patient with SIADH in a chronic giant PRLoma. Of note, exacerbation of prolactin level accompanied the occurrence of SIADH. Findings obtained in this case suggest the possibility of development of SIADH in PRLoma cases due to more than only the effect of the mass.

Topics: Aged; Cabergoline; Humans; Inappropriate ADH Syndrome; Pituitary Neoplasms; Prolactin; Prolactinoma; Vasopressins

Duloxetine is widely used for pain control and depressive syndromes. One of its potential side effects is syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Duloxetine-induced SIADH causes hyponatremia, which leads to a variety of symptoms and has previously been reported in the elderly. In the present case, we experienced a case of the rapid onset of SIADH in a super-elderly woman receiving low-dose duloxetine. Elderly patients tend to have lower duloxetine doses and an earlier onset than non-elderly patients. When hyponatremia occurs after duloxetine administration, duloxetine-induced SIADH should be considered, especially in high-risk elderly patients, regardless of the duloxetine dose or duration of treatment.

Topics: Aged; Duloxetine Hydrochloride; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Middle Aged; Vasopressins

To describe a case of inappropriate antidiuretic hormone (ADH) secretion in a dog secondary to trauma.. A 14-year-old neutered female mixed breed dog presented for evaluation of bite wounds. The dog sustained multiple puncture wounds to the cervical area, stifle, and elbow. Treatment was initiated with isotonic crystalloid fluids, analgesia, broad-spectrum antimicrobials, and gastroprotectants. The dog developed hyponatremia with concurrent serum hypoosmolality and inappropriate urine hyperosmolality and urine sodium secretion, leading to a diagnosis of the syndrome of inappropriate ADH secretion. The hyponatremia improved, and the dog improved clinically and was discharged 3 days after admission.. This is the first case description of the syndrome of inappropriate ADH secretion in a dog suffering from trauma. Inappropriate ADH secretion is largely under-recognized in veterinary patients. Increased awareness of this syndrome can lead to initiation of appropriate treatment and improved outcomes.

Topics: Animals; Dog Diseases; Dogs; Female; Hospitalization; Hyponatremia; Inappropriate ADH Syndrome; Osmolar Concentration; Vasopressins

Topics: Duloxetine Hydrochloride; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

Topics: Duloxetine Hydrochloride; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

To evaluate serum antidiuretic hormone (ADH), its receptors, and renin levels in cerebral salt wasting (CSW) in tuberculous meningitis (TBM).. Patients diagnosed with definite (n = 30) or probable TBM (n = 47) who developed hyponatremia (CSW, SIADH, or miscellaneous causes) were included. Sequential measurement of serum ADH, ADH-R, and renin activity by enzyme-linked immunosorbent assay was done and correlated with serum sodium level, urinary output, and fluid balance.. Out of 79 TBM patients, CSW was observed in 36, SIADH in four, and miscellaneous hyponatremia in eight patients. CSW patients had a longer hospital stay (P < 0.001), lower GCS score (P < 0.007), higher MRC grade (P < 0.007), and a lower serum Na (P < 0.001) compared to non-CSW TBM patients. In severe CSW patients, serum ADH and ADH-R were correlated with hyponatremia and returned to baseline on correction; however, serum renin levels remained elevated. Serum ADH was related to hyponatremia but ADH-R and renin were not. ADH-R and renin levels did not significantly differ in CSW and SIADH.. CSW is the commonest cause of hyponatremia in TBM and correlates with disease severity. ADH is related to hyponatremia, but ADH receptor and renin are not.

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Renin; Tuberculosis, Meningeal; Vasopressins

A giant hypothalamic hamartoma (GHH) is a rare congenital malformation only reported in a few cases in the literature and is often associated with precocious puberty, gelastic seizures, or less commonly, Pallister-Hall syndrome. Persistent syndrome of inappropriate antidiuretic hormone secretion (SIADH) is very rare in infancy, and most patients with GHH do not develop persistent SIADH, usually only transient electrolyte disturbances postoperatively. Previous cases of GHH have not been associated with persistent derangements in antidiuretic hormone levels.. A 7-month-old male infant presented to our hospital with a history of an intracranial cystic lesion diagnosed at 23 weeks gestational age (GA), later impressed as a solid-cystic mass at 37 weeks GA by ultrasound prenatally. Postnatal MRI after birth showed a large mass with a dorsal cyst occupying the hypothalamus, causing hydrocephalus and brainstem compression. The patient started to have subtle seizures on the seventh day after birth and eventually developed dacrystic seizures. Hyponatremia with persistent SIADH was observed at 3 months of age before surgery. He received long-term oral sodium supplementation, polytherapy of anti-epileptic medications, ventriculocystostomy for progressive enlargement of the cystic cavity, and later surgical treatment for disconnection and partial resection which confirmed a histological diagnosis of hypothalamic hamartoma.. In this case study, we present a novel association of GHH with persistent SIADH and a rare presentation of a cystic component at the dorsal part of the tumor. Clinicians should be aware of this potential endocrine derangement and provide emergent treatment.

Topics: Epilepsies, Partial; Hamartoma; Humans; Hypothalamic Diseases; Inappropriate ADH Syndrome; Infant; Male; Seizures; Vasopressins

We report the case of a 68-year-old man, who presented in emergency care with inarticulate speech. The patient was diagnosed with syndrome of inappropriate antidiuretic hormone (SIADH) associated with pancreatic cancer. All diagnostic criteria for SIADH were met, and cancer of the pancreatic tail was identified by computed tomography. Standard treatment for SIADH includes water restriction, oral NaCl, continuous intravenous infusion of 3% NaCl, and intravenous infusion of furosemide. However, these treatments have varying effectiveness and are difficult for both patients and medical staff. Furthermore, unless treatment of the underlying disease is successful, continued hospitalization is needed and the patient's quality of life is significantly impaired. In this case, hyponatremia improved with this standard treatment, but ascites and edema developed. We treated the patient with tolvaptan due to decreased cardiac function, and symptoms improved rapidly. Although surgery and chemotherapy could not be performed for pancreatic cancer, the SIADH was treated for 7 months without relapse. In summary, a case of SIADH complicated by pancreatic cancer was difficult to control with standard treatment, but responded rapidly to tolvaptan, and outpatient treatment could be continued for a long period. Tolvaptan is useful for the treatment of SIADH associated with cancer.

Topics: Aged; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Humans; Inappropriate ADH Syndrome; Male; Pancreatic Neoplasms; Quality of Life; Tolvaptan; Vasopressins

BACKGROUND Cisplatin/5-fluorouracil therapy is the standard therapy for unresectable and recurrent esophageal cancer. Cisplatin-based chemotherapy often causes adverse effects, such as nausea, vomiting, and renal dysfunction, which may necessitate dose modification or treatment prolongation. Therefore, novel combination therapies are urgently needed to improve the efficacy and overcome drug toxicity in this setting. CASE REPORT A 77-year-old man with advanced esophageal cancer received cisplatin/5-fluorouracil therapy as neoadjuvant chemotherapy. On day 8 of administration, the patient had lightheadedness, diaphoresis, and nausea and became unconscious and developed severe hyponatremia. We diagnosed the patient with cisplatin-induced syndrome of inadequate antidiuretic hormone secretion (SIADH). Subsequently, water restriction was started, and treatment with a salt-added diet and 3% hypertonic saline infusion was initiated. The hyponatremia improved and the patient was discharged on day 16 of administration. Therefore, neoadjuvant chemotherapy was discontinued, and surgical treatment was performed. However, the tumor recurred and chemotherapy was required. The patient developed severe hyponatremia while receiving neoadjuvant chemotherapy; hence, folinic acid, fluorouracil, and oxaliplatin therapy (FOLFOX) were administered as an alternative treatment. The patient completed the FOLFOX therapy without developing SIADH. CONCLUSIONS The cisplatin/5-fluorouracil therapy is currently the standard chemotherapy regimen for esophageal cancer. However, SIADH is a known adverse effect when using cisplatin. In patients with esophageal cancer, oxaliplatin appears to have a lower risk of SIADH than cisplatin, suggesting that oxaliplatin can be a therapeutic option for patients with esophageal cancer who are at high risk of SIADH.

Topics: Aged; Antineoplastic Combined Chemotherapy Protocols; Cisplatin; Esophageal Neoplasms; Fluorouracil; Humans; Inappropriate ADH Syndrome; Leucovorin; Male; Neoadjuvant Therapy; Neoplasm Recurrence, Local; Oxaliplatin; Vasopressins

A 67-year-old man with a history of esophageal cancer resection was referred to our hospital because of nausea and appetite loss. Laboratory findings showed severe hyponatremia and were compatible with syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Chest computed tomography (CT) revealed a nodule measuring 13 mm in the lower lobe of the right lung. Right thoracotomy was performed, and the histopathological diagnosis was small-cell lung cancer (T1bN0M0; Stage 1b). Although SIADH is frequently associated with small-cell lung cancer, it is extremely rare as the initial clinical feature in stage I small-cell lung cancer.

Topics: Aged; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Small Cell Lung Carcinoma; Vasopressins

To report on an unusual case of ketamine-precipitated syndrome of inappropriate antidiuretic hormone secretion (SIADH) in an individual managed by an outpatient pain specialty team.. A 78-yr-old male presented to the emergency department with lethargy, malaise, nausea, and abdominal bloating three days following intravenous ketamine infusion for intractable postsurgical lumbar radicular pain with neuropathic features. The patient had a history of resected prostate cancer, hyperlipidemia, chronic kidney disease, and spinal stenosis and the cause of his symptoms was investigated. He was found to be hyponatremic and the treating team excluded reversible surgical and medical causes. A Naranjo score of 7 was calculated, suggesting that the correlation between ketamine and hyponatremia was "likely." Hence, a diagnosis of ketamine-precipitated SIADH was made. The patient was treated with fluid restriction and symptoms were controlled with antiemetics. He returned to baseline function with resolution of the hyponatremia within three days of discharge.. This case is of clinical importance for providers using ketamine in the field of pain management as the effect of this medication reaction can be profound. Clinicians should develop an awareness that ketamine can potentiate adverse effects such as SIADH and they should monitor, detect, and manage as appropriate.. RéSUMé: OBJECTIF: Nous signalons un cas inhabituel de syndrome de sécrétion inappropriée d’hormones antidiurétiques (SIADH - syndrome of inappropriate antidiuretic hormone secretion) précipité par la kétamine chez une personne prise en charge par une équipe spécialisée en douleur en soins ambulatoires. CARACTéRISTIQUES CLINIQUES: Un homme de 78 ans s’est présenté à l’urgence souffrant de léthargie, de malaise, de nausées et de ballonnements abdominaux trois jours après avoir reçu une perfusion intraveineuse de kétamine pour le traitement d’une douleur radiculaire lombaire postopératoire rebelle avec des caractéristiques neuropathiques. Le patient avait des antécédents de résection de cancer de la prostate, d’hyperlipidémie, d’insuffisance rénale chronique et de sténose du canal rachidien, et la cause de ses symptômes a été évaluée. Il s’est avéré hyponatrémique et l’équipe soignante a exclu les causes chirurgicales et médicales réversibles. Un score Naranjo de 7 a été calculé, suggérant que la corrélation entre la kétamine et l’hyponatrémie était « probable ». Par conséquent, un diagnostic de SIADH précipité par la kétamine a été posé. Le patient a été traité par restriction hydrique et les symptômes ont été contrôlés par des antiémétiques. Il est revenu à son fonctionnement de référence avec la résolution de l’hyponatrémie dans les trois jours suivant son congé. CONCLUSION: Ce cas est important d’un point de vue clinique pour les praticiens qui utilisent la kétamine pour la prise en charge de la douleur, car l’effet de cette réaction médicamenteuse peut être profond. Les cliniciens devraient prendre conscience que la kétamine peut augmenter des effets indésirables tels que le SIADH et ils devraient monitorer, dépister et prendre en charge le patient, le cas échéant.

Topics: Drug-Related Side Effects and Adverse Reactions; Humans; Hyponatremia; Inappropriate ADH Syndrome; Ketamine; Male; Pain; Vasopressins

Topics: Humans; Hyponatremia; Hypothyroidism; Inappropriate ADH Syndrome; Vasopressins

The objective of this study was to evaluate the reported associations between the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and a variety of proton pump inhibitors (PPI) through analysis of the reports extracted from the Food and Drug Administration Adverse Event Reporting System (FAERS).. FAERS reports from January 2004 to March 2020 were used to conduct disproportionality and Bayesian analyses. The definition of SIADH relied on the preferred terms provided by the Medical Dictionary for Regulatory Activities. The time to onset, mortality, and hospitalization rates of PPI-related SIADH were also investigated.. The study identified a total of 273 reports of PPI-associated SIADH, which appeared to influence more elderly than middle-aged patients (71.1% vs. 12.5%). Women were more affected than men (48.7% vs. 41.8%). Rabeprazole had a stronger SIADH association than other PPIs based on the highest reporting odds ratio (reporting odds ratio = 13.3, 95% confidence interval (CI) = 7.2, 24.9), proportional reporting ratio (proportional reporting ratio = 13.3, χ. According to our findings, more attention should be paid to SIADH within the first several months after the administration of PPIs. For women older than 65 years, dexlansoprazole may reduce the incidence of PPI-associated SIADH. Nonetheless, larger epidemiological studies are suggested to verify this conclusion.

Topics: Adverse Drug Reaction Reporting Systems; Aged; Bayes Theorem; Female; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Pharmacovigilance; Proton Pump Inhibitors; Vasopressins

A 9-year-old girl with remarkable hyponatremia was diagnosed with SIADH that was likely secondary to varicella. Under appropriate treatment, her serum sodium returned to the normal level. There was no evidence of hyponatremia at a 3-month follow-up. We propose that medical professionals need to consider the existence of that SIADH when treating patients with varicella who present with severe hyponatremia.

Topics: Chickenpox; Child; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

The aim of this work is to examine our experience in the use of urea in patients with SIADH. Observational retrospective analysis of 48 patients with SIADH that have been treated with urea in a third-level hospital. Pre-post analysis of serum sodium levels. The 48 patients with SIADH had a median age of 78.5 (range 26-97 years). The serum sodium nadir was 119.8 ± 5.0 mmoL/L and at the beginning of treatment 125.6 ± 4.1 mmoL/L. The patients continued the treatment for a mean time of 2.95 ± 6.29 months, being the treatment still active in 4 patients. In all patients there was an improvement in serum sodium, being the final serum sodium at the end of treatment 134.4 ± 4.9 mmoL/L (p < 0.01). This improvement was observed from the first week. Adverse events were only detected in 2 patients with mild digestive symptomatology and 2 patients refused the treatment due to the low palatability of the urea. There was an economic cost reduction of 87.9% in comparison with treatment with tolvaptan. Urea has shown to be a safe and cost-effective option for the treatment of hyponatremia caused by SIADH.

Topics: Adult; Aged; Aged, 80 and over; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Humans; Inappropriate ADH Syndrome; Middle Aged; Retrospective Studies; Sodium; Treatment Outcome; Urea; Vasopressins

Hyponatremia and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) are associated with and can be caused by tuberculosis (TB) through meningitis by locally invading the hypothalamus, adrenal, or pituitary glands or possibly through ectopic ADH production. This study assessed the association of TB mortality with hyponatremia and SIADH in a large cohort of a university hospital in Austria.. This retrospective study enrolled patients with hyponatremia and patients diagnosed with TB from 01/2001-11/2019 to assess the prevalence of TB in hyponatremia and TB morbidity and mortality in patients with and without hyponatremia. Sex, age, microbiological results, laboratory tests and comorbidities were analysed and used to calculate survival rates.. Of 107.532 patients with hyponatremia (0.07%) and 186 patients with TB (43%), 80 patients were diagnosed with both-hyponatremia and TB. Only three TB patients had SIADH, precluding further SIADH analysis. In hyponatremia, young age and high CRP levels showed significant associations with TB diagnosis (p<0.0001). Survival rates of patients diagnosed with TB with moderate to profound hyponatremia were significantly lower than those without hyponatremia (p = 0.002).. In this study of a large cohort from a tertiary care hospital in a non-endemic area of TB, 0.07% of patients presenting with hyponatremia, but especially younger patients and patients with high CRP values, were diagnosed with TB. Crucially, patients with moderate to profound hyponatremia had a significantly higher mortality rate and thus required increased medical care.

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Retrospective Studies; Tuberculosis; Vasopressins

Hyponatremia and syndrome of inappropriate antidiuretic hormone (SIADH) is a potentially fatal adverse effect of antidepressants (ADs) and antipsychotics (APs), although its frequency and onset time have not been well documented.. To analyze the frequency and onset time of AD- or AP-induced hyponatremia/SIADH.. We used plural data-mining techniques to search the US Food and Drug Administration Adverse Event Reporting System (FAERS) database for reports on hyponatremia/SIADH induced by psychotropic drugs from January 2004 to June 2020. For each item, we assessed the reporting odds ratio, 95% CI, median onset time, and Weibull distribution parameters.. We identified 36 422 reports related to hyponatremia/SIADH. Signals were detected for all psychotropic drugs that we analyzed, except for clozapine. The median onset time of total AD-induced hyponatremia/SIADH was shorter than that of AP. For all ADs and APs except clozapine, hazards were considered to be the early failure type. In contrast, the hazard of clozapine was considered to be the random failure type. The limitations of this study included several reporting biases and the presence of confounding variables, particularly age.. Most ADs and APs were found to be associated with a risk for hyponatremia/SIADH. In addition, sufficient attention should be paid to signs of hyponatremia/SIADH in the early phase when most ADs and APs are administered. These data are potentially useful for determining AD- or AP-induced hyponatremia/SIADH in the early stage and for preventing its further aggravation into a serious condition.

Topics: Antidepressive Agents; Antipsychotic Agents; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

A 49-year-old man developed severe hyponatremia associated with transient headache and was diagnosed with syndrome of inappropriate antidiuretic hormone secretion (SIADH). Fluid restriction and sodium supplementation corrected the hyponatremia. However, several days later, the patient exhibited hypernatremia with thirst and polyuria. A detailed examination indicated central diabetes insipidus (CDI) with an intrasellar cystic lesion indicative of Rathke's cleft cyst (RCC). A case of RCC exhibiting headache, hyponatremia, and subsequent hypernatremia has been reported. Our case shows that CDI may appear after SIADH in patients with RCC, especially in those with serum sodium levels that unexpectedly increase rapidly beyond the reference range.

Topics: Central Nervous System Cysts; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Vasopressins

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a common problem during the postoperative course after pituitary surgery. Although treatment of this condition is well characterized, prevention strategies are less studied and reported. The authors sought to characterize outcomes and predictive factors of SIADH after implementation of routine postoperative fluid restriction for patients undergoing endoscopic transsphenoidal surgery for pituitary adenoma.. In March 2018, routine postoperative fluid restriction to 1000 ml/day for 7 days was instituted for all patients who underwent surgery for pituitary adenoma. These patients were compared with patients who underwent surgery for pituitary adenoma between March 2016 and March 2018, prior to implementation of routine fluid restriction. Patients with preoperative history of diabetes insipidus (DI) or concern for postsurgical DI were excluded. Patients were followed by neuroendocrinologists and neurosurgeons, and sodium levels were checked between 7 and 10 days postoperatively. SIADH was defined by a serum sodium level less than 136 mmol/L, with or without symptoms within 10 days after surgery. Thirty-day readmission was recorded and reviewed to determine underlying reasons.. In total, 82 patients in the fluid-unrestricted cohort and 135 patients in the fluid-restricted cohort were analyzed. The patients in the fluid-restricted cohort had a significantly lower rate of postoperative SIADH than patients in the fluid-unrestricted cohort (5% vs 15%, adjusted OR [95% CI] 0.1 [0.0-0.6], p = 0.01). Higher BMI was associated with lower rate of postoperative SIADH (adjusted OR [95%] 0.9 [0.9-1.0], p = 0.03), whereas female sex was associated with higher rate of SIADH (adjusted OR [95% CI] 3.1 [1.1-9.8], p = 0.03). There was no difference in the 30-day readmission rates between patients in the fluid-unrestricted and fluid-restricted cohorts (4% vs 7%, adjusted OR [95% CI] 0.5 [0-5.1], p = 0.56). Thirty-day readmission was more likely for patients with history of hypertension (adjusted OR [95% CI] 5.7 [1.3-26.3], p = 0.02) and less likely for White patients (adjusted OR [95% CI] 0.3 [0.1-0.9], p = 0.04).. Routine fluid restriction reduced the rate of SIADH in patients who underwent surgery for pituitary adenoma but was not associated with reduction in 30-day readmission rate.

Topics: Adenoma; Diabetes Insipidus; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Pituitary Neoplasms; Postoperative Complications; Retrospective Studies; Sodium; Vasopressins

Functional pancreatic neuroendocrine tumors (pNETs) rarely produce vasopressin. Here, we reported a case of pNET producing vasopressin in a 78-year-old man with hyponatremia.. The patient presented with anorexia approximately 4 years ago, and the laboratory test results indicated hyponatremia. He was hospitalized 3 times subsequently due to anorexia in the past 4 years, during which laboratory tests consistently indicated severe hyponatremia.. Upon admission, his serum osmolarity, urine osmolarity, urine sodium level, and 24-hour urine sodium level was 277 mOsm/kg H2O, 465 mOsm/kg H2O, 82.5 mmol/L, and 140.25 mmol, respectively. Gallium-68-labeled tetraazacyclododecanetetraacetic acid-Dphel-Tyr3-octreotate positron emission tomography-computed tomography showed a high uptake lesion measuring approximately 1 cm in diameter in the pancreatic body, and the possibility of pNET was considered. Besides, laboratory tests showed that adrenocorticotropic hormone, follicle-stimulating hormone, and luteinizing hormone released by the pituitary was insufficient in the case of low levels of cortisol, estradiol, progesterone, and testosterone. Thus, the diagnosis of the syndrome of inappropriate antidiuresis (SIAD) was considered along with hypopituitarism.. The patient underwent surgery, and pNET was confirmed by pathology examination. The immunohistochemical study showed that the tumor cells were positive for somatostatin receptors 2 and vasopressin.. In the last follow-up 17 months after surgery, the patient was in good condition, taking methylprednisolone 4 mg every other day, and had been free of anorexia or hyponatremia episodes.. This case illustrated the potential ectopic production of vasopressin resulting in SIAD in pNETs, highlighting the adoption of gallium-68-labeled tetraazacyclododecanetetraacetic acid-Dphel-Tyr3-octreotate positron emission tomography-computed tomography and vasopressin immunohistochemical staining in the evaluation of the etiology of SIAD.

Topics: Adrenal Cortex Hormones; Aged; Anorexia; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Neuroendocrine Tumors; Pancreatic Neoplasms; Vasopressins

Topics: Antineoplastic Combined Chemotherapy Protocols; Cisplatin; Female; Humans; Inappropriate ADH Syndrome; Middle Aged; Research Report; Sodium; Urinary Bladder Neoplasms; Vasopressins

Recently, chronic hyponatremia, even mild, has shown to be associated with poor quality of life and high mortality. The mechanism by which hyponatremia contributes to those symptoms, however, remains to be elucidated. Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a primary cause of hyponatremia. Appropriate animal models are crucial for investigating the pathophysiology of SIADH. A rat model of SIADH has been generally used and mouse models have been rarely used. In this study, we developed a mouse model of chronic SIADH in which stable and sustained hyponatremia occurred after 3-week continuous infusion of the vasopressin V2 receptor agonist 1-desamino-8-D-arginine vasopressin (dDAVP) and liquid diet feeding to produce chronic water loading. Weight gain in chronic SIADH mice at week 2 and 3 after starting dDAVP injection was similar to that of control mice, suggesting that the animals adapted to chronic hyponatremia and grew up normally. AQP2 expression in the kidney, which reflects the renal action of vasopressin, was decreased in dDAVP-infused water-loaded mice as compared with control mice that received the same dDAVP infusion but were fed pelleted chow. These results suggest that "vasopressin escape" occurred, which is an important process for limiting potentially fatal severe hyponatremia. Behavioral analyses using the contextual and cued fear conditioning test and T-maze test demonstrated cognitive impairment, especially working memory impairment, in chronic SIADH mice, which was partially restored after correcting hyponatremia. Our results suggest that vasopressin escape occurred in chronic SIADH mice and that chronic hyponatremia contributed to their memory impairment.

Topics: Animals; Behavior, Animal; Chronic Disease; Disease Models, Animal; Hyponatremia; Inappropriate ADH Syndrome; Male; Memory Disorders; Mice; Mice, Inbred C57BL; Vasopressins

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is the most common cause of hyponatraemia in hospital inpatients. We present data on treatment setting, patient characteristics, and outcomes for patients treated with tolvaptan for SIADH across a range of real-world settings in Germany and Spain.. This was a non-interventional, observational, retrospective chart review study. Management was at the discretion of the treating physician, with tolvaptan prescribed according to local clinical practice. Hospital notes and/or medical charts were reviewed from treatment initiation for 6 weeks. Follow-up data were collected when patients were discharged early. Patients were eligible for inclusion if they were ≥ 18 years of age and had been treated with ≥ 2 doses of tolvaptan for one episode of hyponatraemia secondary to SIADH in 2014.. The Full Analysis Set comprised 100 patients from 8 centres. The mean age of patients was 73.9 years. The primary endpoint of the mean increase in serum sodium level from baseline to hospital discharge, or to final available measurement, was 10.3 mmol/L (SD 6.4; 95% CI 9.0, 11.6), from 123.0 mmol/L (SD 6.0) to 133.3 mmol/L (SD 4.9). Seventy-seven patients (77.0%) achieved sodium normalisation within 6 weeks of tolvaptan initiation. Mean daily dose of tolvaptan was 12.7 mg (SD 9.2), and mean treatment duration 28.0 days (SD 16.5). Tolvaptan at off-label doses (< 15 mg/day) was prescribed to 72 patients at some point. A favourable safety and tolerability profile was reported.. Tolvaptan was well tolerated and effectively corrected sodium levels in hospitalised adults with hyponatraemia secondary to SIADH in real-world settings. CLINICALTRIALS.. NCT02545101.

Topics: Adult; Aged; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Germany; Humans; Hyponatremia; Inappropriate ADH Syndrome; Retrospective Studies; Spain; Tolvaptan; Vasopressins

BACKGROUND Syphilis has increased in prevalence in the United States by 72.7% from 2013 to 2017, with the highest rates recorded in men who have sex with men. There is an increased incidence of syphilis in patients with a concomitant HIV infection, estimated at a 77-fold increase. CASE REPORT This report documents an unusual case of neurosyphilis manifesting as syndrome of inappropriate antidiuretic hormone secretion (SIADH) in a 56-year-old man with HIV/AIDS. A 56-year-old man who has sex with men with HIV/AIDS presented with a 4-day history of periumbilical abdominal pain, nausea, and constipation. A physical exam revealed slowing of baseline cognition, but was otherwise unremarkable. Urine and serum osmolality studies were consistent with SIADH as defined by the Bartter and Schwartz Criteria: serum osmolality <275 mOsm/kg, urine osmolality >100 mOsm/kg, urine sodium >20-40 mmol/L, euvolemia, and no other cause for hyponatremia identified. He was fluid-restricted, with improvement in laboratory abnormalities, further supporting the diagnosis of SIADH. A diagnostic work-up included a CT abdomen/pelvis with perirectal lymphadenopathy, colonoscopy negative for malignancy, chest CT with lymphadenopathy, and a head MRI negative for intracranial processes. The patient was ultimately found to have positive results on rapid plasma reagin (RPR) and Venereal Disease Research Laboratory (VDRL) tests, and was diagnosed as having neurosyphilis. He underwent penicillin desensitization and received a 14-day course of penicillin G, with recovery of sodium to normal range on discharge. CONCLUSIONS Our case highlights SIADH as an initial presenting sign of neurosyphilis with HIV infection, which has only been documented in 2 prior case reports. Our case highlights the importance of recognizing atypical presentations of neurosyphilis in patients with HIV to prevent long-term complications.

Topics: HIV Infections; Homosexuality, Male; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Neurosyphilis; Sexual and Gender Minorities; Vasopressins

Small cell carcinoma of the cervix is a rare malignant tumor in the clinical setting. Clinical manifestations of this tumor are mostly similar to those of normal types of cervical cancer. Small cell carcinoma of the cervix only shows symptoms of neuroendocrine tumors, such as syndrome of inappropriate antidiuretic hormone secretion (SIADH). Most of the hyponatremia caused by SIADH can be managed after removal of the cause. Hyponatremia is a predictor of poor prognosis and can be used as an indicator of partial recurrence. We report a case of small cell carcinoma of the cervix complicated by SIADH. Our patient presented with irregular vaginal bleeding after menopause. After one cycle of chemotherapy, there was trembling of the limbs, and a laboratory examination showed low Na

Topics: Carcinoma, Small Cell; Cervix Uteri; Female; Humans; Inappropriate ADH Syndrome; Neoplasm Recurrence, Local; Uterine Cervical Neoplasms; Vasopressins

A previously well 21-year-old girl presented to Hospital Teluk Intan, Perak, Malaysia with a short history of fever, vomiting and altered sensorium. She was diagnosed with dengue encephalitis as her dengue NS-1 antigen was positive and her cerebrospinal fluid (CSF) dengue polymerase chain reaction (PCR) was positive with serotype DENV-2. She also had severe hyponatremia due to Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) which caused an episode of seizure. She recovered well with supportive management. SIADH and dengue encephalitis should be considered as one of the differential diagnosis in patients presenting with fever and altered sensorium especially in dengue endemic countries like Malaysia.

Topics: Adult; Dengue; Encephalitis; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins; Young Adult

Topics: Acrylamides; Aged; Aniline Compounds; Carcinoma, Non-Small-Cell Lung; Drug Substitution; Female; Humans; Inappropriate ADH Syndrome; Treatment Outcome; Vasopressins

Syndrome of inappropriate antidiuretic hormone (SIADH) secretion is a recognisable complication of acute porphyria. We report a nine-year-old female patient with hereditary tyrosinaemia type 1 and poor adherence to nitisinone therapy who presented with acute abdominal pain, vomiting and lethargy at Sultan Qaboos University Hospital, Muscat, Oman in 2016. She subsequently developed generalised tonic-clonic seizures attributable to severe hyponatremia that met the diagnostic criteria of SIADH. The acute porphyria screen also appeared positive. The patient responded well to fluid restriction and was discharged home without immediate neurological sequelae. Although acute porphyria is also a recognised complication of uncontrolled tyrosinaemia type 1, to the best of the authors' knowledge, no patient with tyrosinaemia type 1 has been reported to present with SIADH.

Topics: Child; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Oman; Tyrosinemias; Vasopressins

Topics: Aged; Amnesia, Transient Global; Diagnosis, Differential; Diuretics; Female; Humans; Inappropriate ADH Syndrome; Vasopressins

We present a case of severe hyponatraemia due to syndrome of inappropriate antidiuretic hormone (SIADH) in a patient with respiratory syncytial virus (RSV) infection. A retrospective analysis of all patients admitted to our hospital with RSV in the preceding 3-year period revealed hyponatraemia in 41 (28%) cases, of which 13 (8.9%) were moderate or severe. SIADH was explored and confirmed in five (3.4%) patients, raising this as an important, previously unrecognised, complication of RSV infection in adults. Physician awareness of SIADH as a potential complication of RSV will facilitate early diagnosis and treatment of this potentially fatal disorder.

Topics: Adult; Humans; Hyponatremia; Inappropriate ADH Syndrome; Respiratory Syncytial Virus Infections; Retrospective Studies; Vasopressins

Paraneoplastic syndromes are frequently observed in lung cancer, especially in small cell lung cancer (SCLC). Although there have been many reports on paraneoplastic syndromes, few reports have been published on SCLC that simultaneously produces antidiuretic hormone (ADH) and adrenocorticotropic hormone (ACTH), and these reports described the prognosis of such cases as extremely poor. We herein present a rare case of a Japanese woman with SCLC accompanied by syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and Cushing's syndrome. The survival of the patient was prolonged by the long-term administration of amrubicin.

Topics: Adrenocorticotropic Hormone; Aged; Anthracyclines; Antineoplastic Agents; Cushing Syndrome; Female; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Paraneoplastic Syndromes; Prognosis; Small Cell Lung Carcinoma; Survival Rate; Vasopressins

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Lymphoma, Large B-Cell, Diffuse; Vasopressins

Topics: Diuretics; Humans; Inappropriate ADH Syndrome; Multiple Myeloma; Vasopressins

Syndrome of inappropriate antidiuretic hormone release (SIADH) is a condition defined by the unsuppressed release of antidiuretic hormone (ADH) from the pituitary gland or nonpituitary sources or its continued action on vasopressin receptors. Of the many causes of SIADH, an important one includes tumours that secrete ADH. We describe a rare case of a patient with colonic adenocarcinoma presenting initially as SIADH. A 60-year-old man presented with confusion and vomiting. Over the previous month he had fatigue and loss of weight. Baseline investigations showed a low serum sodium level of 108mmol/l. He was euvolaemic on examination and fulfilled the criteria for SIADH. Further evaluation and imaging tests revealed that the patient had adenocarcinoma of the colon. It is remarkable that our patient did not present with any of the cardinal symptoms/signs suggestive of colorectal carcinoma including haematochezia, change in bowel habits or iron-deficiency anaemia. Initial therapy with hypertonic saline, fluid restriction and salt diet for management of SIADH was unsuccessful. Tolvaptan was added to the treatment regimen and the patient improved dramatically. Oncology consultation was initiated, and chemotherapy for the carcinoma was planned.

Topics: Adenocarcinoma; Colon; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Tolvaptan; Vasopressins

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is a known cause of hyponatremia, caused by excessive ADH secretion which, in turn, leads to water retention. SIADH has been associated with multiple etiologies, one of which is traumatic brain injury (TBI). Most cases of SIADH after TBI describe a course in which hyponatraemia develops several days to weeks after the trauma and then resolves within a few weeks. We demonstrate a case of SIADH after TBI, which persisted several years after initial presentation, but eventually did resolve spontaneously after five years.

Topics: Brain Injuries, Traumatic; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

Nephrogenic syndrome of inappropriate antidiuresis (NSIAD) is a recently identified chromosome X-linked disease associated with gain-of-function mutations of the V2 vasopressin receptor (V2R), a G-protein-coupled receptor. It is characterized by inability to excrete a free water load, hyponatremia, and undetectable vasopressin-circulating levels. Hyponatremia can be quite severe in affected male children. To gain a deeper insight into the functional properties of the V2R active mutants and how they might translate into the pathological outcome of NSIAD, in this study, we have expressed the wild-type V2R and three constitutively active V2R mutants associated with NSIAD (R137L, R137C, and the F229V) in MCD4 cells, a cell line derived from renal mouse collecting duct, stably expressing the vasopressin-sensitive water channel aquaporin-2 (AQP2). Our findings indicate that in cells expressing each active mutant, AQP2 was constitutively localized to the apical plasma membrane in the absence of vasopressin stimulation. In line with these observations, under basal conditions, osmotic water permeability in cells expressing the constitutively active mutants was significantly higher compared to that of cells expressing the wild-type V2R. Our findings demonstrate a direct link between activating mutations of the V2R and the perturbation of water balance in NSIAD. In addition, this study provides a useful cell-based assay system to assess the functional consequences of newly discovered activating mutations of the V2R on water permeability in kidney cells and to screen the effect of drugs on the mutated receptors.

Topics: Animals; Aquaporin 2; Cell Line; Gain of Function Mutation; Genetic Diseases, X-Linked; Humans; Inappropriate ADH Syndrome; Mice; Receptors, Vasopressin; Renal Reabsorption; Vasopressins; Water; Water-Electrolyte Balance

Small cell carcinoma (SCC) of the bladder is a rare malignancy, representing less than 1% of bladder cancers diagnosed annually in the USA. In contrast to SCC of the lung, paraneoplastic syndromes are rarely documented in cases of extrapulmonary SCCs, particularly those of genitourinary origin. We present a case of SCC of the bladder presenting with paraneoplastic syndrome of inappropriate antidiuretic hormone, which resolved after treatment with sequential chemoradiation.

Topics: Aged, 80 and over; Carcinoma, Small Cell; Chemoradiotherapy; Cystoscopy; Fluorine Radioisotopes; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Paraneoplastic Syndromes; Positron Emission Tomography Computed Tomography; Treatment Outcome; Urinary Bladder; Urography; Vasopressins

The objective of the study is to report a rare case of pancreatic neuroendocrine tumor (pNET) producing insulin and vasopressin. We describe the clinical presentation and management of a metastatic pNET with refractory hypoglycemia and progressive severe hyponatremia. A 52-year-old patient had abdominal pain leading to the diagnosis of a tumor that was initially presumed to be splenic in origin. Investigations ultimately identified a pancreatic mass that on biopsy proved to be a pNET. Eventually, he developed extensive liver metastases, and with tumor progression, he manifested hypoglycemia and severe hyponatremia. He was managed with multiple therapies including somatostatin analogue, peptide-receptor-radionuclide-therapy (PRRT), diazoxide, and everolimus; none of these therapeutic modalities was successful in controlling functional and structural progression of the tumor. Ultimately, the pNET proved fatal and autopsy confirmed widely metastatic disease that stained strongly and diffusely for vasopressin, a feature not seen in the previous liver biopsy. This case illustrates the challenges of diagnosis and management of aggressive insulin-producing pNETs and highlights the potential concomitant ectopic production of vasopressin leading to refractory hyponatremia.

Topics: Humans; Inappropriate ADH Syndrome; Insulin; Male; Middle Aged; Neuroendocrine Tumors; Neurophysins; Pancreatic Neoplasms; Protein Precursors; Vasopressins

Topics: Antidiuretic Hormone Receptor Antagonists; Benzazepines; Drug Resistance; Fatal Outcome; Female; Genetic Diseases, X-Linked; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Middle Aged; Small Cell Lung Carcinoma; Sodium; Tolvaptan; Vasopressins

Topics: Antidiuretic Hormone Receptor Antagonists; Humans; Hyponatremia; Inappropriate ADH Syndrome; Tolvaptan; Vasopressins

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is defined by euvolemic hyponatremia due to an inappropriate retention of free water under the effect of antidiuretic hormone. It is underdiagnosed despite well-defined criteria. Diagnosis involves a precise evaluation of volemia and the elimination of differential diagnoses. The etiologies are classified into four main groups : tumors, drugs, diseases of the central nervous system and lung diseases. In the case of a newly diagnosed SIADH, investigations depend on the clinical context and should at least include a chest radiograph or a chest CT-scan. Fluid restriction is the recommended first-line treatment for mild or moderate hyponatremia. However, only the etiologic treatment leads to the disappearance of SIADH.. Le syndrome de sécrétion inappropriée d’hormone antidiurétique (SIADH) est défini par une hyponatrémie euvolémique induite par une rétention d’eau libre sous l’effet de l’hormone antidiurétique. Il est sous-diagnostiqué malgré des critères bien définis. Le diagnostic implique une évaluation fine de la volémie et l’élimination des diagnostics différentiels. Les étiologies sont classées en quatre groupes : tumeurs, médicaments, affections neurologiques et affections pulmonaires. La conduite à tenir devant un SIADH sans étiologie évidente est mal codifiée. Elle est orientée par le contexte clinique et doit comprendre au minimum une imagerie thoracique. La restriction hydrique est le traitement recommandé de première ligne en cas d’hyponatrémie légère ou modérée. Toutefois, seul le traitement de l’étiologie permet une disparition du SIADH.

Topics: Diagnosis, Differential; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) may develop in association with several malignancies. However, as an immunohistochemical analysis is not performed in the majority cases, its true cause is often uncertain. We herein report a case of SIADH following chemotherapy due to tumor-derived ADH production in a patient with mucosa-associated lymphoid tissue (MALT) lymphoma. A retrospective immunohistochemical analysis demonstrated ADH expression by lymphoma cells. These findings highlight the importance of using an immunohistochemical analysis to determine ADH production by tumor cells in patients with SIADH. Such analyses play an important role in elucidating the pathogenesis of SIADH and determining the most appropriate treatment.

Topics: Aged; Antineoplastic Agents; Asian People; Humans; Inappropriate ADH Syndrome; Lymphoma, B-Cell, Marginal Zone; Male; Retrospective Studies; Treatment Outcome; Vasopressins

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is an extremely rare cause of hyponatremia post-liver transplantation. A 15-year-old Japanese girl with recurrent cholangitis after Kasai surgery for biliary atresia underwent successful living donor liver transplantation. Peritonitis due to gastrointestinal perforation occurred. Hyponatremia gradually developed but improved after hypertonic sodium treatment. One month later, severe hyponatremia rapidly recurred. We considered the hyponatremia's cause as SIADH. We suspected that tacrolimus was the disease's cause, so we used cyclosporine instead, plus hypertonic sodium plus water intake restriction, which improved the hyponatremia. Symptomatic hyponatremia manifested by SIADH is a rare, serious complication post-liver transplantation.

Topics: Adolescent; Cholangitis; Diagnosis, Differential; Female; Humans; Hyponatremia; Immunosuppressive Agents; Inappropriate ADH Syndrome; Liver Transplantation; Postoperative Complications; Tacrolimus; Vasopressins

Topics: Aged, 80 and over; Benzamides; Humans; Inappropriate ADH Syndrome; Male; Nitriles; Phenylthiohydantoin; Prognosis; Prostatic Neoplasms, Castration-Resistant; Vasopressins

A 78-year-old woman with a history of bronchial asthma presented with distal dominant sensory disturbance and weakness in the upper and lower extremities. A biopsy of the left peroneus brevis muscle showed active vasculitis with inflammation extending into muscle fascicles and fibrinoid necrosis of the vessel wall, consistent with eosinophilic granulomatosis with polyangiitis (EGPA). Despite her decreased serum osmolarity, her serum antidiuretic hormone level was not reduced, consistent with the syndrome of inappropriate antidiuretic hormone (SIADH). Intravenous and oral steroid therapy improved her neurological symptoms. Clinicians should consider EGPA as a concurrent, and potentially causative, disorder in cases of SIADH.

Topics: Adrenal Cortex Hormones; Aged; Eosinophilia; Female; Granulomatosis with Polyangiitis; Humans; Inappropriate ADH Syndrome; Vasopressins

Hyponatremia is often caused by the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Hypersecretion of vasopressin from malignant tumors can be considered a cause of SIADH. Most of these ectopic productions of vasopressin are complications of small cell lung cancer. Cases concomitant with ovarian tumors are very rare, and a specific causative substance from the ovary is often unknown. A 16-year-old woman was diagnosed with an ovarian tumor. She developed hyponatremia that was resistant to medical treatment, but immediately improved after surgical resection of the tumor. Her diagnosis was SIADH caused by an ovarian tumor; however, her serum vasopressin level was normal. It is possible that a vasopressin-like substance causing SIADH was secreted by either nervous system tissue within an immature teratoma or small cell lung cancer. We should be cautious when SIADH is a complication of an ovarian tumor.

Topics: Adolescent; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Ovarian Neoplasms; Teratoma; Vasopressins

Topics: Biopsy, Needle; Carcinoma, Non-Small-Cell Lung; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Vasopressins

During the past 50 years the molecular mechanisms of renal reabsorption of sodium and water have been described and molecules specifically interfering with these mechanisms have been developed (diuretics, vasopressin receptor antagonists). Chronic hyponatremia is caused by relative excess of free water, it occurs within a broad spectrum of diseases associated with hypervolemia (heart failure, liver cirrhosis), normovolemia and hypovolemia and it is a negative prognostic factor for patients with chronic heart failure and cirrhotic ascites. Vaptans (vasopressin antagonists, vasopressin V2-receptor inhibitors) reduce reabsorption of water in the distal nephron, they increase free water excretion and normalize serum concentrations of sodium in normovolemic and hypervolemic conditions associated with hyponatremia. Hyponatremia can be corrected (depending on cause, severity and speed of development) through the reduction of fluid intake, administration of a hypertonic solution NaCl, diuretics, oral administration of urea and by vaptans. The role of vaptans in the treatment of hyponatremia should be defined even better, in Europe vaptans can be used to treat the syndrome of inadequate antidiuretic hormone secretion (SIADH).Key words: hyponatremia - liver cirrhosis - heart failure - syndrome of inadequate secretion ADH - tolvaptan - vasopressin.

Topics: Antidiuretic Hormone Receptor Antagonists; Benzazepines; Europe; Heart Failure; Humans; Hyponatremia; Inappropriate ADH Syndrome; Liver Cirrhosis; Receptors, Vasopressin; Sodium; Tolvaptan; Vasopressins

The syndrome of inappropriate secretion of antidiuretic hormone is a disorder of impaired water excretion caused by the inability to suppress secretion of antidiuretic hormone. It has been commonly associated with small cell carcinoma. The association of this syndrome with squamous cell lung carcinoma has rarely been reported, with only 4 cases over the past two decades in the English literature. We describe the case of a 75-year-old Caucasian male who developed the syndrome after a right pneumonectomy for down-staged squamous cell lung cancer previously treated with neoadjuvant platinum-based chemotherapy and radiotherapy.

Topics: Aged; Carcinoma, Squamous Cell; Chemoradiotherapy; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Paraneoplastic Syndromes; Pneumonectomy; Vasopressins

Neonatal hyponatraemia is common, and related to significant morbidity and mortality. We report a case of a preterm newborn (gestational age of 36 weeks) with hyponatraemia, and with a prenatal diagnosis of cleft lip and palate, with a normal fetal karyotype. On the seventh day of life, a biochemical evaluation for jaundice and mild signs of dehydration showed hyponatraemia of 124 mmol/L. Investigation showed normal adrenal and thyroid functions, plasma hyposmolality (258 mOsm/kg); high urinary sodium (73 mmol/L) and high urinary osmolality (165 mOsm/kg). Despite oral sodium supplementation and fludrocortisone treatment, sodium levels remained between 124 and 130 mmol/L. Cranial ultrasound, brain MRI and renal ultrasound were normal. The diagnosis of hyponatraemia was unpredicted and the investigation was suggestive of reset osmostat, a subtype of the syndrome of inappropriate secretion of antidiuretic hormone, characterised by a subnormal threshold for antidiuretic hormone secretion.

Topics: Anti-Inflammatory Agents; Dehydration; Fludrocortisone; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant, Newborn; Jaundice; Magnetic Resonance Imaging; Male; Osmolar Concentration; Premature Birth; Sodium; Vasopressins

Hyponatraemia, defined as a serum sodium concentration <135 mmol/l, is the most common disorder of body fluid and electrolyte balance encountered in clinical practice. It can lead to a wide spectrum of clinical symptoms, from subtle to severe or even life threatening, and is associated with increased mortality, morbidity and length of hospital stay in patients presenting with a range of conditions. Despite this, the management of patients remains problematic. The prevalence of hyponatraemia in widely different conditions and the fact that hyponatraemia is managed by clinicians with a broad variety of backgrounds have fostered diverse institution- and speciality-based approaches to diagnosis and treatment. To obtain a common and holistic view, the European Society of Intensive Care Medicine (ESICM), the European Society of Endocrinology (ESE) and the European Renal Association - European Dialysis and Transplant Association (ERA-EDTA), represented by European Renal Best Practice (ERBP), have developed the Clinical Practice Guideline on the diagnostic approach and treatment of hyponatraemia as a joint venture of three societies representing specialists with a natural interest in hyponatraemia. In addition to a rigorous approach to methodology and evaluation, we were keen to ensure that the document focused on patient-important outcomes and included utility for clinicians involved in everyday practice.

Topics: Adult; Algorithms; Blood Glucose; Brain Edema; Critical Care; Endocrinology; Evidence-Based Medicine; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infusions, Intravenous; Kidney Diseases; Male; Nephrology; Osmolar Concentration; Saline Solution, Hypertonic; Sodium; Vasopressins

Hyponatraemia, defined as a serum sodium concentration <135 mmol/l, is the most common disorder of body fluid and electrolyte balance encountered in clinical practice. It can lead to a wide spectrum of clinical symptoms, from subtle to severe or even life threatening, and is associated with increased mortality, morbidity and length of hospital stay in patients presenting with a range of conditions. Despite this, the management of patients remains problematic. The prevalence of hyponatraemia in widely different conditions and the fact that hyponatraemia is managed by clinicians with a broad variety of backgrounds have fostered diverse institution- and speciality-based approaches to diagnosis and treatment. To obtain a common and holistic view, the European Society of Intensive Care Medicine (ESICM), the European Society of Endocrinology (ESE) and the European Renal Association - European Dialysis and Transplant Association (ERA-EDTA), represented by European Renal Best Practice (ERBP), have developed the Clinical Practice Guideline on the diagnostic approach and treatment of hyponatraemia as a joint venture of three societies representing specialists with a natural interest in hyponatraemia. In addition to a rigorous approach to methodology and evaluation, we were keen to ensure that the document focused on patient-important outcomes and included utility for clinicians involved in everyday practice.

Topics: Adult; Algorithms; Blood Glucose; Brain Edema; Critical Care; Endocrinology; Evidence-Based Medicine; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infusions, Intravenous; Kidney Diseases; Male; Nephrology; Osmolar Concentration; Saline Solution, Hypertonic; Sodium; Vasopressins

Although the syndrome of inappropriate antidiuretic hormone has connection with various malignant tumors, there are few reports associated with advanced gastric cancer.. We describe the case of a 63-year-old Korean male with inappropriate antidiuretic hormone syndrome due to an ectopic antidiuretic hormone-producing advanced gastric adenocarcinoma manifested with overt serum hypo-osmolar hyponatremia and high urinary sodium concentrations. His adrenal, thyroidal, and renal functioning were normal, and the hyponatremia improved following removal of the tumor. The cancer cells were immunostained and found to be positive for the antidiuretic hormone. To our knowledge, this is the first report of an antidiuretic hormone-secreting advanced gastric adenocarcinoma associated with the syndrome of inappropriate antidiuretic hormone, showing cancer cells immunostained for the antidiuretic hormone.. Although a strong relationship between gastric cancer and the syndrome of inappropriate antidiuretic hormone remains to be established, we suggest that gastric cancer could be included as a differential diagnosis of cancer that is associated with the syndrome of antidiuretic hormone.

Topics: Adenocarcinoma; Humans; Hyponatremia; Immunohistochemistry; Inappropriate ADH Syndrome; Male; Middle Aged; Paraneoplastic Endocrine Syndromes; Stomach Neoplasms; Tomography, X-Ray Computed; Vasopressins

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Urea; Vasopressins

Topics: Diagnosis, Differential; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Polydipsia, Psychogenic; Rhabdomyolysis; Vasopressins; Water Intoxication

Apelin and vasopressin levels are regulated in opposite directions to maintain body fluid homeostasis.. We thus assessed plasma apelin to copeptin ratios, with plasma copeptin concentrations as a reliable index of vasopressin secretion, in pathological states combining high levels of vasopressin secretion with hyponatremia.. We carried out a cross-sectional study including 113 healthy subjects, 21 hyponatremic patients with the syndrome of inappropriate antidiuretic hormone (SIADH), and 16 normonatremic and 16 hyponatremic patients with chronic heart failure (CHF) in an academic hospital.. Individual apelin to copeptin ratios were plotted against natremia and compared with those of 10 healthy subjects of a previous study acutely challenged by water loading or hypertonic saline infusion. We calculated the percentage of SIADH/CHF patients whose apelin to copeptin ratio for a given natremia lies outside the 95% prediction limits of the physiological relationship.. In healthy subjects, median (interquartile range) plasma apelin and copeptin concentrations were 254 fmol/mL (225-311) and 4.0 fmol/mL (2.6-6.9), respectively. Sex- and age-adjusted plasma apelin concentrations were 26% higher in SIADH and normonatremic and hyponatremic CHF patients than in healthy subjects. Sex- and age-adjusted plasma copeptin concentration was 75%, 187%, and 207% higher in SIADH and normonatremic and hyponatremic CHF patients, respectively, than in healthy subjects. During an acute osmotic challenge, the plasma apelin to copeptin ratio decreased exponentially with natremia. Apelin to copeptin ratios as a function of natremia were outside the 95% predicted physiological limits for 86% of SIADH patients and 81% of hyponatremic CHF patients.. Inappropriate apelin concentrations and apelin to copeptin ratios as a function of natremia in SIADH and CHF patients suggest that the increase in plasma apelin secretion cannot compensate for the higher levels of vasopressin release and may contribute to the corresponding water metabolism defect.

Topics: Adolescent; Adult; Aged; Apelin; Biomarkers; Cross-Sectional Studies; Female; Glycopeptides; Heart Failure; Humans; Hyponatremia; Inappropriate ADH Syndrome; Intercellular Signaling Peptides and Proteins; Male; Middle Aged; Models, Biological; Neurophysins; Pituitary Gland, Posterior; Protein Precursors; Saline Solution, Hypertonic; Up-Regulation; Vasopressins; Young Adult

Topics: Enalapril; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

Hyponatremia is a serious, but often overlooked, electrolyte imbalance that has been independently associated with a wide range of deleterious changes involving many different body systems. Untreated acute hyponatremia can cause substantial morbidity and mortality as a result of osmotically induced cerebral edema, and excessively rapid correction of chronic hyponatremia can cause severe neurologic impairment and death as a result of osmotic demyelination. The diverse etiologies and comorbidities associated with hyponatremia pose substantial challenges in managing this disorder. In 2007, a panel of experts in hyponatremia convened to develop the Hyponatremia Treatment Guidelines 2007: Expert Panel Recommendations that defined strategies for clinicians caring for patients with hyponatremia. In the 6 years since the publication of that document, the field has seen several notable developments, including new evidence on morbidities and complications associated with hyponatremia, the importance of treating mild to moderate hyponatremia, and the efficacy and safety of vasopressin receptor antagonist therapy for hyponatremic patients. Therefore, additional guidance was deemed necessary and a panel of hyponatremia experts (which included all of the original panel members) was convened to update the previous recommendations for optimal current management of this disorder. The updated expert panel recommendations in this document represent recommended approaches for multiple etiologies of hyponatremia that are based on both consensus opinions of experts in hyponatremia and the most recent published data in this field.

Topics: Adrenal Insufficiency; Antidiuretic Hormone Receptor Antagonists; Clinical Trials as Topic; Diagnosis, Differential; Diuretics; Gastrointestinal Diseases; Genetic Diseases, X-Linked; Humans; Hyponatremia; Hypothyroidism; Hypovolemia; Inappropriate ADH Syndrome; Liver Cirrhosis; Polydipsia; Receptors, Vasopressin; Sodium Chloride; Vasopressins

The aims of this study were to describe the characteristics of hyponatremia in elderly users of antidepressants, to determine the prevalence and risk factors for hyponatremia, and to identify the underlying mechanisms.. Cross-sectional study (March 2007-April 2009) with prospectively collected data. Patients were older than 60 years, used antidepressants, and had a complete geriatric assessment.. Serum sodium and antidiuretic hormone levels, serum osmolality, urine sodium level, and urine osmolality were measured. The prevalence of hyponatremia (serum sodium <135 mM) as an adverse reaction to an antidepressant (AR-AD), defined with Naranjo's algorithm, was calculated. Hyponatremic patients were compared to normonatremic patients with regard to gender, age, weight, history of hyponatremia, hyponatremia-associated medications and disorders, and type and duration of antidepressant use.. Of 358 eligible patients, 345 were included. The prevalence of hyponatremia as an AR-AD was 9.3%. Risk factors were a history of hyponatremia (adjusted OR 11.17, 95%CI 2.56-40.41), weight<60 kg (adjusted OR 3.47, 95%CI 1.19-10.13), and psychosis (adjusted OR 3.62, 95%CI 1.12-11.73). Non-suppressed ADH was found in a minority of hyponatremic patients.. In elderly patients, the prevalence of hyponatremia as adverse reaction to all types of antidepressants was 9%. Patients with previous hyponatremia, weight <60 kg, and psychosis were at risk. Beside SIADH, the nephrogenic syndrome of inappropriate antidiuresis, in which ADH secretion was normal, is postulated as an underlying mechanism. This has consequences for treatment of antidepressant-induced hyponatremia with vasopressin receptor antagonists.

Topics: Aged; Aged, 80 and over; Antidepressive Agents; Cross-Sectional Studies; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Odds Ratio; Prevalence; Prospective Studies; Risk Factors; Sodium; Vasopressins

Binding of vasopressin to its type 2 receptor in renal collecting ducts induces cAMP signaling, transcription and translocation of aquaporin (AQP)2 water channels to the plasma membrane, and water reabsorption from the prourine. Demeclocycline is currently used to treat hyponatremia in patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Demeclocycline's mechanism of action, which is poorly understood, is studied here. In mouse cortical collecting duct (mpkCCD) cells, which exhibit deamino-8-D-arginine vasopressin (dDAVP)-dependent expression of endogenous AQP2, demeclocycline decreased AQP2 abundance and gene transcription but not its protein stability. Demeclocycline did not affect vasopressin type 2 receptor localization but decreased dDAVP-induced cAMP generation and the abundance of adenylate cyclase 3 and 5/6. The addition of exogenous cAMP partially corrected the demeclocycline effect. As in patients, demeclocycline increased urine volume, decreased urine osmolality, and reverted hyponatremia in an SIADH rat model. AQP2 and adenylate cyclase 5/6 abundances were reduced in the inner medulla but increased in the cortex and outer medulla, in the absence of any sign of toxicity. In conclusion, our in vitro and in vivo data indicate that demeclocycline mainly attenuates hyponatremia in SIADH by reducing adenylate cyclase 5/6 expression and, consequently, cAMP generation, AQP2 gene transcription, and AQP2 abundance in the renal inner medulla, coinciding with a reduced vasopressin escape response in other collecting duct segments.

Topics: Adenylyl Cyclases; Animals; Anti-Bacterial Agents; Aquaporin 2; Cells, Cultured; Cyclic AMP; Deamino Arginine Vasopressin; Demeclocycline; Disease Models, Animal; Hyponatremia; In Vitro Techniques; Inappropriate ADH Syndrome; Kidney Medulla; Male; Mice; Minocycline; Rats; Rats, Wistar; Vasopressins

Because of antidiuretic hormone (ADH) disorder on production or function we can observe dysnatremia. In the absence of production by posterior pituitary, central diabetes insipidus (DI) occurs with hypernatremia. There are hereditary autosomal dominant, autosomal recessive or X- linked forms. When ADH is secreted but there is an alteration on his receptor AVPR2, it is a nephrogenic diabetes insipidus in acquired or hereditary form. We can make difference on AVP levels and/or on desmopressine response which is negative in nephrogenic forms. Hyponatremia occurs when there is an excess of ADH production: it is a euvolemic hypoosmolar hyponatremia. The most frequent etiology is SIADH (syndrome of inappropriate secretion of ADH), a diagnostic of exclusion which is made after eliminating corticotropin deficiency and hypothyroidism. In case of brain injury the differential diagnosis of cerebral salt wasting (CSW) syndrome has to be discussed, because its treatment is perfusion of isotonic saline whereas in SIADH, the treatment consists in administration of hypertonic saline if hyponatremia is acute and/or severe. If not, fluid restriction demeclocycline or vaptans (antagonists of V2 receptors) can be used in some European countries. Four types of SIADH exist; 10 % of cases represent not SIADH but SIAD (syndrome of inappropriate antidiuresis) due to a constitutive activation of vasopressin receptor that produces water excess. c 2013 Published by Elsevier Masson SAS.

Topics: Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diagnosis, Differential; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Pituitary Diseases; Pituitary Gland, Posterior; Receptors, Vasopressin; Sodium Chloride; Vasopressins; Water-Electrolyte Imbalance

This study evaluated the osmoregulatory system changes in 39 patients with severe ovarian hyperstimulation syndrome. Plasma osmolality (Posm) less or more than 280 mOsm/kg body weight were associated with inappropriate antidiuretic hormone secretion syndrome and hypovolemia, respectively.

Topics: Adult; Dinoprostone; Female; Humans; Hypovolemia; Inappropriate ADH Syndrome; Osmolar Concentration; Ovarian Hyperstimulation Syndrome; Ovulation Induction; Severity of Illness Index; Vasopressins; Water-Electrolyte Balance; Young Adult

Topics: Amitriptyline; Carbamazepine; Comorbidity; Demeclocycline; Diabetic Neuropathies; Diuretics; Furosemide; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Saline Solution, Hypertonic; Spain; Urea; Vasopressins

The Asian variant of intravascular large B cell lymphoma is a special type of intravascular lymphoma with hemophagocytic syndrome and hypercytokinemia including interleukin-6, which stimulates antidiuretic hormone synthesis in the hypothalamus. We present here that the syndrome of inappropriate antidiuretic hormone secretion frequently occurs in patients with the Asian variant of intravascular large B cell lymphoma. The syndrome of inappropriate antidiuretic hormone secretion was found in eight of 118 (6.8%) lymphoma patients at the first diagnosis. Although there were six (5.1%) among 118 lymphoma patients with the Asian variant of intravascular large B cell lymphoma, four of the six patients (66.7%) developed the syndrome of inappropriate antidiuretic hormone secretion. In four patients with the Asian variant of intravascular large B cell lymphoma with the syndrome of inappropriate antidiuretic hormone secretion, elevated serum interleukin-6 and low sodium levels were almost normalized after chemotherapy. The Asian variant of intravascular large B cell lymphoma patients frequently develop the syndrome of inappropriate antidiuretic hormone secretion, and interleukin-6 might play a role in the occurrence of this disease. We should pay attention to hyponatremia caused by the syndrome of inappropriate antidiuretic hormone secretion in patients with the Asian variant of intravascular large B cell lymphoma.

Topics: Adult; Aged; Aged, 80 and over; Asia; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Interleukin-6; Lymphoma, Large B-Cell, Diffuse; Male; Middle Aged; Sodium; Syndrome; Vasopressins; Young Adult

Topics: Critical Care; Humans; Hyponatremia; Inappropriate ADH Syndrome; Osmolar Concentration; Urea; Vasopressins; Water-Electrolyte Balance

A 60-year-old female underwent right upper lobectomy of the lung and lymph node dissection under a diagnosis of cancer in the upper lobe of the right lung. Pathological examination showed stage IIIA adenocarcinoma with mediastinal lymph node metastasis. One month after the operation, adjuvant chemotherapy with carboplatin (CBDCA) and paclitaxel (PTX) was initiated. Four days after the chemotherapy, hyponatremia progressed, and central nervous system disorder developed. A diagnosis of syndrome of inappropriate secretion of antidiuretic hormone (SIADH) was made. She recovered after fluid intake restriction and electrolyte correction. SIADH was considered to be due to the adverse effects of anticancer drugs. In postoperative adjuvant chemotherapy, attention should be paid to the serum Na level.

Topics: Adenocarcinoma; Adenocarcinoma of Lung; Animals; Antineoplastic Agents; Antineoplastic Agents, Phytogenic; Antineoplastic Combined Chemotherapy Protocols; Carboplatin; Carcinoma, Non-Small-Cell Lung; Combined Modality Therapy; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lung; Lung Neoplasms; Lymphatic Metastasis; Middle Aged; Paclitaxel; Vasopressins

Topics: Aged; Diuretics; Humans; Hydrochlorothiazide; Inappropriate ADH Syndrome; Male; Severity of Illness Index; Vasopressins

Nephrogenic syndrome of inappropriate antidiuresis (NSIAD), the X-linked disease resulting from activating mutation of the vasopressin V2 receptor gene (AVPR2), is a recently described condition causative of episodes of hyponatremia in boys and male and female adults.. The objective of the study was the pathophysiological characterization of NSIAD.. A family with NSIAD was identified and investigated for hyponatremic episodes and degrees of urine dilution defects. For the first time, the impact of the mutated V2R on aquaporin 2 (AQP2) excretion is reported.. The study was conducted at a referral center.. Five patients of seven carriers (two young brothers and their mother and her two sisters) were investigated together with age-matched controls.. There were no interventions.. In NSIAD patients, urinary AQP2 excretion occurred independently of concomitant vasopressin excretion and strongly correlated with urine osmolality, confirming direct AQP2 involvement in urine concentration. Water loading was followed by a very slow and incomplete elimination in the asymptomatic hemizygous boy with no suppression of AQP2 excretion and a delayed elimination in the heterozygous women because of an incomplete suppression of AQP2, and it induced hyponatremia in all NSIAD patients. Two hemizygous carriers presented with severe hyponatremia-induced seizures, and the repetition in one of them led to mental retardation.. Hyponatremia was a constant and characteristic aspect of the abnormal response to even mild water-loading tests in an asymptomatic hemizygous child as well as heterozygous adults. We confirm the phenotypic variability of NSIAD, a disease that should be regarded in pediatric intensive care units in presence of severe and/or recurrent hyponatremia, and also in adults, because carriers are prone to hyponatremia.

Topics: Adult; Aquaporin 2; Case-Control Studies; Child, Preschool; DNA Mutational Analysis; Family; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant; Male; Pedigree; Receptors, Vasopressin; Vasopressins

A 66-year-old man was referred to our hospital with esophageal tumor. He was diagnosed with esophageal small cell carcinoma by endoscopic biopsy. He had a low serum sodium level at admission and was diagnosed syndrome of inappropriate secretion of antidiuretic hormone (SIADH). His CT scan revealed esophageal wall thickness and swelling of thoracic and abdominal lymph nodes. He was classified as Stage IV a (cT3cN4cM0). He received systemic chemotherapy with CDDP and CPT-11. After three courses of chemotherapy, his tumor disappeared on CT scan and endoscopy. He was diagnosed as in complete remission and his SIADH recovered. The patient was then discharged and visited our outpatient clinic. Seven months after diagnosis, a tumor recurrence was indicated by CT scan and endoscopy. He received radiation therapy, and chemotherapy of paclitaxel, followed by CBDCA+VP-16. He is presently alive sixteen months after diagnosis.

Topics: Aged; Biopsy; Carcinoma, Small Cell; Combined Modality Therapy; Esophageal Neoplasms; Humans; Inappropriate ADH Syndrome; Male; Tomography, X-Ray Computed; Vasopressins

Topics: Humans; Inappropriate ADH Syndrome; Urinalysis; Vasopressins

We describe a rare case of thymic neuroblastoma with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). A 60-year-old male patient was admitted to our hospital for further examination and treatment of anterior mediastinal tumor found at a regular health check-up. On examination there was hyponatremia, decrease in plasma osmolarity and elevation of plasma antidiuretic hormone (ADH) level. Thus, he underwent total thymectomy under the diagnosis of thymoma with SIADH. The tumor was located in the right lobe of the thymus and the final diagnosis was thymic neuroblastoma. To our knowledge, this is the first reported case of thymic neuroblastoma in which production of ADH by tumor cells is demonstrated immunohistochemically. This case highlights the need to consider functional activity of thymic neuroblastoma and complete resection of the tumor is warranted for treatment.

Topics: Biomarkers; Biopsy; Humans; Hyponatremia; Immunohistochemistry; Inappropriate ADH Syndrome; Magnetic Resonance Imaging; Male; Middle Aged; Neuroblastoma; Osmolar Concentration; Thymectomy; Thymus Neoplasms; Tomography, X-Ray Computed; Treatment Outcome; Up-Regulation; Vasopressins

Patients having the nephrogenic syndrome of inappropriate antidiuresis present either the R137C or R137L V2 mutated receptor. While the clinical features have been characterized, the molecular mechanisms of functioning of these two mutants remain elusive. In the present study, we compare the pharmacological properties of R137C and R137L mutants with the wild-type and the V2 D136A receptor, the latter being reported as a highly constitutively active receptor. We have performed binding studies, second messenger measurements and BRET experiments in order to evaluate the affinities of the ligands, their agonist and antagonist properties and the ability of the receptors to recruit beta-arrestins, respectively. The R137C and R137L receptors exhibit small constitutive activities regarding the G(s) protein activation. In addition, these two mutants induce a constitutive beta-arrestin recruitment. Of interest, they also exhibit weak sensitivities to agonist and to inverse agonist in term of G(s) protein coupling and beta-arrestin recruitment. The small constitutive activities of the mutants and the weak regulation of their functioning by agonist suggest a poor ability of the antidiuretic function to be adapted to the external stimuli, giving to the environmental factors an importance which can explain some of the phenotypic variability in patients having NSIAD.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Arrestins; beta-Arrestins; Chlorocebus aethiops; COS Cells; Fluorescence Resonance Energy Transfer; Humans; Inappropriate ADH Syndrome; Mutant Proteins; Protein Binding; Receptors, Vasopressin; Vasopressins

To study any possible relation between hyponatremia following brain injury and the presence of cerebral salt-wasting syndrome (CSWS) or the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), and if vasopressin, brain natriuretic peptide (BNP) and aldosterone have a role in its mechanism.. Patients with brain injury admitted to the intensive care unit were included and had their BNP, aldosterone and vasopressin levels dosed on day 7.. Twenty six adult patients were included in the study. Nine (34.6%) had hyponatremia and presented with a negative water balance and higher values of urinary sodium, serum potassium and diuresis than patients with normonatremia. The serum levels of BNP, aldosterone, and vasopressin were normal and no relation was observed between plasma sodium and BNP, aldosterone or vasopressin.. The most likely cause of hyponatremia was CSWS and there was no correlation between BNP, aldosterone and vasopressin with serum sodium level.

Topics: Adolescent; Adult; Aldosterone; Brain Diseases, Metabolic; Brain Injuries; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Natriuretic Peptide, Brain; Vasopressins; Young Adult

Topics: Aquaporins; Brain Edema; Burns; Diarrhea; Fluid Therapy; Humans; Hypotonic Solutions; Inappropriate ADH Syndrome; Isotonic Solutions; Kidney; Neurons; Transcription Factors; Vasopressins; Vomiting; Water-Electrolyte Balance

Syndrome of inappropriate antidiuretic hormone secretion is frequent in small-cell lung carcinomas. We report on a case of syndrome of inappropriate antidiuretic hormone secretion after each of the first 2 cycles of chemotherapy for small-cell lung cancer. The association with chemotherapy-induced tumor lysis is proposed, particularly based on the course of antidiuretic hormone levels, and a review of the literature is presented. Syndrome of inappropriate antidiuretic hormone secretion can occur during tumor lysis syndrome.

Topics: Carcinoma, Small Cell; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Middle Aged; Paraneoplastic Syndromes; Tumor Lysis Syndrome; Vasopressins

We report a 74-year-old woman with histologically confirmed neuroendocrine carcinoma of the nasal cavity disclosing a syndrome of inappropriate antidiuretic hormone secretion (SIADH). Since SIADH is a paraneoplastic syndrome commonly associated with small cell lung cancer, an extra-pulmonary localisation of neuroendocrine carcinoma has to be investigated.

Topics: Aged; Carcinoma, Neuroendocrine; Humans; Inappropriate ADH Syndrome; Male; Nose Neoplasms; Paranasal Sinuses; Vasopressins

A 61-year-old man had hyponatremia (serum Na 112 mmol/L), which was associated with disturbance of consciousness. Therefore, administration of hypertonic saline was commenced. Eventually he was diagnosed with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Hypertonic saline was continued for 45 days, and plasma Na concentration rose to 138 mmol/L. At that time we were consulted regarding further administration of hypertonic saline. At the time of the consultation marked edema had developed affecting the whole body. The cardiothoracic ratio was increased and pleural effusion was evident on the chest X-ray. Administration of hypertonic saline was discontinued to prevent further worsening of the edema. Furthermore, water restriction (500 mL/day) was started. Body weight decreased by 4.3 kg in 7 days and the edema was diminished. However, plasma Na concentration decreased to 117 mmol/L. At that stage, we needed to balance the treatment of hyponatremia to the increased extracellular fluid volume (ECF). To normalize the ECF, we carried out ultrafiltration (UF) three times. Resolution of edema by using an extracorporeal UF method allowed the control of plasma Na concentration. In this case increased ECF volume hindered the adjustment of plasma Na concentration. The infusion of hypertonic saline is now used commonly by physicians. It is necessary to consider the potential risks of such treatment.

Topics: Edema; Esthesioneuroblastoma, Olfactory; Humans; Inappropriate ADH Syndrome; Magnetic Resonance Imaging; Male; Middle Aged; Nasal Cavity; Nose Neoplasms; Pleural Effusion; Radiography; Saline Solution, Hypertonic; Sodium; Ultrafiltration; Vasopressins

Topics: Animals; Dogs; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins; Water-Electrolyte Imbalance

Vasopressin is a critical regulator of water homeostasis. There are two major receptors for vasopressin: V1 and V2 receptors. Disturbances in water balance are commonly encountered in clinical practice and can be divided into disorders of urinary dilution and concentration. The major representatives of such disorders are diabetes insipidus and the syndrome of inappropriate secretion of antidiuretic hormone (SI ADH). Recent studies show that genetic forms of nephrogenic diabetes insipidus are due to mutations in the genes coding for the vasopressin V2 receptor (V2R) or aquaporin-2 (AQP2). Identification of the genes involved and analysis of the cellular fate of the V2R and AQP2 mutants are relevant for understanding the functioning of the V2R and AQP2 protein. These developments also have implications for future therapeutic options. The development of nonpeptide vasopressin receptor antagonists (VRAs) offers prospects for the treatment of euvolaemic (SI ADH) or hypervolaemic hyponatraemia (congestive heart failure or cirrhosis). Several nonpeptide VRAs are now in various stages of clinical trials. At present, only conivaptan is registered by the FD A for intravenous treatment of euvolaemic and hypervolaemic hyponatremia. A recent long-term study comparing tolvaptan with placebo in patients with chronic heart failure showed no reduction in risk of death and hospitalisation.

Topics: Antidiuretic Hormone Receptor Antagonists; Diabetes Insipidus, Nephrogenic; Humans; Inappropriate ADH Syndrome; Mutation; Receptors, Vasopressin; Vasopressins; Water; Water-Electrolyte Balance; Water-Electrolyte Imbalance

A 71-year old man with failed back syndrome was admitted to hospital with oliguria that had occurred 4 days after his dose of paroxetine had been increased to 40 mg x day(-1). Laboratory data on admission revealed hyponatremia (124 mmol x l(-1)), low serum osmolarity (267 mOsm x l(-1)) with a normal level of serum antidiuretic hormone (1.7 pg x ml(-1)), and concentrated urine (430 mOsm x l(-1)). He was diagnosed as having syndrome of inappropriate secretion of antidiuretic hormone, associated with paroxetine; this drug was discontinued immediately after admission. The hyponatremia was treated with saline infusion, water restriction, and furosemide; serum sodium level returned to normal on hospital day 5. Paroxetine is being increasingly used for depression and chronic pain management because of its favorable side-effect profile; however, we should be alert to hyponatremia in patients on paroxetine by carrying out periodic monitoring of serum electrolytes, especially in elderly patients.

Topics: Aged; Antidepressive Agents, Second-Generation; Chronic Disease; Depressive Disorder; Electrolytes; Humans; Hyponatremia; Inappropriate ADH Syndrome; Intervertebral Disc Displacement; Male; Pain; Paroxetine; Sodium; Spinal Stenosis; Vasopressins

Two children with complete congenital anterior hypopituitarism developed hyponatremia; inappropriate secretion of antidiuretic hormone was documented despite adequate hormonal replacement therapy. These cases show that congenital hypopituitarism can be associated with SIADH in children later than the neonatal period, despite adequate replacement therapy.

Topics: Adolescent; Child, Preschool; Female; Fluid Therapy; Hormone Replacement Therapy; Humans; Hyponatremia; Hypopituitarism; Inappropriate ADH Syndrome; Magnetic Resonance Imaging; Male; Pituitary Gland, Anterior; Treatment Outcome; Vasopressins

Nonosmotic antidiuretic hormone (ADH) activity can cause severe hyponatremia during involuntary fluid administration. We looked for evidence of this before and during intravenous (IV) fluid administration in children treated for gastroenteritis.. In this prospective observational study, plasma ADH, electrolytes, osmolality, and glucose were measured in 52 subjects before (T0) and 4 hours after (T4) starting 0.45% saline + 2.5% dextrose and subsequently when indicated. Hormonal markers of stress were measured at T0. Urine samples were collected to measure electrolytes and osmolality.. The nonosmotic stimuli of ADH secretion that we identified were vomiting (50 of 52), dehydration (median: 5%; range: 3-8%), hypoglycemia (2 of 52), and raised hormonal markers of stress (mean +/- SD: cortisol, 1094 +/- 589 nmol/L; reverse triiodothyronine, 792 +/- 293 pmol/L). At T0, half the children were hyponatremic (plasma sodium concentration of < 135 mmol/L; n = 27). The median plasma ADH concentration at T0 was significantly elevated (median: 7.4 pg/mL; range: < 1.9-85.6 pg/mL). ADH was high in both hyponatremic and normonatremic children and remained high at T4 in 33 of the 52 children, 22 of whom were concurrently hyponatremic. At T4, mean plasma sodium concentration was unchanged in the hyponatremic children but was 2.6 mmol/L (+/-2.0) lower in those who were initially normonatremic. Urine tonicity was high compared with 0.45% saline in 16 of 19 children at baseline and in 20 of 37 children after 3 to 12 hours of IV fluids.. Nonosmotic stimuli of ADH secretion are frequent in children with gastroenteritis. Their persistence during IV-fluid administration predisposes to dilutional hyponatremia. The use of hypotonic saline for deficit replacement needs to be reassessed.

Topics: Child; Child, Preschool; Female; Fluid Therapy; Gastroenteritis; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant; Male; Prospective Studies; Vasopressins

The use of vasopressin for the treatment of septic shock is increasing. Few reports of fluid and electrolyte complications of this therapy have been reported. A neurologically impaired, 53-year-old man with a history of syndrome of inappropriate antidiuretic hormone developed apparent transient diabetes insipidus and acute hypernatremia after being treated with vasopressin. He was treated for presumed septic shock with intravenous vasopressin 0.01-0.10 U/minute. His blood pressure did not improve with this therapy, and his course was complicated by hyponatremia during the vasopressin infusion. Discontinuation of the infusion was followed by a profound (8.4 L) diuresis and rapid onset of hypernatremia (serum sodium concentration increased from 132 to 157 mEq/L over 8 hrs). Although urine osmolality was not measured during the patient's diuresis, the rapid changes in serum sodium concentration can be explained only by an inappropriate water diuresis. The diuresis ceased when the vasopressin infusion was resumed. We concluded that these findings are most consistent with transient diabetes insipidus. The safety and efficacy of intravenous vasopressin have not been established in patients with septic shock and underlying disorders of water homeostasis. The drug may have diminished vasoconstrictive effects in this patient population. Careful monitoring of water and sodium balance is warranted in all patients treated with vasopressin for septic shock.

Topics: Acute Disease; Diabetes Insipidus; Humans; Hypernatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Vasoconstrictor Agents; Vasopressins

Inappropriate antidiuretic hormone secretion syndrome is rare in patients with gynecologic tumors.. A 22-year-old woman presented with inappropriate antidiuretic hormone secretion symptoms during the 2 months preceding the diagnosis of an immature ovarian teratoma. Vasopressin levels in serum and in the urine were very low. Restriction of water intake and surgical removal of the teratoma resulted in the definitive correction of the hyponatremia. This observation suggests that immature teratoma cells can produce a vasopressin-like factor, and the syndrome may be a sign of an ovarian malignancy.. Pelvic organs should be examined when the more common causes of inappropriate antidiuretic hormone secretion syndrome have been ruled out.

Topics: Adult; Antineoplastic Combined Chemotherapy Protocols; Drinking; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Ovarian Neoplasms; Teratoma; Vasopressins

The syndrome of inappropriate antidiuretic hormone (SIADH) is associated with water retention and hyponatremia. The kidney adapts via a transient natriuresis and persistent diuresis, i.e., vasopressin escape. Previously, we showed an increase in the whole kidney abundance of aldosterone-sensitive proteins, the alpha- and gamma (70-kDa-band)-subunits of the epithelial Na(+) channel (ENaC), and the thiazide-sensitive Na-Cl cotransporter (NCC) in our rat model of SIADH. Here we examine mean arterial pressure via radiotelemetry, aldosterone activity, and cortical vs. medullary ENaC subunit and 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD-2) protein abundances in escape. Eighteen male Sprague-Dawley rats (300 g) were sham operated (n = 6) or infused with desmopressin (dDAVP; n = 12, a V(2) receptor-selective analog of AVP). After 4 days, one-half of the rats receiving dDAVP were switched to a liquid diet, i.e., water loaded (WL) for 5-7 additional days. The WL rats had a sustained increase in urine volume and blood pressure (122 vs. 104 mmHg, P < 0.03, at 7 days). Urine and plasma aldosterone levels were increased in the WL group to 844 and 1,658% of the dDAVP group, respectively. NCC and alpha- and gamma-ENaC (70-kDa band) were increased significantly in the WL group (relative to dDAVP), only in the cortex. Beta- and gamma-ENaC (85-kDa band) were increased significantly by dDAVP in cortex and medulla relative to control. 11beta-HSD-2 was increased by dDAVP in the cortex and not significantly affected by water loading. These changes may serve to attenuate Na(+) losses and ameliorate hyponatremia in vasopressin escape.

Topics: 11-beta-Hydroxysteroid Dehydrogenase Type 2; Aldosterone; Animals; Blood Pressure; Blotting, Western; Deamino Arginine Vasopressin; Diuresis; Electrolytes; Epithelial Sodium Channels; Immunoenzyme Techniques; Immunohistochemistry; Inappropriate ADH Syndrome; Kidney; Male; Natriuresis; Osmolar Concentration; Rats; Rats, Sprague-Dawley; Renal Agents; Sodium Channels; Vasopressins

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterized by hyponatremia and the plasma hypoosmolality induced by water retention attributable to persistent antidiuretic hormone (ADH) release. It has been reported that SIADH may occur due to various factors in patients with malignant tumor. We report a case of hypopharyngeal cancer complicated by SIADH following chemotherapy. A 72-year-old woman with hypopharyngeal cancer was treated by oral administration of S-1 and intravenous administration of low-dose cisplatin following radiation therapy. General fatigue and coma occurred during the third course of this chemotherapy, using S-1 and low-dose cisplatin. We believed that she had SIADH because of the results of examinations including hyponatremia, serum hypoosmolality and increasing serum ADH level. We treated her by fluid restriction and intravenous administration of hypertonic saline and furosemide, and she recovered. Unfortunately, her hypopharyngeal cancer gradually progressed and she died of acute pneumonia three months later.

Topics: Aged; Antimetabolites, Antineoplastic; Antineoplastic Agents; Carcinoma, Squamous Cell; Cisplatin; Drug Combinations; Fatal Outcome; Female; Humans; Hyponatremia; Hypopharyngeal Neoplasms; Inappropriate ADH Syndrome; Osmolar Concentration; Oxonic Acid; Pyridines; Radiotherapy, Adjuvant; Tegafur; Vasopressins

Pituitary apoplexy may be associated with visual deterioration that may be severe in some cases. Misdiagnosis of this condition is not uncommon, resulting in delayed treatment, which may adversely affect the outcome and visual prognosis. We present a case of pituitary apoplexy, who presented with features of syndrome of inappropriate anti-diuretic hormone secretion (SIADH) and monocular blindness. He had remarkable improvement to normal vision along with normalisation of serum sodium following emergency trans-sphenoidal surgery.

Topics: Decompression, Surgical; Humans; Inappropriate ADH Syndrome; Magnetic Resonance Imaging; Male; Middle Aged; Neurophysins; Pituitary Apoplexy; Pituitary Gland; Protein Precursors; Sodium; Vasopressins

To assess the frequency of vasopressin deficiency in septic shock.. Prospective cohort study.. Intensive care unit at Raymond Poincaré University Hospital.. A cohort of 44 patients who met the usual criteria for septic shock for < 7 days. A second cohort of 18 septic shock patients were enrolled within the first 8 hrs of disease onset.. None.. General demographics, severity scores, vital signs, standard biochemical data, and circulating vasopressin levels were systematically obtained at baseline in the two cohorts. Vasopressin deficiency was defined by a normal plasma vasopressin level in the presence of a systolic blood pressure of <100 mm Hg or in the presence of hypernatremia. Baroreflex sensitivity was systematically evaluated in patients of the first cohort when vasopressin deficiency was noted. In the second cohort of patients, plasma levels of vasopressin were obtained at baseline, 6, 24, 48, and 96 hrs after shock onset. In the first population, plasma vasopressin levels were inversely correlated to the delay from shock onset. Fourteen patients had relative vasopressin deficiency: 12 patients had systolic blood pressure <100 mm Hg, with impaired baroreflex sensitivity in four, and three patients had hypernatremia. In the second population, only two patients had relative vasopressin deficiency. The plasma levels of vasopressin significantly decreased over time (p < 10-3).. Plasma vasopressin levels are almost always increased at the initial phase of septic shock and decrease afterward. Relative vasopressin deficiency is seen in approximately one-third of late septic shock patients.

Topics: Analysis of Variance; Baroreflex; Blood Pressure; Female; France; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Osmolar Concentration; Prospective Studies; Shock, Septic; Sodium; Statistics, Nonparametric; Time Factors; Vasopressins; Water-Electrolyte Balance

Hypopituitarism and hyponatremia, especially when severe, are infrequent findings particularly when the cause of hypopituitarism at presentation is unknown and untreated. Interestingly, hyponatremia is usually seen in elderly patients with hypopituitarism due to various causes. We present a case with unrecognized and untreated hypopituitarism due to a large aneurysm of the internal carotid artery in the sellar region causing the syndrome of inappropriate secretion of antidiuretic hormone (SIADH).

Topics: Aneurysm; Carotid Artery, Internal; Female; Humans; Hyponatremia; Hypopituitarism; Inappropriate ADH Syndrome; Magnetic Resonance Angiography; Magnetic Resonance Imaging; Middle Aged; Radiography; Vasopressins

An autopsy case of primary small cell carcinoma (SCC) of the prostate in a 68-year-old man is reported. The patient was admitted to hospital because of a bloody stool and suspected rectal cancer. However, a diagnosis of prostate cancer was made on the basis of a digital rectal examination, the serum level of prostate-specific antigen, and a needle biopsy of the prostate. The patient also experienced a syndrome of inappropriate secretion of antidiuretic hormone. He died 29 days after admission. At autopsy, the tumor had invaded the rectum, bladder and pelvic peritoneum. Metastases to the heart, vertebrae and lymph nodes were observed. Microscopically, the tumor was composed of small round cells that showed a solid growth pattern. Rosette formations were observed. Immunohistochemically, the tumor cells were positive for a prostatic epithelial marker and neuroendocrine markers. A high level of antidiuretic hormone was detected in the tumor tissue. To our knowledge, this is the first reported case of SCC of the prostate in which both a prostatic epithelial marker and neuroendocrine markers have been found in the same tumor. This finding supports the hypothesis that SCC of the prostate originates from a multipotential stem cell of the prostatic epithelium.

Topics: Aged; Biomarkers, Tumor; Carcinoma, Small Cell; Fatal Outcome; Humans; Immunohistochemistry; Inappropriate ADH Syndrome; Male; Neuroendocrine Tumors; Prostate-Specific Antigen; Prostatic Neoplasms; Vasopressins

The syndrome of inappropriate antidiuretic hormone (SIADH) secretion has been well described in patients with meningeal spread from metastatic carcinomatosis and bacterial or mycobacterial infections. We describe a 39-year-old white man who was diagnosed with coccidioidomycosis pneumonia 7 years before presentation. He displayed evidence for meningitis with the onset of SIADH. We reviewed the diagnosis of coccidioidomycosis and radiological findings in the central nervous system. Last, we discussed the findings that led to the diagnosis of SIADH.

Topics: Adult; Coccidioides; Humans; Inappropriate ADH Syndrome; Magnetic Resonance Imaging; Male; Meningitis, Fungal; Vasopressins

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Renal Agents; Vasopressins

We describe a 74-year-old man with rheumatoid arthritis (RA) who developed syndrome of inappropriate secretion of antidiuretic hormone (SIADH) 1.5 months after commencement of mizoribin prescription when his arthritis was improved. He noticed nausea and headache and serum Na fell as low as 118 mEq/l. Normal urinary Na excretion without hypotension or hemoconcentration negated the possibility of dehydration resulting from urinary Na loss. Serum antidiuretic hormone (ADH) remained elevated at 0.59 pg/ml in spite of a significant reduction in serum osmolality to 254 mosm/kg. He had no organic disease likely to cause SIADH. Despite infusion of hypertonic saline, his serum Na was not restored to normal. Shortly after mizoribin withdrawal, his serum Na increased significantly from 128 to 139 mEq/l and plasma osmolality from 265 to 287 mosm/kg. ADH hypersecretion in relation to plasma osmolality was reversed by mizoribin withdrawal, suggesting that bredinin might adversely induce SIADH. Additional predisposing factors were the patient's age and difficulty in urination due to benign prostatic hypertrophy. In summary, we report herein the first case of SIADH believed to be an adverse effect of mizoribin, which may therefore needed to be added to the list of drugs which can induce SIADH.

Topics: Aged; Anti-Inflammatory Agents, Non-Steroidal; Arthritis, Rheumatoid; Drinking; Humans; Inappropriate ADH Syndrome; Male; Neurophysins; Osmolar Concentration; Protein Precursors; Ribonucleosides; Sodium; Vasopressins

Topics: Aged; Aged, 80 and over; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Renal Agents; Self Medication; Vasopressins

Topics: Aged; Aging; Humans; Hyponatremia; Inappropriate ADH Syndrome; Middle Aged; Renal Agents; Vasopressins

Hyponatremia after cranial vault remodeling has been noted in a pediatric patient population. If left untreated, the patients may develop a clinical hypoosmotic condition that can lead to cerebral edema, increased intracranial pressure, and eventually, to central nervous system and circulatory compromise. The hyponatremia has traditionally been attributed to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH); however, in our patients the treatment has been resuscitation with normal saline as opposed to fluid restriction (the accepted treatment of SIADH), thus placing the diagnosis of SIADH in question. Patients who developed hyponatremia after intracranial injury or surgery were, until recently, grouped together as having SIADH. However, there are diagnosis and treatment differences between SIADH and another distinct but poorly understood disorder that is designated cerebral salt wasting syndrome (CSW). CSW is associated with increased urine output and increased urine sodium concentration and volume contraction, and it is frequently seen after a central nervous system trauma. We therefore developed a prospective study to evaluate the cause of the sodium imbalance.Ten consecutive pediatric patients who underwent intracranial surgery for various craniosynostotic disorders were postoperatively monitored in the pediatric intensive care unit for hemodynamic, respiratory, and fluid management. The first four patients were evaluated for electrolyte changes and overall fluid balance to determine the consistency with which these changes occurred. The remaining six patients had daily (including preoperative) measurement of serum electrolytes, urine electrolytes, urine osmolarity, serum antidiuretic hormone (ADH), aldosterone, and atrial natriuretic hormone (ANH). All patients received normal saline intravenous replacement fluid in the postoperative period. All of the patients developed a transient hyponatremia postoperatively, despite normal saline resuscitation. Serum sodium levels as low as 128 to 133 mEq per liter (normal, 137 to 145 mEq per liter) were documented in the patients. All patients had increased urine outputs through the fourth postoperative day (>1 cc/kg/h). The six patients who were measured had an increased ANH level, with a peak value as high as 277 pg/ml (normal, 25 to 77 pg/ml). ADH levels were low or normal in all but one patient, who had a marked increase in ADH and ANH. Aldosterone levels were variable. On the basis of t

Topics: Aldosterone; Atrial Natriuretic Factor; Child, Preschool; Craniosynostoses; Electrolytes; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant; Infusions, Intravenous; Male; Postoperative Complications; Prospective Studies; Resuscitation; Skull; Sodium; Sodium Chloride; Vasopressins

Our purpose was to investigate the proportion of tyrosine hydroxylase (TH)-immunoreactive (IR) neurons expressing vasopressin (VP) mRNA in the human paraventricular and supraoptic nuclei by combining in situ hybridization with immunohistochemistry on the same tissue section. A variability in the proportion of TH-IR neurons synthesizing VP mRNA was observed in adults which was usually more than 50%. In neonates almost all the TH-IR neurons appeared to contain VP mRNA.

Topics: Adult; Aged; Aged, 80 and over; Antibodies; Female; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Paraventricular Hypothalamic Nucleus; RNA, Messenger; Supraoptic Nucleus; Tyrosine 3-Monooxygenase; Vasopressins

We report an unusual case of inappropriate antidiuresis with undetectable vasopressin in an elderly man presenting with confusion due to severe hyponatremia. Further investigations led to the diagnosis of non-functional pituitary macroadenoma. The patient had normal thyroid and adrenal function. The abnormal water balance resolved promptly after transsphenoidal removal of the tumor, confirmed by a repeat water loading test. We conclude that inappropriate antidiuresis in the absence of excess vasopressin secretion may implicate mass effect from an underlying pituitary tumor.

Topics: Adenoma; Aged; Confusion; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Pituitary Neoplasms; Vasopressins

To evaluate effects of anesthesia, surgery, and intravenous administration of fluids on plasma concentrations of antidiuretic hormone (ADH), concentration of total solids (TS), PCV, arterial blood pressure (BP), plasma osmolality, and urine output in healthy dogs.. 22 healthy Beagles.. 11 dogs did not receive fluids, and 11 received 20 ml of lactated Ringer's solution/kg of body weight/h. Plasma ADH adn TS concentrations, PCV, osmolality, and arterial BP were measured before anesthesia (T0) and after administration of preanesthetic agents (T1), induction of anesthesia (T2), and 1 and 2 hours of surgery (T3 and T4, respectively). Urine output was measured at T3 and T4.. ADH concentrations increased at T1, T3, and T4, compared with concentrations at T0. Concentration of TS and PCV decreased at all times after administration of preanesthetic drugs. Plasma ADH concentration was less at T3 in dogs that received fluids, compared with those that did not. Blood pressure did not differ between groups, and osmolality did not increase > 1% from To value at any time. At T4, rate of urine production was less in dogs that did not receive fluids, compared with those that did.. Plasma ADH concentration increased and PCV and TS concentration decreased in response to anesthesia and surgery. Intravenous administration of fluids resulted in increased urine output but had no effect on ADH concentration or arterial BP. The causes and effects of increased plasma ADH concentrations may affect efficacious administration of fluids during the perioperative period in dogs.

Topics: Anesthesia; Animals; Blood Pressure; Body Temperature; Dog Diseases; Dogs; Fluid Therapy; Hematocrit; Inappropriate ADH Syndrome; Injections, Intravenous; Osmolar Concentration; Surgical Procedures, Operative; Tidal Volume; Urine; Vasopressins

a) To determine if antidiuretic hormone (ADH) is elevated in patients undergoing spinal fusion, especially in those who have clinical evidence of syndrome of inappropriate antidiuretic hormone (SIADH); b) to evaluate the relationship between ADH secretion and the secretion of atrial natriuretic peptide (ANP).. Tertiary care pediatric intensive care unit (ICU) in a university hospital.. A prospective cross-sectional, observational study with factorial design.. Thirty patients > or = 10 yrs of age undergoing spinal fusion admitted to the ICU for postoperative care.. Patients underwent anterior, posterior, or both anterior/posterior spinal fusion. Blood was collected for serial measurements of ADH, ANP and serum electrolyte levels. Heart rate, blood pressure and central venous pressure were measured.. Thirty children were studied. Nineteen had idiopathic scoliosis, nine had neuromuscular scoliosis, one had Marfan's disease, and one had congenital scoliosis. Ten (33%) children met clinical criteria of SIADH. There was no difference in duration of surgery, blood loss, volume of iv fluid administration pre- and intraoperatively, or type of scoliosis between those who developed SIADH and those who did not. Hemodynamic variables were similar in both groups. ADH levels increased in both groups immediately postoperatively and at 6 hrs after surgery, but were much more elevated in those patients with SIADH. Patients with SIADH also had significantly higher ADH levels preoperatively. In relation to serum osmolality, ADH was considerably higher in those with SIADH compared with those who did not. Although ANP values tended to be higher in the group with SIADH, this did not reach statistical significance.. SIADH occurs in a subset of children who undergo spinal fusion. The diagnosis of SIADH can be made easily using clinical parameters which are well-defined. In the face of SIADH, continued volume expansion may be harmful, and should therefore be avoided.

Topics: Adolescent; Analysis of Variance; Atrial Natriuretic Factor; Cross-Sectional Studies; Electrolytes; Female; Hemodynamics; Humans; Inappropriate ADH Syndrome; Intensive Care Units, Pediatric; Male; Postoperative Complications; Prospective Studies; Scoliosis; Sodium; Spinal Fusion; Vasopressins

A 79-year-old woman suffering from urinary incontinence and unsteady gait was diagnosed as having idiopathic normal pressure hydrocephalus (NPH) with hyponatremia due to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The concentration of antidiuretic hormone was high while the plasma osmolality was low in the presence of concentrated urine during the episodes of hyponatremia. Magnetic resonance imaging (MRI) of the head showed enlargement of the third and lateral ventricles. After ventriculoperitoneal shunt surgery, the symptoms of NPH and hyponatremia improved. It may be possibly explained that mechanical pressure on the hypothalamus from the third ventricle is responsible for hyponatremia.

Topics: Aged; Cerebral Ventricles; Female; Follow-Up Studies; Humans; Hydrocephalus, Normal Pressure; Hyponatremia; Inappropriate ADH Syndrome; Magnetic Resonance Imaging; Myelography; Radionuclide Imaging; Sodium; Vasopressins; Ventriculoperitoneal Shunt

We experienced four cases with hyponatremia due to SIADH, which seems to be related to inflammation. The plasma Na concentration decreased when the patients had fever and increased plasma CRP level. In such conditions, plasma vasopressin concentration (PAVP) and the plasma interleukin-6 (IL-6) concentration were increased. There was significant correlation between them. The animal experiments were carried out to investigate the role of interleukin in the development of SIADH. Intravenous administrations of IL-1 beta increased AVP, atrial natriuretic hormone (ANH) and ACTH. The changes in AVP and ACTH were abolished by the pretreatment with an intravenous administration of indomatacin. Moreover, the intracerebroventricular administration (ICV) of IL-1 beta also increased AVP, atrial natriuretic hormone (ANH) and ACTH. The pretreatment of indomatacin attenuated the changes in AVP and ACTH. The intravenous administration of IL-1 beta increased the urinary sodium excretion. The pretreatement of HS142-1, an ANH antagonist, abolished the increase in urinary sodium excretion induced by IL-1 beta. These results suggested that the interleukin play an important role in the development of SIADH associated with inflammation.

Topics: Adrenocorticotropic Hormone; Adult; Aged; Aged, 80 and over; Animals; Atrial Natriuretic Factor; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Inflammation; Interleukin-1; Interleukin-6; Male; Rats; Rats, Sprague-Dawley; Vasopressins

A 65-year-old man who had muscle weakness and dysarthria was admitted for investigation of motor neuron disease. He had lost 12 kg of weight in 6 months. Neurological findings disclosed upper and lower motor neuron disturbances with normal sensory nerve function, and needle electromyography showed a neurogenic pattern. Laboratory findings on admission demonstrated dilutional hyponatraemia due to an excessive secretion of antidiuretic hormone (ADH). Based on these findings, the patient was diagnosed as having the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with amyotrophic lateral sclerosis (ALS). During the night of first hospital day, the patient complained of severe dyspnoea, and mechanical ventilation was commenced. Following the mechanical ventilation, plasma ADH levels and serum sodium concentration were normalized. We propose that respiratory failure secondary to the atrophy of respiratory muscle might be responsible for the development of SIADH.

Topics: Aged; Amyotrophic Lateral Sclerosis; Blood Gas Analysis; Diagnosis, Differential; Electromyography; Humans; Inappropriate ADH Syndrome; Male; Respiration, Artificial; Respiratory Insufficiency; Saline Solution, Hypertonic; Sodium; Vasopressins

Topics: Adrenal Insufficiency; Humans; Hyponatremia; Hypothalamo-Hypophyseal System; Inappropriate ADH Syndrome; Pituitary-Adrenal System; Practice Guidelines as Topic; Vasopressins

A 60-year-old woman was admitted with severe hyponatremia. Basal values of adrenocorticotropic hormone (ACTH), thyroid hormone and cortisol were normal on admission. Impairment of water diuresis was observed by water loading test. Initially, we diagnosed her condition as the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). By provocation test, we finally confirmed that the hyponatremia was caused by hypothalamic adrenal insufficiency. The basal values of ACTH and cortisol might not be sufficient to exclude the possibility of adrenal insufficiency. Therefore, it is necessary to evaluate adrenal function by provocation test or to re-evaluate it after recovery from hyponatremia.

Topics: Adrenal Insufficiency; Adrenocorticotropic Hormone; Female; Humans; Hydrocortisone; Hyponatremia; Hypothalamo-Hypophyseal System; Inappropriate ADH Syndrome; Middle Aged; Pituitary-Adrenal System; Thyrotropin; Vasopressins

Topics: Aged; Antidepressive Agents, Second-Generation; Humans; Inappropriate ADH Syndrome; Male; Paroxetine; Selective Serotonin Reuptake Inhibitors; Vasopressins

Topics: Extracellular Space; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant, Newborn; Infant, Very Low Birth Weight; Intensive Care Units, Neonatal; Lung Diseases; Pressoreceptors; Sodium-Potassium-Exchanging ATPase; Vasopressins

The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with neuropsychiatric lupus (NP-SLE) is rare. We report a case of SIADH associated with the new onset of SLE in an 88-yr-old female. The unique features of this case include the extreme age of onset of SLE presenting with neuropsychiatric manifestations and positive antiribosomal P antibody titres. Both the NP manifestations of SLE and SIADH were highly correlated with the SLE disease activity. This case illustrates a novel presentation of NP-SLE with SIADH which may develop due to antibody-mediated hypothalamic dysfunction.

Topics: Aged; Aged, 80 and over; Aldosterone; Antibodies, Antinuclear; Brain; Complement C3; Complement C4; Depressive Disorder; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lupus Erythematosus, Systemic; Magnetic Resonance Imaging; Protozoan Proteins; Renin; Ribosomal Proteins; Vasopressins

A patient with a ganglioglioma of the neurohypophysis developed the syndrome of inappropriate antidiuretic hormone secretion (SIADH). We present the case and describe its microscopic and ultrastructural features. Malignant neoplasms were thought to be the main cause of ectopic production of vasopressin. Head trauma, infection, or drugs, however, can also induce hypersecretion of vasopressin. Mechanical compression of the pituitary stalk can lead to an excessive antidiuretic hormone (ADH) release by affecting the inhibitory system. Primary neuroendocrine tumors of the hypothalamic-neurohypophyseal system are extremely rare. We demonstrate the presence of vasopressin in the tumor cells by immunocytochemistry. This represents the first case of SIADH caused by a tumor of the neurohypophysis.

Topics: Aged; Cell Nucleus; Cytoplasm; Ganglioglioma; Humans; Immunohistochemistry; Inappropriate ADH Syndrome; Male; Microscopy, Electron; Pituitary Neoplasms; Vasopressins

A 72-year-old man was hospitalized with asymptomatic hyponatremia. Despite hyponatremia, urinary sodium excretion with urine osmolality exceeding plasma osmolality persisted. Plasma vasopressin levels were high and independent of plasma osmolality during hypertonic saline infusion. Computed tomography of the chest showed enlarged mediastinal and right hilar lymph nodes. Microscopically, a specimen of lymph nodes obtained by biopsy represented vasopressin-producing small cell lung carcinoma. Chemotherapy plus irradiation improved the hyponatremia. Thus, careful evaluation is necessary to determine the cause of hyponatremia disorders in elderly patients.

Topics: Aged; Antineoplastic Combined Chemotherapy Protocols; Biomarkers, Tumor; Biopsy; Bronchoscopy; Carcinoma, Small Cell; Follow-Up Studies; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lung Neoplasms; Magnetic Resonance Imaging; Male; Osmosis; Radiotherapy, Adjuvant; Sodium; Tomography, X-Ray Computed; Vasopressins

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant, Newborn; Vasopressins; Water-Electrolyte Balance

Fluoxetine is widely prescribed for depressed patients. Hyponatremia secondary to inappropriate secretion of antidiuretic hormone has been reported in a few cases associated with routine use of fluoxetine, especially in elderly patients. The mechanism has been postulated to be linked to the inappropriate secretion of antidiuretic hormone. Serum concentrations of antidiuretic hormone and fluoxetine have not been reported in previously published reports.. We report two new cases of severe and reversible hyponatremia associated with routine use of fluoxetine therapy in two elderly women. Fluoxetine-induced inappropriate secretion of antidiuretic hormone was confirmed by elevated serum concentrations of antidiuretic hormone and fluoxetine.

Topics: Aged; Aged, 80 and over; Antidepressive Agents, Second-Generation; Contraindications; Female; Fluoxetine; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

For unclear reasons, life-threatening water intoxication often coincides with acute psychosis in polydipsic schizophrenic patients with chronic hyponatremia. In contrast, most polydipsic schizophrenic patients are normonatremic and never manifest hyponatremia. To explore whether the effect of acute psychosis on water balance differs in these 2 schizophrenic subgroups, we compared their responses to drug-induced psychotic exacerbations.. Matched polydipsic schizophrenic patients with (n = 6) and without (n = 8) hyponatremia were identified based on past and current indexes of fluid intake and hydration. A transient psychotic exacerbation was induced with an infusion of the psychotomimetic methylphenidate hydrochloride (0.5 mg/kg of body weight over a 60-second period). Antidiuretic hormone levels, subjective desire for water, and factors known to influence water balance were measured at 15-minute intervals for 2 hours.. Except for the expected differences in plasma osmolality and sodium, basal measures were similar in the 2 groups. Following methylphenidate administration, antidiuretic hormone levels increased more in the hyponatremic patients (P < .02), despite their consistently lower plasma osmolality (P < .007). No known or putative antidiuretic hormone stimulus could account for this finding. Only basal positive psychotic symptoms (P < .09) and plasma sodium (P < .18) were even marginally associated with the peak antidiuretic hormone responses, but neither factor could explain the difference in the response by the 2 groups.. Psychotic exacerbations are associated with enhanced antidiuretic hormone secretion, for unknown reasons, in schizophrenic patients with hyponatremia and polydipsia, thereby placing them at increased risk of life-threatening water intoxication.

Topics: Acute Disease; Adult; Arginine Vasopressin; Blood Pressure; Drinking; Female; Heart Rate; Humans; Hydrocortisone; Hyponatremia; Inappropriate ADH Syndrome; Male; Methylphenidate; Osmolar Concentration; Psychiatric Status Rating Scales; Schizophrenia; Schizophrenic Psychology; Sodium; Thirst; Vasopressins; Water Intoxication

We describe a 78-year-old female patient with severe hyponatremia owing to inappropriate antidiuresis. Despite hyponatremia, the urinary sodium excretion persisted with urine osmolality exceeding plasma osmolality. Although a water load decreased plasma sodium concentration and osmolality, the patient excreted only 40% of the water load after 4 h without decreased urine sodium concentrations and osmolality. The plasma vasopressin levels relative to plasma osmolality were not inappropriately elevated. Intravenous administration of the selective nonpeptide vasopressin V2 antagonist OPC-31260 decreased sodium concentration and osmolality in urine to lower values than in plasma. Concomitantly, the urine volume excretion increased markedly. In addition, restriction of water or administration of demeclocycline improved plasma sodium and plasma vasopressin levels relative to plasma osmolality to be normal. The findings indicate that the inappropriate antidiuresis in this patient was related to hyperfunction of the arginine vasopressin V2 receptor in the kidney which is not due to inappropriately secreted vasopressin.

Topics: Aged; Antidiuretic Hormone Receptor Antagonists; Benzazepines; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Injections, Intravenous; Sodium; Vasopressins

The antidiuretic hormone (vasopressin) is involved, either directly or indirectly, in the pathogenesis of almost all forms of hyponatremia. This means that blockage of the ADH effect at the renal ADH receptor represents a rational approach in the treatment of hyponatremia, in particular in difficult-to-treat and symptomatic forms. Recently, orally absorbable, non-peptidergic competitive ADH antagonists (aquaretics) have been introduced, which bind with high affinity to renal ADH receptor subtypes. Initial investigations in humans show that the substance is well tolerated. Numerous studies on patients with hyponatremia of varying genesis have since been started. It is to be expected that the availability of this new dass of substances will result in marked improvements in the treatment of acute and chronic forms of hyponatremia.

Topics: Antidiuretic Hormone Receptor Antagonists; Benzazepines; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Male; Vasopressins

We report 2 autopsy-proven cases of motor neuron disease/amyotrophic lateral sclerosis (MND/ALS), who developed the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) prior to the respiratory failure. With respect to the underlying mechanisms of SIADH in the cases, we considered two factors; 1) dysfunction of the feedback system in ADH secretion via intrathoracic volume receptors caused by changes in intrathoracic circulation, and 2) primarily functional abnormalities in the limbic system which could influence hypothalamic osmoreceptors. It appears that SIADH can be followed by an exacerbation of respiratory dysfunction in MND/ALS.

Topics: Amyotrophic Lateral Sclerosis; Feedback; Humans; Hypothalamus; Inappropriate ADH Syndrome; Limbic System; Male; Middle Aged; Motor Neuron Disease; Neurologic Examination; Respiratory Insufficiency; Vasopressins; Water-Electrolyte Balance

A 61-year-old woman was admitted to the hospital because of general fatigue. Laboratory examinations showed hyponatremia, plasma hypo-osmolarity, and inappropriate increased concentration of the plasma antidiuretic hormone (ADH) in the presence of concentrated urine. Magnetic resonance imaging revealed a mass lesion in the anterior mediastinum. An extended thymectomy was performed under the diagnosis of thymoma with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Histologically the tumor was located in the thymic tissue and was diagnosed as ganglioneuroblastoma. Immunohistochemical studies showed the existence of ADH in the tumor cells. To the knowledge of the authors, this is the first case of ganglioneuroblastoma of the thymus with SIADH.

Topics: Female; Ganglioneuroblastoma; Humans; Inappropriate ADH Syndrome; Microscopy, Electron; Middle Aged; Thymus Neoplasms; Vasopressins

In a 59-year-old woman suffering from the syndrome of inappropriate antidiuretic hormone secretion, a small cell carcinoma of the uterine cervix was detected. The tumor was immunoreactive for antidiuretic hormone as well as for neuron specific enolase, chromogranin A, and Leu-7, but not vimentin. Electron microscopic examination of the tumor revealed neurosecretory granules. To our knowledge, this is only the second report of the syndrome of inappropriate antidiuretic hormone secretion with small cell carcinoma of the uterine cervix and the first one confirmed immunohistopathologically.

Topics: Carcinoma, Small Cell; CD57 Antigens; Chromogranin A; Chromogranins; Female; Humans; Immunohistochemistry; Inappropriate ADH Syndrome; Middle Aged; Phosphopyruvate Hydratase; Uterine Cervical Neoplasms; Vasopressins

We describe a 73-year old man with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) due to an ectopic ADH-producing pancreatic adenocarcinoma. His laboratory findings showed marked hyponatremia, and the water load test showed uncontrolled ADH secretion. The imaging studies revealed pancreatic body cancer. Histological examination revealed an adenocarcinoma of the pancreas, which was positive for ADH immuno-staining. The ADH in the tumor extract was 53.3 pg/g wet weight. In attempt to diagnose ADH-production from the tumor, the ADH in his pancreatic juice was measured and found to be 2.1 pg/ml. We conclude that it is valid to measure the ADH in pancreatic juice to diagnose ectopic ADH production by tumors.

Topics: Adenocarcinoma; Aged; Hormones, Ectopic; Humans; Inappropriate ADH Syndrome; Male; Pancreatic Juice; Pancreatic Neoplasms; Vasopressins

Topics: Adult; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Porphobilinogen; Porphyria, Acute Intermittent; Transaminases; Vasopressins

A 58-year-old postmenopausal woman with primary ovarian serous carcinoma presented with the syndrome of inappropriate antidiuresis (SIAD). Preoperative workup showed serum sodium level of 110 mEq/liter and antidiuretic hormone level of 3.3 pg/ml. The serum and urine osmolarity were 239 and 371, respectively. Antidiuretic hormone was demonstrated in tumor cells by immunohistochemistry. To the best of the authors' knowledge, this represents the first case of SIAD due to primary ovarian tumor.

Topics: Adenocarcinoma; Female; Humans; Immunohistochemistry; Inappropriate ADH Syndrome; Middle Aged; Osmolar Concentration; Ovarian Neoplasms; Sodium; Vasopressins

delta-Aminolevulinic acid dehydratase deficiency porphyria (ALAD porphyria, ADP) with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in a 69-year-old woman is reported. The patient was admitted to our hospital complaining of slight cough with low-grade fever, and treated with piperacillin sodium, resulting in complete resolution of the symptoms, following a diagnosis of bronchopneumonia. Thereafter, however, she began to complain of vomiting, abdominal pain, facial numbness and paresis of the extremities with gait disturbance, and became comatose with hyponatremia (serum Na concentration 119 mEq/L) in a few days. Laboratory tests revealed an antidiuretic hormone (ADH) level of 13.5 pg/mL, plasma osmolality 218 mOsm/KgH2O, urinary osmolality 429 mOsm/KgH20, urinary Na concentration > 20 mEq/L, and no abnormalities of thyroid, adrenal or renal function. Neither edema nor dehydration was evident. These data indicated the presence of SIADH. No abnormalities suggestive of malignant or infectious diseases such as lung cancer, pneumonia and Guillain-Barré syndrome were evident from laboratory and roentgenographic findings. As the cause of SIADH, therefore, porphyria was suspected. Metabolites and activities of enzymes in the heme biosynthetic pathway were examined, and very low activity of delta-aminolevulinic acid dehydratase (ALA-D) (0.14 mumol PBG/mL RBC/h) was found. The patient was neither an alcoholic nor a heavy smoker, and she had no past history of heavy metal intoxication, photosensitivity or tyrosinemia. On the basis of these data and clinical features, she was diagnosed as having ADP. We consider this to be the first case of ADP reported in Japan.

Topics: Abdominal Pain; Aged; Coma; Female; Humans; Inappropriate ADH Syndrome; Japan; Osmolar Concentration; Paresis; Porphobilinogen Synthase; Porphyrias; Porphyrins; Sodium; Vasopressins; Vomiting

We report three lymphoma patients in whom the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) was observed during the course of lymphoma-associated hemophagocytic syndrome (LAHS). The clinical course was devoid of any known mechanism for SIADH which could be attributable to lymphoma or antineoplastic treatment. Alternatively, high serum levels of interleukin-1 beta and tumor necrosis factor-alpha, which stimulate the secretion of antidiuretic hormone, may have contributed to the development of SIADH in our patients, who were receiving glucocorticoids. In conclusion, LAHS patients should be considered to be at high risk for SIADH.

Topics: Aged; Female; Histiocytosis, Non-Langerhans-Cell; Humans; Inappropriate ADH Syndrome; Interleukin-1; Lymphoma; Lymphoma, T-Cell; Male; Middle Aged; Nose Neoplasms; Risk Factors; Sodium; Tumor Necrosis Factor-alpha; Vasopressins

An old women was in an 8-year-period 9 times admitted to the hospital because of severe mental disturbances. The average serum sodium concentration was 126.25 +/- 2.43 mmol/l at the admissions; it increased to 139.44 +/- 1.40 mmol/l after intravenous infusion of hypertonic solutions accompanied with the disappearance of the mental disturbances. The patient was usually chronically hyponatremic due to the increased water intake and the insufficient water excretion. The latter was induced by the augmented vasopressin levels. The remarkable feature of the syndrome of inappropriate antidiuretic hormone secretion was its association with lowered blood level of atrial natriuretic factor accompanied by sodium, and volume depletion. Discontinuation of the exaggerated water intake resulted in the elimination of the permanent hyponatremia; no episode of water intoxication occurred during the last 3 and 1/2 years.

Topics: Aged; Atrial Natriuretic Factor; Cognition Disorders; Drinking Behavior; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins; Water Intoxication

Topics: Animals; Atrial Natriuretic Factor; Brain; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney Failure, Chronic; Vasopressins; Water-Electrolyte Balance

The syndrome of inappropriate secretion of antidiuretic hormone (ADH) or SIADH has been so far reported in various disorders. However, to our knowledge, no case of SIADH associated with adult onset Still's disease (AOSD) has been described in the literature. We report on a patient who developed inappropriate secretion of antidiuretic hormone (SIADH) during the course of adult onset Still's disease (AOSD). The patient developed SIADH associated with pleuritis and improved when pleuritis subsided during the course of steroid therapy. Thus, it seems suggest that SIADH was induced by AOSD which is considered to be related with vasculitis.

Topics: Female; Humans; Inappropriate ADH Syndrome; Middle Aged; Pleurisy; Still's Disease, Adult-Onset; Vasopressins

A 76-year-old man with small cell lung cancer associated with the syndrome of inappropriate secretion of ADH (SIADH) visited our hospital. The serum Na level was normal on the first visit, but 2 weeks later it decreased to 114 mEq/L with an extremely high plasma vasopressin (VP) level of 1520 pg/ml. Serum Na was normalized after the reduction of the tumor size by chemotherapy, but the plasma VP level remained between 150 to 600 pg/ml. On gel filtration of plasma VP two peaks of immunoreactive VP were eluted at the positions of a larger molecule than authentic VP and authentic VP, and VP in urine gave only one peak compared to that of authentic VP. The dilution curve of plasma VP was almost parallel and that of urine was completely parallel to the standard curve. These findings suggest that a larger VP with low physiological activity was predominantly secreted in the present patient and manifested relatively mild symptoms despite the extremely high plasma VP level.

Topics: Aged; Carcinoma, Small Cell; Chromatography, Gel; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Sodium; Vasopressins

Topics: Adrenocorticotropic Hormone; Corticotropin-Releasing Hormone; Cushing Syndrome; Cytokines; Humans; Inappropriate ADH Syndrome; Interleukin-6; Polyuria; Vasopressins

Overhydration can contribute to fatal complications of falciparum malaria, even though renal function may be normal. In this context, the role of inappropriate secretion of antidiuretic hormone (ADH) has been controversial. Therefore, we have analyzed ADH serum concentrations together with serum osmolality and sodium levels in serum and urine of 17 consecutively studied patients with severe falciparum malaria. Serum sodium levels were low in 13 of 17 patients upon admission and returned to normal levels during antiparasitic therapy. Urine sodium levels were low in seven of 13 patients before treatment and increased during therapy. Urine sodium concentrations were high, however, in the remaining six patients. Serum osmolality was lower in these six patients than in the other seven hyponatremic patients (P < 0.002). In relation to serum osmolality, ADH levels were inappropriately high in these six patients, which confirms the presence of inappropriate secretion of ADH. Serum creatinine levels were not higher in these six patients than in those without inappropriate secretion of ADH. Inappropriate secretion of ADH seemed to be a major cause of hyponatremia, since other factors that could lead to this condition were not found in these six patients. In conclusion, we have shown, that human falciparum malaria can be associated with inappropriate secretion of ADH.

Topics: Adult; Creatinine; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Malaria, Falciparum; Male; Middle Aged; Osmolar Concentration; Potassium; Sodium; Thyroxine; Tumor Necrosis Factor-alpha; Vasopressins

To evaluate the effect of Brain Tomour (BT) and Neurosurgery (NS) on the renal handling of H2O and Na, and the clinical importance of SIADH in this setting.. Fourteen patients with BT pre-op for NS and 6 controls (C) pre-op for general surgery, were assessed in a controlled prospective trial. All patients were normovolaemic, with normal renal function. They received 400 mg of lithium carbonate (Li) 8 hours before each of two test periods (I and II) and a standard water load only before period II. Clearances studies were performed pre-op (period I) and 24 hours post-op (period II).. Serum Na was normal at all times. Despite normovolaemia, a 1% decrement in serum osmolality and the water load, ADH dramaticaly increased from time I to II mainly in the BT group (36.2 +/- 9.4 vs 7.1 +/- 0.6 pmol/L, p = 0.02). FENa, FELi and FEUricA were significantly more elevated in the BT group pre and post-op (at time II respectively 4.6 +/- 1.6 vs 1.1 +/- 0.3%; 29.3 +/- 4.9 vs 22.6 +/- 5.5; 26.0 +/- 8.1 vs 11.3 +/- 2.2, p = 0.03). Proximal and distal H2O re-absorption and distal fractional Na re-absorption were identical in both groups pre and post-operatively.. 1-BT and NS always induce a SIADH. 2-There was a primary Na loss at the proximal tubule level not explained by ADH increment, that did not significantly changed H2O handling. 3-To prevent hyponatraemia, hypotonic I.V. fluids should be avoided, but more importantly saline must be provided to this potentially salt-wasting condition.

Topics: Adult; Aged; Brain Neoplasms; Craniotomy; Female; Humans; Inappropriate ADH Syndrome; Kidney Concentrating Ability; Kidney Tubules; Lithium Carbonate; Male; Middle Aged; Postoperative Complications; Reference Values; Vasopressins; Water-Electrolyte Balance

The present study was undertaken to determine whether the non-peptide V2 antidiuretic hormone (ADH) antagonist 5-dimethylamino-1[4-(2- methylbenzoylamino)benzoyl]-2,3,4,5-tetrahydro-1H-benzazepine (OPC-31260) normalized hyponatremia in rats with an experimental syndrome of inappropriate secretion of ADH (SIADH). Rats were administered V2 agonist 1-deamino-8-D-arginine vasopressin (dDAVP) subcutaneously at a rate of 5 ng/hr using an osmotic minipump and a 40 ml/day liquid diet. Serum sodium levels (SNa) and serum osmolality (SOsm) markedly decreased to 119 mEq/liter and 249 mOsm/kg H2O, respectively, 48 hours after the start of dDAVP administration. Hyponatremia persisted in a similar magnitude during the observation period of 14 days. On days 7 to 13 OPC-31260, administered 5 mg/kg per day orally, promptly raised SNa and SOsm to 134 mEq/liter and 282 mOsm/kg H2O in half a day, respectively, followed by the normalization of SNa and SOsm during the rest of the observation period. The cease of administration of OPC-31260 again decreased SNa and SOsm in rats receiving dDAVP. In contrast, SNa and SOsm were within the normal values in rats receiving 0.15 M NaCl, a vehicle for dDAVP, in the presence or absence of OPC-31260. The administration of OPC-31260 promptly caused marked water diuresis on day 7 in the hyponatremic rats receiving dDAVP, namely 5 mg/kg OPC-31260 markedly increased urinary volume and decreased UOsm. These results indicate that there is dilutional hyponatremia in rats receiving dDAVP and 40 ml/day liquid diets, and that OPC-31260 is an effective therapeutic for hyponatremia associated with dDAVP-induced SIADH.

Topics: Animals; Benzazepines; Deamino Arginine Vasopressin; Hyponatremia; Inappropriate ADH Syndrome; Male; Osmolar Concentration; Rats; Rats, Sprague-Dawley; Sodium; Vasopressins

Topics: Animals; Arginine Vasopressin; Body Water; Brain; Brain Edema; Electrolytes; Inappropriate ADH Syndrome; Male; Rats; Rats, Wistar; Subarachnoid Hemorrhage; Vasopressins

Topics: Animals; Benzazepines; Cells, Cultured; Hyponatremia; Inappropriate ADH Syndrome; Kidney Tubules, Collecting; Muscle, Smooth, Vascular; Piperidines; Quinolones; Rats; Rats, Brattleboro; Rats, Sprague-Dawley; Vasopressins

Topics: Follow-Up Studies; Humans; Inappropriate ADH Syndrome; Male; Nasopharyngeal Neoplasms; Vasopressins; Xerostomia

Topics: Antipsychotic Agents; Combined Modality Therapy; Electroconvulsive Therapy; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Middle Aged; Schizophrenia; Schizophrenic Psychology; Vasopressins

A 59 year old man presenting fever, serum hyponatremia and hypoosmolality in association with hyperosmotic urine was hospitalized in our unit in February 1988. We demonstrated evidence of systemic sarcoidosis and inappropriate secretion of antidiuretic hormone (ADH). The patient was treated with corticosteroid therapy for a period of about 1 year, with regression of signs of the inappropriate vasopressin secretion as well as the symptomatology related to systemic sarcoidosis. This study identified systemic sarcoidosis as a definite cause of "syndrome of inappropriate ADH secretion".

Topics: Arginine Vasopressin; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Prednisone; Radioimmunoassay; Sarcoidosis; Vasopressins

The syndrome of inadequate secretion of antidiuretic hormone (SIADH) following treatment with a tricyclic antidepressant is demonstrated using the example of a 70 year-old man admitted for weakness and cognitive disturbances. Because of incontinence he had been periodically treated since 1989 with imipramine (Tofranil) by his family doctor. On admission he was seriously hyponatriemic and had low plasmatic osmolality, significantly lower than urinary osmolality. Creatinine, urea and uric acid in serum were also below normal values. Like other drugs tricyclic antidepressants can rarely induce an increased release of ADH by direct hypothalamic stimuli. In this patient imipramine was terminated and within a few days of reduced fluid intake and substitution of sodium a sustained clinical improvement and normalisation of laboratory parameters was noted. The patient was discharged to his home after three weeks.

Topics: Aged; Humans; Hyponatremia; Imipramine; Inappropriate ADH Syndrome; Male; Osmolar Concentration; Vasopressins

Seventeen unselected, consecutive patients with intracranial disease and accompanying hyponatraemia were studied. All would previously have been diagnosed as having the syndrome of inappropriate antidiuretic hormone (ADH) secretion on the basis of spot plasma/urinary electrolyte testing with the application to them of existing standard laboratory criteria. Timed urinary collections and matching plasma samples were available in all but three cases for the derivation of creatinine, osmotic and free-water clearances, tubular reabsorbed water, and fractional water and sodium excretions. In a number of patients the plasma renin, aldosterone and ADH levels were also assayed. On the basis of the overall findings, 13 patients were diagnosed as in fact having a salt-wasting state whilst in only four patients was the diagnosis of inappropriate ADH secretion (SIADH) substantiated. It is suggested that obtaining simple derived parameters of sodium and water homeostasis can add significantly in differentiating between these quite opposite syndromes.

Topics: Aged; Aldosterone; Brain Diseases; Female; Homeostasis; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Postoperative Complications; Renin; Vasopressins; Water-Electrolyte Balance

A 71-year-old female with amyotrophic lateral sclerosis (ALS) developed the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) during respiratory failure due to atrophy of the respiratory muscles. Serum sodium concentration fell to 116 mEq/l and then returned to the normal range after water restriction and respiratory care. This is considered to be the first case report of ALS associated with SIADH.

Topics: Aged; Amyotrophic Lateral Sclerosis; Blood Chemical Analysis; Electromyography; Female; Humans; Inappropriate ADH Syndrome; Respiratory Insufficiency; Sodium; Vasopressins

A patient with a primary undifferentiated carcinoma of the nasopharynx manifested the clinical syndrome of inappropriate antidiuretic hormone secretion (SIADH). Immunohistochemical techniques demonstrated the presence of vasopressin, neurophysin, and their precursor (propressophysin) in the cancer cells. In situ hybridization additionally confirmed the expression of propressophysin messenger RNA in these cells. To the knowledge of the authors, this represents not only the first case of SIADH caused by carcinoma of the nasopharynx, but also the first report of pathologic confirmation of the syndrome with the use of both molecular and immunologic probes.

Topics: Arginine Vasopressin; Carcinoma, Squamous Cell; DNA, Neoplasm; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Nasopharyngeal Neoplasms; Neurophysins; Nucleic Acid Hybridization; Oxytocin; Protein Precursors; Vasopressins

A 66-year-old Japanese man presented with persistent hyponatremia without polydipsia and polyuria. Laboratory examination showed serum sodium of 117 mEq/l, plasma osmolality 239 mosm/kg, urine sodium 108 mEq/l, urine osmolality 577 mosm/kg, and normal levels (less than 2.0 pg/ml) of serum antidiuretic hormone (ADH). ADH release was regulated normally with changes in plasma osmolality. No obvious cause for the syndrome of inappropriate secretion of ADH (SIADH) could be detected. However, 20 months later, the patient had bouts of hematuria and was found to have cancer of the urinary bladder. Increased renal sensitivity to ADH was suspected as the underlying mechanism of SIADH.

Topics: Aged; Carcinoma, Squamous Cell; Diuresis; Humans; Inappropriate ADH Syndrome; Kidney; Male; Urinary Bladder Neoplasms; Vasopressins

A five-year-old girl with known sickle cell disease presented with severe hyponatremia and findings compatible with syndrome of inappropriate secretion of antidiuretic hormone (SIADH). She was found to have lead levels in the Class III category. By exclusion, we postulated that the SIADH was in some way related to the high lead levels, since this was the only abnormality the patient exhibited. The toxic lead levels and the elevated vasopressin levels rapidly responded to dimercaprol and calcium EDTA chelation therapy.

Topics: Anemia, Sickle Cell; Chelation Therapy; Child, Preschool; Dimercaprol; Edetic Acid; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lead; Lead Poisoning; Vasopressins

Forty-one male alcoholics suffering from alcohol withdrawal syndrome were investigated to assess the relationship between vasopressin (ADH), water homeostasis and alcohol withdrawal. During 10 d, we found a significant decrease in serum vasopressin, from 3.08 +/- 0.61 to 1.71 +/- 0.22 pg/nl. There were no concomitant changes in osmolality, so that a general dysregulatory state of vasopressin secretion during alcohol withdrawal cannot be assumed. Only patients with delirium tremens (8/41) had higher vasopressin levels despite lowered serum osmolalities. These findings support the hypothesis of an inappropriate rebound secretion of vasopressin in severe alcohol withdrawal. Furthermore, they may contribute to the pathogenesis of focal alcoholic brain damage, because rapid and/or profound changes in osmolality are suspected to cause circumscribed cerebral demyelinization.

Topics: Adult; Alcohol Withdrawal Delirium; Alcoholism; Hospitalization; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Vasopressins; Water-Electrolyte Balance

Syndrome of inappropriate secretion of antidiuretic hormone (SIADH), hypothalamic hypogonadism and alopecia universalis occurred in a 31-year-old female with insulin-dependent diabetes mellitus (IDDM). Despite various clinical investigations and careful observation for 20 months, the cause and pathogenesis of SIADH and hypothalamic hypogonadism were not elucidated. The complex of these disorders had not been described. The presence of IDDM and alopecia universalis, in which an autoimmune process has been assumed to be involved, is interesting in considering the pathogenesis of the SIADH and hypothalamic hypogonadism.

Topics: Adrenocorticotropic Hormone; Adult; Alopecia; Clomiphene; Diabetes Mellitus, Type 1; Female; Follicle Stimulating Hormone; Growth Hormone; Humans; Hydrocortisone; Hypogonadism; Inappropriate ADH Syndrome; Insulin; Luteinizing Hormone; Pituitary Gland; Prolactin; Thyroid Hormones; Thyrotropin; Vasopressins

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Central Nervous System Diseases; Child; Child, Preschool; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant; Kallikreins; Male; Middle Aged; Sex Factors; Uric Acid; Vasopressins

Topics: Body Water; Dehydration; Diabetes Insipidus; Diuretics; Drinking; Feedback; Glomerular Filtration Rate; Homeostasis; Humans; Inappropriate ADH Syndrome; Polyuria; Vasopressins; Water Intoxication

We measured urine vasopressin (VP) once daily on days 1 through 3 in 18 patients hospitalized with meningitis. Urine VP values were 215 +/- 100, 116 +/- 44, and 69 +/- 23 pg/mL on days 1 through 3, respectively, for children with bacterial meningitis and 34 +/- 14, 20 +/- 4, and 15 +/- 4 pg/mL for those with aseptic meningitis. Urinary VP levels of infants with bacterial meningitis were significantly greater than those of healthy ambulatory subjects (n = 18) on all three study days; VP values of infants with bacterial meningitis were also greater than those of infants with aseptic meningitis on study days 2 and 3. The VP levels for the subjects with aseptic meningitis were significantly greater than those of the controls on day 1 only. None of the infants exhibited the clinical syndrome of inappropriate antidiuretic hormone secretion.

Topics: Bacterial Infections; Humans; Inappropriate ADH Syndrome; Infant; Meningitis; Meningitis, Aseptic; Osmolar Concentration; Risk Factors; Sodium; Time Factors; Vasopressins

We describe two sisters with chronic hypernatremia, lack of thirst, and inappropriate osmoregulated vasopressin secretion. Only one sister, who presented with microcephaly and developmental delay, showed signs of dysplasia of the midline structures (ie, septum pellucidum and corpus callosum) and a large intracranial cyst. Neither sister showed any signs of thirst, even when osmolality exceeded 337 mmol/kg. In both patients, the vasopressin secretion did not respond to either osmotic or nonosmotic stimuli or was suppressed by a water load. Plasma osmolality values returned to normal after treatment with forced hydration and a vasopressin analogue, desamino-D-arginine vasopressin. These findings indicate a severe defect in the hypothalamic osmoreceptors that control thirst and vasopressin secretion. To our knowledge, this is the first report of such a disorder in two sisters.

Topics: Aldosterone; Blood Urea Nitrogen; Female; Humans; Hypernatremia; Hypothalamus; Inappropriate ADH Syndrome; Infant; Osmolar Concentration; Renin; Sodium; Spasms, Infantile; Thirst; Vasopressins

To examine a possible role for atrial natriuretic peptide (ANP) in water and sodium metabolism disturbances associated with abnormal vasopressin (AVP) secretion, we measured plasma ANP concentrations in 15 patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and in 17 patients with central diabetes insipidus (DI). The mean plasma ANP concentration (30.2 +/- 10.4 pmol/L) in SIADH patients who had hyponatremia, plasma hypoosmolality, hyperosmolar urinary compared to plasma sodium levels, and increased plasma AVP levels relative to plasma osmolality was significantly higher than that in normal subjects (12.6 +/- 4.9 pmol/L), although there was a considerable individual variation in plasma ANP ranging from normal to clearly elevated levels (15.1-47.0 pmol/L). When hyponatremia was corrected by water restriction or demeclocycline administration, plasma ANP levels decreased significantly and fell into the normal range (12.5 +/- 4.3 pmol/L). DI patients who complained of polyuria and polydipsia and had hypoosmolar urine, normal or elevated plasma sodium concentrations, and decreased plasma AVP levels relative to plasma osmolality, on the other hand, had a significantly lower mean plasma ANP level (7.6 +/- 2.9 pmol/L) than normal subjects. There was, again, a considerable overlap between plasma ANP levels in individual DI patients (4.2-13.9 pmol/L) and those in normal subjects. Treatment with 1-desamino-8-D-arginine vasopressin resulted in a significant increase in the mean plasma ANP level (18.6 +/- 8.0 pmol/L). There were no significant correlations between plasma ANP and AVP levels in either group of patients. The results indicate that ANP secretion is modulated by changes in plasma volume consequent to abnormal AVP secretion, which may have a pathophysiological significance in maintaining volume homeostasis.

Topics: Adolescent; Adult; Aged; Atrial Natriuretic Factor; Blood Volume; Deamino Arginine Vasopressin; Demeclocycline; Diabetes Insipidus; Female; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Polyuria; Sodium; Vasopressins; Water-Electrolyte Balance

We report a case of 47-year-old woman with an isolated deficiency of adrenocorticotropic hormone. She was admitted complaining of fatigue and frequent loss of consciousness. The patient developed severe hyponatremia (100 mEq/l) after five days of the admission. Her plasma renin activity and plasma aldosterone concentration were low though she was dehydrated. After the treatment of dehydration, plasma osmolality was low but high plasma antidiuretic hormone (ADH) level sustained. Both high urinary sodium excretion and low urinary aldosterone excretion still remained after one month of replacement therapy with prednisolone. But, glomerular filtration rate and a response of urinary volume to acute water loading were normalized. These results suggested that severe hyponatremia of the patient was caused by an inappropriate secretion of ADH and suppression of renin-aldosterone system. We consider the suppression of renin-aldosterone system was partially independent of an inappropriate secretion of ADH.

Topics: Adrenocorticotropic Hormone; Aldosterone; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Middle Aged; Renin-Angiotensin System; Vasopressins

Twenty-two of 23 consecutive infants with bronchiolitis, 5.5 +/- 3.5 mo of age, showed a 1.9 +/- 1.4% increase in body weight, increased urinary osmolality of 737 +/- 193 mmol/L with low plasma osmolality of 275 +/- 4 mmol/L, and markedly elevated plasma antidiuretic hormone (ADH) levels of 114 +/- 225 pg/mL. Increased ADH, which usually suppresses plasma renin activity, was associated with increased plasma renin activity of 11-55 ng angiotensin 1/mL/h (normal for age less than 10 ng angiotensin 1/mL/h). Hyperaldosteronism was evident from the low fractional excretion of sodium of 0.27 +/- 0.2% and high fractional excretion of potassium of 21 +/- 15%. Serum sodium concentrations were normal. All of the pathologic findings returned to normal when the bronchiolitis subsided. A control group of 10 infants with nonrespiratory febrile illness did not show any of the above abnormalities. Thus, bronchiolitis of infancy is characterized by both increased ADH secretion and hyperreninemia with secondary hyperaldosteronism, which induce water retention but counterbalance each other with respect to serum sodium. Increased ADH secretion as well as increased plasma renin activity are not "inappropriate," but rather suggest a response to the perception of hypovolemia by intrathoracic receptors. We therefore conclude that the clinical management of bronchiolitis requires close monitoring of body wt and plasma osmolality-urinary osmolality relationship; serum sodium levels may be misleading.

Topics: Blood Volume; Bronchiolitis; Endocrine Glands; Female; Homeostasis; Humans; Inappropriate ADH Syndrome; Infant; Male; Osmolar Concentration; Renin; Vasopressins; Water-Electrolyte Balance

Oliguria is common in critically ill patients and may result from prerenal, renal, and postrenal causes. Oliguria also frequently develops in patients with normal concentrations of blood urea nitrogen and creatinine. Most of these patients do not develop renal failure. The authors prospectively studied 100 patients admitted to the ICU to determine the etiology of oliguria in these patients. Eighteen patients (18%) developed oliguria (less than 0.33 ml.kg-1.h-1 X 2 h). Seven and eleven patients were felt on clinical assessment to be hypovolemic or normovolemic, respectively. Compared with the hypovolemic patients, the normovolemic oliguric patients had significantly lower serum osmolalities (278 +/- 3 vs. 290 +/- 5 mOsm/kg H2O) and serum sodium concentrations (138 +/- 3 vs. 132 +/- 1 mEq/l). In addition, normovolemic patients had significantly higher urine sodium concentrations (83 +/- 12 vs. 13 +/- 2 mEq/l), fractional excretion of sodium (1.14 +/- 0.2 vs. 0.15 +/- 0.03), and renal failure indices (1.5 +/- 0.3 vs. 0.21 +/- 0.04). ADH concentrations in six hypovolemic and six normovolemic patients were increased in both groups but not significantly different. The hypovolemic patients increased their urine output from 17 +/- 2 ml/h to greater than 0.5 ml.kg-1.h-1 following a 500-ml bolus of normal saline. The normovolemic oliguric patients remained oliguric following the saline bolus (13 +/- 2 to 19 +/- 3 ml/h). The authors conclude that oliguria is common in critically ill patients and results from renal hypoperfusion and ADH excess.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Anuria; Blood Volume; Diuresis; Furosemide; Humans; Inappropriate ADH Syndrome; Kidney; Oliguria; Osmolar Concentration; Reference Values; Sodium Chloride; Vasopressins

Hypouricemia in coexistence with hyponatremia often differentiates the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) from most other causes of hyponatremia. We report clearance studies in 5 cases of hyponatremia and hypouricemia that were not due to SIADH. One had metastatic pancreatic carcinoma with ascites, edema, hypoalbuminemia and hypophosphatemia. Two had adenocarcinoma of the lung with metastasis to the brain in 1, 1 had disseminated cryptococcus and 1 had Hodgkin's disease. None received radiation or known nephrotoxins at least 4 months prior to study. None had serum creatinine greater than 106.1 mumol/l (1.2 mg/dl). Two had postural hypotension and hyponatremia that responded to saline therapy. Fluid restriction corrected the hyponatremia in all patients, but the hypouricemia, high fractional excretion (FE) of urate, and high urine sodium concentration persisted. In 2 patients studied, ADH was appropriately suppressed after volume repletion but there was a defect in free water clearance due to high renal solute excretion. In contrast to patients with SIADH who correct their defect in renal urate transport with correction of hyponatremia by water restriction, our patients appear to have a persistent renal urate transport defect and abnormality in sodium conservation. Elevated FE urate of greater than 10% after correction of hyponatremia can thus differentiate these patients from SIADH. The diametrically opposing goals of fluid therapy emphasize the importance of differentiating one group from the other.

Topics: Adult; Diagnosis, Differential; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Male; Middle Aged; Sodium; Uric Acid; Vasopressins; Xanthine Oxidase

Topics: Blood Pressure; Cerebral Hemorrhage; Cerebral Ventricles; Humans; Inappropriate ADH Syndrome; Infant, Newborn; Infant, Premature, Diseases; Vasopressins

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

The authors describe a case of subarachnoid hemorrhage with hyponatremia accompanied by elevation of plasma atrial natriuretic peptide (ANP). The early phase of hyponatremia was classified as the syndrome of inappropriate secretion of antidiuretic hormone (ADH) due to subarachnoid hemorrhage. However, in the later phase, hyponatremia and natriuresis were accompanied by suppression of ADH while plasma ANP remained elevated. The patient was effectively treated with demeclocycline and hypertonic saline. The significance of ANP in the pathophysiology of increased natriuresis is discussed.

Topics: Aged; Atrial Natriuretic Factor; Demeclocycline; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Intracranial Aneurysm; Natriuresis; Saline Solution, Hypertonic; Subarachnoid Hemorrhage; Vasopressins

A rare case with Guillain-Barré syndrome complicated by inappropriate secretion of antidiuretic hormone (SIADH) and hypertension was reported. This case showed clinically mild symptoms without respiratory muscle paralysis and had a complete neurological recovery. It should, therefore, be considered that the Guillain-Barré syndrome may cause SIADH and hypertension independent of the severity of the disease.

Topics: Child; Epinephrine; Humans; Hypertension; Inappropriate ADH Syndrome; Male; Neurologic Examination; Norepinephrine; Polyradiculoneuropathy; Renin-Angiotensin System; Sodium; Sympathetic Nervous System; Vagus Nerve; Vasopressins

Topics: Aged; Antineoplastic Agents; Atrial Natriuretic Factor; Humans; Inappropriate ADH Syndrome; Lung Diseases; Male; Neoplasms; Vasopressins

Severe hyponatremia occurs in some patients with untreated hypopituitarism, but it is not known whether such hyponatremia is caused by the hypersecretion of vasopressin (antidiuretic hormone). This report describes severe, symptomatic hyponatremia in five women 59 to 83 years old (serum sodium, 111 to 118 mmol per liter) who presented with hypopituitarism (which had been previously undiagnosed in four). Plasma vasopressin was inappropriately high (1.3 to 25.8 pmol per liter [1.4 to 28 ng per liter]) in relation to plasma osmolality (236 to 260 mOsm per kilogram of body weight). All five patients had normal renal function and no signs of dehydration or volume depletion. The hyponatremia was resolved within a few days after the institution of hydrocortisone therapy, after infusion of normotonic or hypertonic saline had been found to be less effective. When four of the patients were later restudied while receiving maintenance hydrocortisone treatment, the relation between plasma vasopressin and osmolality was normal. We conclude that ACTH deficiency may cause the syndrome of inappropriate secretion of antidiuretic hormone. The beneficial effect of hydrocortisone is probably exerted through the suppression of vasopressin secretion.

Topics: Adrenocorticotropic Hormone; Aged; Aged, 80 and over; Female; Humans; Hydrocortisone; Hyponatremia; Hypopituitarism; Inappropriate ADH Syndrome; Middle Aged; Osmolar Concentration; Retrospective Studies; Vasopressins

Topics: Adult; Animals; Cell Membrane; Humans; Hyponatremia; Inappropriate ADH Syndrome; Kidney; Male; Syndrome; Vasopressins; Water

Topics: Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Pituitary Function Tests; Radioimmunoassay; Reagent Kits, Diagnostic; Reference Values; Saline Solution, Hypertonic; Specimen Handling; Vasopressins

Vasopressin levels, together with plasma and urinary electrolytes, were measured in the acute and convalescent stages of 17 patients with malaria and 11 patients with other febrile illnesses. There was a significantly lower serum sodium in the acute stages of both groups (p less than 0.01 and p less than 0.02). There was no significant difference between the malaria and control groups. There were no significant changes in the vasopressin levels, although one patient with malaria showed evidence of inappropriate vasopressin secretion which returned to normal after treatment. This study suggests the mild hyponatraemia sometimes seen in the acute stages of malaria is not related to inappropriate secretion of vasopressin, although this condition may be of importance in more severe cases of hyponatraemia.

Topics: Adolescent; Adult; Animals; Electrolytes; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Malaria; Male; Middle Aged; Plasmodium falciparum; Vasopressins

The effect of therapy for hyponatremia with central origin (cerebrovascular disease and head injury) was investigated in order to examine contributing factors. Out of a total of 58 subjects admitted to the hospital during the previous three years with cerebrovascular disease (49 cases), and head injuries (9 cases), hyponatremia with central origin occurred within 2 weeks. Special treatment for hyponatremia was not given in 30 of the 58 cases (control group). The group (28 cases) which underwent therapy was optionally selected in terms of the following-SIADH, natriuretic polypeptide involvement and sick cells resulting from Na-K pump disorder. These 28 cases were classified into subgroups: water restricted (7 cases), hypertonic NaCl load (9 cases), glucose/insulin/potassium (GIK) therapy (4 cases), phenytoin administration (8 cases). In all of the 58 patients, the serum sodium, potassium and osmolarity and urinary sodium and potassium were measured daily. The balance of water, sodium and potassium were calculated on hyponatremic phase. Plasma levels of such hormones as antidiuretic hormone, aldosterone and cortisol were measured on hyponatremic phase. For each group, onset day and duration of hyponatremia and lowest sodium value were investigated for the sake of comparison. No significant difference for onset day and lowest sodium value was found between each group. Duration was as follows: control group 9.4 +/- 3.3 days, water restricted 7.4 +/- 2.1 days, hypertonic NaCl load 3.3 +/- 1.4 days, GIK therapy 7.3 +/- 2.9 days and phenytoin administration 8.9 +/- 3.7 days. Hypertonic NaCl load indicated a significantly shorter duration compared with the other groups. Hypertonic NaCl load was found to be most effective for hyponatremia with central origin.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aldosterone; Cerebrovascular Disorders; Craniocerebral Trauma; Glucose; Humans; Hydrocortisone; Hyponatremia; Inappropriate ADH Syndrome; Insulin; Phenytoin; Potassium; Saline Solution, Hypertonic; Sodium; Vasopressins; Water-Electrolyte Balance

The syndrome of inappropriate secretion of antidiuretic hormone is associated with head trauma; however, there are no reports concerning vasopressin levels in pediatric patients with head trauma. Urine vasopressin in eight children (mean +/- SEM, age 7.5 +/- 1.6 years, range 1 to 15 years) was measured by radioimmunoassay during their hospitalization for head trauma. Urine vasopressin values for ten healthy children (mean age 5.4 +/- 1.3 years) and for eight children hospitalized for systemic antibiotic treatment of infections (age 5.9 +/- 1.8 years) also were obtained. Urine vasopressin, urine and serum sodium concentration and osmolality, urea nitrogen, creatinine, and fluid intake were measured within 24 hours of admission and daily for the following two days. For the first three days following head trauma, mean urine vasopressin levels in pediatric patients with head trauma were increased (P less than .05) compared with those of healthy children. Despite fluid restriction to 85% of maintenance level, 25% of patients with head trauma exhibited the clinical syndrome of inappropriate secretion of antidiuretic hormone (hyponatremia, increased urinary sodium, diminished serum osmolality, and urine osmolality greater than serum osmolality). Urine osmolality greater than 800 mosm/kg was associated with markedly increased urine vasopressin levels (200 to 1,650 pg/mL); children with this finding may be at particular risk for the syndrome of inappropriate secretion of anti-diuretic hormone without restrictive water intake.

Topics: Adolescent; Child; Child, Preschool; Craniocerebral Trauma; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant; Osmolar Concentration; Sodium; Vasopressins

We studied a 41 year old patient who had pathologic fluid intake of 10 1/day together with syndrome of inappropriate antidiuretic hormone. Imaging studies revealed a lesion of the anterior wall of the third cerebral ventricle. A review of relevant literature indicated several different disturbances by which alterations of thirst, vasopressin-secretion and abnormalities of anterior third ventricle may be associated. The present case presents an unusual and potentially dangerous combination in this spectrum of changes.

Topics: Adult; Calcinosis; Cerebral Ventricles; Drinking; Humans; Hypothalamic Diseases; Hypothalamus; Inappropriate ADH Syndrome; Male; Tomography, X-Ray Computed; Vasopressins; Water-Electrolyte Balance

An inappropriate antidiuretic hormone secretion (SIADH) has been recognized as the cause of hypotonic hyponatremia, and the occurrence of this syndrome, accompanied by an ADH-producing adenocarcinoma in the nasal cavity, is reported. In February, 1987, a 50-year-old male, showing sights of delirium, disorientation, and irritability was admitted to the hospital. The patient was observed to be healthy, except for a neck lymphnode metastasis that was present up to the time of his hospitalization. The hyponatremia was incidentally found, although dehydration or intravascular volume depletion were not noted. These neuropsychiatric symptoms were considered to be associated with hyponatremia due to SIADH. He had had a partial maxillectomy, a neck dissection, and irradiation to the nose and nasal cavity 32 months earlier, and then underwent a surgical resection of the neck metastasis; he had a total of 10 other operations before the onset of the symptoms. Upon initial inspection, since neither an intracranial invasion nor a brain metastasis was found, we diagnosed that his symptoms were due to an autonomic disturbance caused by surgical and mental "stress". When he died of cardiac failure due to a mediastinal invasion 8 months after the onset of SIADH, tumor tissues was extirpated in an autopsy and was then cultured. In this manner, it was proved that the tumor cells had been producing ADH. This procedure clarified that the syndrome had resulted from an ADH-producing tumor of the nasal cavity.

Topics: Adenocarcinoma; Combined Modality Therapy; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Nose Neoplasms; Paraneoplastic Endocrine Syndromes; Vasopressins

In neurosurgical patients with hyponatraemia (plasma sodium less than 130 mmol/l) and natriuresis, increased antidiuretic hormone (ADH) secretion may be appropriate rather than inappropriate. Ten such patients were studied prospectively to assess circulating ADH concentration and body fluid volumes. Compared with a control group, the mean plasma ADH level was significantly elevated (0.9 pmol/l (s.e.m. = 0.2) versus 0.2 pmol/l (s.e.m. = 0.1], the total body water was normal (101% (s.e.m. = 3) versus 100% (s.e.m. = 6], while the blood volume was significantly reduced (89% (s.e.m. = 3) versus 104% (s.e.m. = 5]. The elevated ADH level was therefore appropriate to a reduced blood volume. This suggests that, in neurosurgical patients with hyponatraemia, fluid restriction could be dangerous. Serial observations in this small group of patients showed that salt replacement and normal fluid intake resulted in a fall in the elevated ADH levels.

Topics: Acute Disease; Adult; Blood Volume; Body Water; Brain Diseases; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Natriuresis; Plasma Volume; Prospective Studies; Vasopressins

In this study we have identified and characterized several vasopressin-like peptides in the plasma of a patient with the syndrome of inappropriate antidiuretic hormone secretion and oat cell carcinoma of the lung. Immunoreactive plasma vasopressin was measured after gel filtration (Sephadex G-25) or C-18 cartridge extraction using two different region-specific antisera: AS1 and AS2. Antiserum AS1 is more specifically directed towards the antigenic site of the hexapeptidic ring of arginine-vasopressin (AVP), whereas AS2 is more specifically directed towards the C-terminal region of AVP. Unexpectedly, the Sephadex G-25 gel filtration elution profile of the immunoreactive vasopressin was very heterogeneous, indicating the presence of several molecular species. After extraction of total AVP and AVP-like peptides of this plasma, an unusual AS1/AS2 ratio of immunoreactivity was observed, suggesting the presence of vasopressin-like peptides which differ from AVP in the C-terminus.

Topics: Aged; Arginine Vasopressin; Carcinoma, Small Cell; Chromatography, Gel; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Molecular Conformation; Radioimmunoassay; Trypsin; Vasopressins

This study explored whether atrial natriuretic hormone (ANH) might be involved in the escape from salt and water retention that occurs in patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Sixteen patients with low serum Na+ concentrations [123 +/- 1 (+/- SE) mmol/L] were studied. Each patient excreted urine that was hyperosmolar (mean, 391 +/- 4 mosmol/kg) in relation to serum osmolality (mean, 258 +/- 4 mosmol/kg). Sodium excretion (81 +/- 20 mmol/L) also was inappropriate to the low serum Na+ level. The probable causes of SIADH were head trauma (4), pneumonia (5), lung cancer (3), and chlorpropamide therapy (4). In the nontumor patients, plasma and/or urinary vasopressin (AVP) concentrations were in the normal range, but inappropriate for serum osmolality. Urinary AVP values of 50 pg/mL or more (greater than 46 pmol/L) were found in the three tumor patients. The mean plasma ANH concentration was 6-fold higher than that in normal subjects [296 +/- 51 vs. 51 +/- 13 pg/mL (100 +/- 20 vs. 17 +/- 4 pmol/L); P less than 0.01]. Six SIADH patients were studied again after brief (1-3 days) water restriction. Although serum osmolality increased in each, their plasma AVP concentrations decreased very little, and urinary AVP excretion and plasma ANH did not change. These results indicate that plasma ANH levels are markedly increased in patients with SIADH. Their increased ANH secretion may antagonize water retention resulting from the inappropriate AVP secretion.

Topics: Adult; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Electrolytes; Female; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Osmolar Concentration; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Aged; Atrial Natriuretic Factor; Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Middle Aged; Pituitary Gland, Posterior; Renin-Angiotensin System; Vasopressins

Topics: Humans; Inappropriate ADH Syndrome; Osmolar Concentration; Pneumonia; Vasopressins

This prospective study is based on 256 patients with severe brain injury. Six patients (2.3%) developed the clinical picture of inappropriate secretion of antidiuretic hormone (SIADH): 3 in the first 3 days following the injury, 3 after more than a week. Their ADH plasmatic level were measured by radio-immunoassay. In the former, many factors, largely iatrogenic, can explain the increased secretion of ADH we found and which is then definitely "appropriate". It should be prevented by fluid restriction. In the latter, we found adequately low ADH levels, when the hypo-osmolarity is taken into account. Here, the aetiology seems to be a renal salt loss, eventually in relation to a natriuric factor (e.g. atrial natriuretic factor), justifying the term: "Cerebral salt wasting syndrome". With the resistance to fluid restriction, the treatment still remains a problem.

Topics: Adult; Brain Injuries; Child; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Osmolar Concentration; Prospective Studies; Vasopressins

Patients with small-cell lung cancer and hyponatremia were examined for the syndrome of inappropriate antidiuresis (SIAD). A comparison was made between the definition based on hyponatremia, serum hypoosmolality and urine hyperosmolality (classic SIAD, 12 patients) and a definition based on measurement of plasma ADH concentration by radioimmunoassay (RIA-SIAD, nine patients) and patients without SIAD (eight patients). A standard water load test was performed as a reference before initiation of cytostatic treatment. All tests were repeated if remission of the malignant disease occurred. RIA-SIAD patients were a subgroup of classic SIAD patients, with more pronounced homeostatic abnormalities. Biochemical abnormalities were reduced after tumor regression but a completely normal renal water handling was achieved in only few patients, even when complete remission of the tumor was achieved, presumably due to the persistence of subclinical disease. However, an effect of other yet unknown factors might be of influence.

Topics: Carcinoma, Small Cell; Female; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Osmolar Concentration; Radioimmunoassay; Remission Induction; Vasopressins

Topics: Adrenocorticotropic Hormone; Child, Preschool; Female; Humans; Inappropriate ADH Syndrome; Periodicity; Vasopressins

Topics: Aged; Carcinoma, Squamous Cell; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Vasopressins

Topics: Child; Child, Preschool; Humans; Inappropriate ADH Syndrome; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Humans; Inappropriate ADH Syndrome; Tuberculosis, Pulmonary; Vasopressins

Topics: Adult; Female; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Myotonic Dystrophy; Vasopressins; Water

Our purpose was to investigate a method of prolonged desmopressin (DDAVP) infusion in a free roaming rat to better understand the SIADH (syndrome of inappropriate antidiuretic hormone secretion) syndrome in man. DDAVP was infused for 2 weeks from implanted self-powered osmotic minipumps. At the end of that time, plasma DDAVP and urine osmolality were both significantly elevated in experimental as compared with control animals. However, hyponatremia and hypoosmolality, which are characteristic in the SIADH, did not develop. Our observations suggest that inappropriate high antidiuretic hormone levels do not necessarily lead to the SIADH either by urine sodium loss or by water retention if animals decrease water intake.

Topics: Animals; Deamino Arginine Vasopressin; Drinking; Female; Inappropriate ADH Syndrome; Infusion Pumps; Osmolar Concentration; Rats; Rats, Inbred Strains; Sodium; Vasopressins; Water-Electrolyte Balance

The role of vasopressin in human hypertension was examined in a series of studies. In patients with primary hyperaldosteronism and benign essential hypertension, circulating vasopressin was generally lower than in normotensive subjects. In contrast, plasma vasopressin was increased (p less than 0.001) in patients with malignant-phase hypertension. However, compared to infused vasopressin in normal subjects, when plasma levels of up to 120 pg/ml did not affect blood pressure, the increased levels found in malignant hypertension could not account for the hypertension. The possibility that there may be an increased pressor sensitivity to vasopressin in hypertension was examined by infusing the peptide into nine patients with essential hypertension. This showed a slight increase in sensitivity compared to normotensive subjects, but again this was insufficient to account for the discrepancy between the circulating level of vasopressin and the extent of the raised blood pressure in the hypertensive patients. The effect of chronically elevated levels of vasopressin was studied in a group of patients with the syndrome of inappropriate ADH excess as a consequence of bronchogenic carcinoma. In spite of having chronically elevated levels of vasopressin, these patients had normal blood pressures for their age and sex. Our results suggest that, although vasopressin is elevated in malignant hypertension, it does not contribute significantly to the raised blood pressure, and its increase is probably a consequence of volume shrinkage through renal salt and water loss.

Topics: Blood Pressure; Female; Humans; Hypertension; Inappropriate ADH Syndrome; Infusions, Intravenous; Male; Middle Aged; Vasopressins

Vasopressin is the primary physiological factor regulating renal water reabsorption in mammals. Inhibitors of vasopressin-stimulated water reabsorption have previously been used as water diuretic agents in both experimental animals and man. The present studies describe and characterize the pharmacological effects of the potent vasopressin antagonist desGly d(CH2)5D-Tyr(Et)VAVP (SK&F 101926) and related analogs on renal water and solute excretion in conscious rats. Administration of SK&F 101926 was associated with dose-dependent increases in renal water excretion in conscious hydropenic rats. A selective vasopressin pressor (V1) antagonist (SK&F 100273) was inactive as a diuretic agent in these tests. SK&F 101926 antagonized, in a competitive fashion, exogenous vasopressin-stimulated antidiuresis in conscious water-loaded rats. Only modest increases in renal excretion of Na+, K+, and urea were observed when SK&F 101926 was administered. No changes in endogenous creatinine excretion were associated with the administration of SK&F 101926, suggesting that this drug does not affect glomerular filtration rate. The rank order of bioequivalency of alternative routes of administration of SK&F 101926 was intraperitoneal = intravenous = intramuscular = subcutaneous greater than intranasal much greater than rectal, ocular, and oral. SK&F 101926 (20 micrograms/kg/day) was effective in blocking the development of hyponatremia in a rat model of the syndrome of inappropriate antidiuretic hormone (SIADH). SK&F 100273 (100 micrograms/kg) hastened the onset of endotoxin-associated shock in rats. We conclude that SK&F 101926 is a potent water diuretic (aquaretic) agent in rats. The mechanism of action is most probably antagonism of vasopressin at renal epithelial (V2) receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Arginine Vasopressin; Dehydration; Diuresis; Dose-Response Relationship, Drug; Inappropriate ADH Syndrome; Male; Osmolar Concentration; Rats; Shock, Septic; Vasopressins

Review of clinical data from 350 patients with small-cell lung cancer (SCLC) revealed hyponatremia (sodium less than 130 mEq/L) attributable to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in 40 patients (11%). Although hyponatremia was severe in most instances (median, sodium 117 mEq/L), symptoms attributable to water intoxication were identified in only 27% of hyponatremic episodes. Development of SIADH showed no correlation with clinical stage, distribution of metastatic sites, sex, or histologic subtype of small-cell carcinoma. SIADH occurred most often with initial presentation (33 of 40), and resolved promptly (less than 3 weeks) with initiation of combination chemotherapy in 80% of evaluable patients. The presence of SIADH did not influence response to chemotherapy or overall survival as an independent variable. However, in five patients profound hyponatremia developed immediately following primary cytotoxic therapy (range, one to five days). Despite initial control of SIADH, dilutional hyponatremia recurred in 70% of patients with tumor progression. Our findings suggest that development of clinically demonstrable SIADH in patients with SCLC is dependent on functional properties of the neoplastic cells, rather than tumor burden or metastatic site. The potential for development of clinically significant hyponatremia early in the course of cytotoxic therapy emphasizes the need to closely monitor patients, particularly those receiving chemotherapy regimens requiring substantial intravenous hydration.

Topics: Antineoplastic Combined Chemotherapy Protocols; Carcinoma, Small Cell; Female; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Neoplasm Metastasis; Neoplasm Staging; Osmolar Concentration; Paraneoplastic Endocrine Syndromes; Sodium; Vasopressins

Two patients with squamous cell carcinoma of the head and neck are reported in whom the syndrome of inappropriate antidiuretic hormone (SIADH) secretion occurred transiently during the rapid cytolytic phase of tumor destruction after chemotherapy with cis-platinum diamminedichloride and bleomycin. Immunoperoxidase staining for ADH of the original biopsy specimens from both patients was negative. Possible mechanisms for and the implications of the production of SIADH in this setting are discussed.

Topics: Antineoplastic Agents; Carcinoma, Squamous Cell; Female; Head and Neck Neoplasms; Humans; Immunoenzyme Techniques; Inappropriate ADH Syndrome; Male; Middle Aged; Vasopressins

A new rat model of the Schwartz--Bartter syndrome was created by the administration of 1-deamino-8-D-arginine vasopressin together with a forced water intake. The treatment led to water retention, hypernatriuria, marked hyponatraemia (in 4-5 days) and severe cerebral oedema. These changes could be prevented by the simultaneous administration of [1-(beta-mercapto-beta, beta-cyclopentamethylene-propionic acid)- 2-o-ethyltyrosine-4-valine] arginine vasopressin. The observations indicate that this vasopressin antagonist analogue might be of use in the future as an effective drug against the Schwartz--Bartter syndrome.

Topics: Animals; Arginine Vasopressin; Deamino Arginine Vasopressin; Disease Models, Animal; Inappropriate ADH Syndrome; Male; Rats; Vasopressins; Water Intoxication

A study was conducted on 16 schizophrenic patients with compulsive water drinking (CWD) and 10 normal controls, and the relation between serum antidiuretic hormone (ADH) and serum osmolality measured under ordinary conditions of free water intake. A water deprivation test and a water load test were also carried out on 10 schizophrenics with CWD and 10 normal controls. A comparison between the patients and controls showed the following results: the patients showed a significantly high level of serum ADH for their serum osmolality level, and 3 of them were consistent with the syndrome of inappropriate secretion of ADH (SIADH); the urine osmolality after the water deprivation in the patients was relatively low for their serum ADH; inhibition of ADH secretion after the water load was insufficient in the patients; and the water load test proved favorable to water diuresis (106%) in the patients with CWD of less than a 5-year duration, and insufficient diuresis (62.6%) in the patients with CWD of more than a 5-year duration. Two cases of the latter group had SIADH. The dilution and concentration of the urine after the water load were delayed also in the schizophrenic patients without SIADH. These findings suggest a strong possibility that the regulatory mechanism of ADH secretion might be impaired in the schizophrenic patients with CWD.

Topics: Adult; Compulsive Behavior; Drinking; Female; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Schizophrenic Psychology; Vasopressins; Water Deprivation; Water Intoxication; Water-Electrolyte Balance

Topics: Adult; Aged; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Vasopressins; Water-Electrolyte Imbalance

Vasopressin (ADH) was measured in CSF and plasma in 75 evaluable patients with known or suspected CNS metastases from small-cell bronchogenic carcinoma (SCBC), and in 66 control patients having neither malignant disease nor organic CNS disease. The presence of CNS metastases was confirmed or excluded on the basis of computed tomographic scans, neurologic examination, and autopsy. Twenty-four of the 75 patients had no CNS metastases. Ten of the 51 patients with CNS metastases had leptomeningeal carcinomatosis (MC). CSF-ADH was significantly increased in patients with MC (P less than .05), but not in patients having exclusively parenchymatous CNS metastases. Taking 2 pg/mL (95th percentile of control patients) as the upper limit of normal, 15 SCBC patients had elevated CSF-ADH, including 12 patients with CNS metastases and six patients with MC. The CSF-ADH to plasma ADH ratio was significantly increased in patients with CNS metastases (P less than .05). Patients without CNS metastases had a ratio less than or equal to 0.8 whereas the ratio was greater than 0.8, in 21 of the 51 patients with CNS metastases. The positive and negative predictive values with 95% confidence limits were 84% to 100% and 31% to 59%, respectively. Patients with inappropriate secretion of ADH (SIADH) constituted a significantly greater proportion of patients with elevated CSF-ADH than of patients with normal CSF-ADH levels (P less than .05). In addition, patients with SIADH constituted a significantly greater proportion of patients with MC than of patients with parenchymatous metastases (P less than .05). The diagnostic application of these findings is limited because of the large number of false-negative results, but it may prove to be of value in conjunction with the measurement of other tumor markers.

Topics: Carcinoma, Bronchogenic; Carcinoma, Small Cell; Central Nervous System Diseases; Humans; Inappropriate ADH Syndrome; Intracranial Pressure; Lung Neoplasms; Meningeal Neoplasms; Neoplasm Metastasis; Vasopressins

Topics: Aged; Humans; Hyponatremia; Inappropriate ADH Syndrome; Middle Aged; Vasopressins; Water-Electrolyte Balance

Topics: Humans; Inappropriate ADH Syndrome; Vasopressins; Water-Electrolyte Imbalance

A prospective study was undertaken to determine whether there was a relationship between the pharyngeal flap operation and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). From August 1982 to November 1983, 25 patients underwent pharyngeal flap procedures. They were compared to a control group made up of five patients who underwent major cleft lip revisions. Twelve of the twenty-five patients (48%) who underwent pharyngeal flap procedures had inappropriately elevated serum ADH levels, low serum osmolality, and hyponatremia in the postoperative period. There was a statistically significant (p less than 0.001) drop in the serum sodium levels in the pharyngeal flap group from the preoperative to postoperative period. There was neither a statistically significant change in the serum sodium levels nor inappropriate elevation of ADH levels in the control group. Two patients who underwent pharyngeal flap procedures developed SIADH. To our knowledge this complication has not been reported in association with the pharyngeal flap operation. No specific causes were found that would explain why SIADH developed.

Topics: Adolescent; Child; Child, Preschool; Female; Humans; Inappropriate ADH Syndrome; Male; Osmolar Concentration; Pharynx; Sodium; Surgical Flaps; Vasopressins; Velopharyngeal Insufficiency

Hyponatremia developing some days after transsphenoidal pituitary adenectomy is a treacherous complication of uncertain cause. Of 19 patients monitored in a pilot study at the Wessex Neurological Centre, plasma sodium fell below 125 mmol/liter in three patients at times ranging from 6 to 9 days postoperatively. One patient had evidence of inappropriate secretion of arginine vasopressin (AVP), and the other two probably had steroid insufficiency despite apparently adequate steroid cover. In a more detailed study, the fluid and sodium balance of a further 16 patients was monitored for 7 to 11 days following transsphenoidal surgery together with plasma cortisol, renin, and AVP concentrations. No patient became severely hyponatremic. Three developed partial diabetes insipidus. Two patients with Cushing's disease had evidence of postoperative corticosteroid insufficiency despite normal steroid protection. An inappropriately low plasma cortisol concentration was recorded in both. Plasma AVP concentrations did not show a delayed surge postoperatively. Delayed hyponatremia appears to occur most often in patients with hypoadrenalism, as glucocorticoid cover is decreased. It results from water retention combined with natriuresis, and is reversed by glucocorticoid treatment.

Topics: Adenoma; Adult; Arginine Vasopressin; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Pituitary Neoplasms; Vasopressins; Water-Electrolyte Imbalance

Topics: Aged; Humans; Inappropriate ADH Syndrome; Male; Osmolar Concentration; Pneumonia; Radioimmunoassay; Sodium; Vasopressins

Nine children with Schwartz-Bartter-syndrome are described. Seven suffered from severe diseases of the CNS, 2 developed the syndrome during treatment with vincristine, the damaging action of which on the CNS is known. The main symptoms of the syndrome are: hyponatremia with consecutive hypotonia of the extracellular space caused by excessive urinary sodium loss. The plasma volume is not diminished. Therapeutically administered NaCl appears in the urine which is hyperosmolar in spite of the hypoosmolarity of the plasma. The increased secretion of ADH which Schwartz et al. postulated to be the cause of the syndrome has been confirmed in recent years. The organism attempts to excrete the increased fluid volume which is retained by ADH, probably by means of a natriuretic hormone, so-called third factor. Enhanced activity of such a factor was assessed in one of our cases.

Topics: Brain Diseases; Brain Injuries; Cerebrospinal Fluid Shunts; Child; Cysts; Female; Humans; Inappropriate ADH Syndrome; Infant; Male; Tuberculosis, Meningeal; Vasopressins; Vincristine

Topics: Diagnosis, Differential; Humans; Hyponatremia; Inappropriate ADH Syndrome; Vasopressins

Topics: Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Polyuria; Syndrome; Thirst; Vasopressins

Topics: Female; Humans; Inappropriate ADH Syndrome; Male; Subarachnoid Hemorrhage; Vasopressins

Although the syndrome of inappropriate ADH secretion (SIADH) has many causes, principally pulmonary, central nervous system or neoplastic disease, and drugs, patients may present with SIADH in whom the etiology is not readily evident. We measured serum ADH levels in such an individual in both the eunatremic and water-loaded states and found levels to be undetectable despite failure to dilute the urine. A small oat cell pulmonary carcinoma was ultimately diagnosed with lung tomograms and cytology. Following a partial response to water restriction, demeclocycline was effective in producing a water diuresis that restored the serum sodium concentration to normal. Patients with clinical SIADH but low serum ADH levels can harbor a malignant or benign process that, notwithstanding the low ADH levels, may still remain responsive to demeclocycline, suggesting either neoplastic production of a biologically-active, immunologically-inactive ADH-like peptide, or increased renal tubular sensitivity to ADH.

Topics: Carcinoma, Small Cell; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Middle Aged; Vasopressins

Topics: Humans; Inappropriate ADH Syndrome; Male; Schizophrenia; Thirst; Vasopressins

Topics: Humans; Inappropriate ADH Syndrome; Subarachnoid Hemorrhage; Vasopressins

The effects of lorcainide, a new antiarrhythmic drug, on serum electrolytes and osmolality are described in a series of 33 patients with organic heart disease and complex ventricular arrhythmias treated with lorcainide. In eight patients, a mean decrease in serum Na+ of 8.25 +/- 3.2 mEq/L was observed after a single 200 mg intravenous dose of lorcainide. Sixteen of 33 patients developed significant hyponatremia and hypoosmolality during oral treatment with lorcainide. In all except two patients, serum Na+ returned to normal values within 3 to 12 months of continued lorcainide therapy. Low serum Na+ and hypoosmolality in the absence of volume depletion, clinically manifest edema, and unaltered renal, adrenal, cardiac, or thyroid function suggest that this antiarrhythmic drug produced the syndrome of inappropriate antidiuretic hormone secretion (SIADH). SIADH appeared to be transient and asymptomatic in our patients. One patient developed severe hyponatremia with serum Na+ of 108 mEq/L when hydrochlorothiazide was given to control hypertension. It is concluded that SIADH is an important side effect of lorcainide therapy. We recommend that serum Na+ be carefully monitored in patients started on lorcainide therapy, and extreme caution should be exercised in prescribing diuretics to patients with persistent hyponatremia.

Topics: Adult; Aged; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Benzeneacetamides; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Piperidines; Potassium; Sodium; Vasopressins

A monkey model of subarachnoid hemorrhage (SAH) was used to study both the incidence of hyponatremia and natriuresis and the associated changes in antidiuretic hormone (ADH) secretion and salt and water balance. Following SAH, seven of nine monkeys became natriuretic and hyponatremic. The natriuretic period lasted an average of 4.4 +/- 0.4 days. The mean nadir of serum sodium content was 125.7 +/- 1.6 mEq/liter, and occurred on the average on the 5th day following SAH. The sodium balance after SAH was negative as compared to the preoperative positive sodium balance (p less than 0.001). The plasma vasopressin level was usually elevated for a day following surgery, but there was no significant difference in the levels during the preoperative period and during the period of natriuresis following SAH. The daily urine output and aldosterone levels were not significantly different, and the plasma volume was slightly, but not significantly, decreased after SAH. Four of the animals that had a hyponatremic and natriuretic response following SAH showed a normal regulation of vasopressin in response to both a water challenge and hypertonic saline challenge. The three monkeys that underwent sham procedures did not become hyponatremic and natriuretic postoperatively. The sham-operated monkeys did not show significant differences in their plasma vasopressin levels, urine volume, plasma volume, and aldosterone levels following surgery. These observations are more consistent with primary natriuresis as the cause of hyponatremia rather than the syndrome of inappropriate secretion of ADH. The cause of the renal loss of sodium is not known, but the possibility of a brain natriuretic factor or an alteration in the neural control of the kidney should be considered.

Topics: Animals; Hyponatremia; Inappropriate ADH Syndrome; Macaca fascicularis; Male; Models, Biological; Natriuresis; Subarachnoid Hemorrhage; Vasopressins

Topics: Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Vasopressins

A rat model of the Schwartz-Bartter syndrome was created by the administration of a high dose of a long-acting vasopressin preparation (pitressin tannate ) together with a forced water intake. The treatment led to water retention, hypernatriuria , marked hyponatraemia (in 4-5 days) and severe cerebral oedema. These changes could be prevented by the simultaneous administration of [1-(beta-mercapto-beta, beta- cyclopentamethylene -propionic acid),2-0- ethyltyrosine ,4-valine]arginine vasopressin. The observations indicate that this vasopressin antagonist analogue might be of use in the future as an effective drug against the Schwartz-Bartter syndrome.

Topics: Animals; Arginine Vasopressin; Body Water; Brain; Brain Edema; Diuresis; Hyponatremia; Inappropriate ADH Syndrome; Male; Osmolar Concentration; Rats; Rats, Inbred Strains; Urination; Vasopressins

The effect of [1-(beta-mercapto-beta,beta- cyclopentamethylene -propionic acid)2-0- ethyltyrosine ,4-valine] arginine vasopressin on the water metabolism was studied in rat. The compound was found to be able to block the antidiuretic action of both exogenous and endogenous vasopressin. A rat model of the Schwartz-Bartter syndrome was created by the administration of a high dose of a posterior pituitary preparation (Pitressin tannate ) together with a forced water intake. The antagonist prevented water retention and averted the enhanced natriuresis and hyponatraemia, and cerebral oedema did not develop. The observations suggest that this vasopressin antagonist might be of use in the future as an effective drug against the Schwartz-Bartter syndrome.

Topics: Animals; Arginine Vasopressin; Brain; Brain Edema; Disease Models, Animal; Diuresis; Female; Inappropriate ADH Syndrome; Male; Natriuresis; Osmolar Concentration; Rats; Sodium; Vasopressins

Topics: Humans; Inappropriate ADH Syndrome; Postoperative Period; Stress, Physiological; Vasopressins; Water

The role played by prostaglandins in the secretion of ADH and modulation of its action was investigated by testing the effects of prostaglandin synthesis inhibition in patients with SIADH of cerebral or pulmonary origin. Three patients with SIADH of central origin and 3 with SIADH of peripheral origin were subjected to 4 successive water-loading tests. In the first and fourth tests, the patients absorbed water 20 ml/kg bodyweight; in the second test they absorbed alcohol 2.5 ml/kg followed by water 17.5 ml/kg. The third test was preceded by a 3-day inhibition of prostaglandin synthesis with indomethacin 200 mg/day and aspirin 1.5 g/day. In patients with SIADH of peripheral origin the percent water-load excreted after 4 hours was low (less than 35%) with the 4 tests, whereas it reached 80% (p less than 0.001) with the third test (prostaglandin inhibition) in those with SIADH of central origin. Alcohol did not significantly correct the antidiuretic effect in any of the patients in both groups. It is concluded that prostaglandins reduce ADH secretion in central SIADH but do not modify antidiuresis in peripheral SIADH, since ectopic secretion probably does not depend on prostaglandins. The prostaglandin inhibition test therefore seems to be more helpful than the alcohol test to differentiate between central and peripheral SIADH. Further studies, however, are required to confirm these findings.

Topics: Adult; Aged; Aspirin; Brain Diseases; Ethanol; Female; Humans; Inappropriate ADH Syndrome; Indomethacin; Lung Diseases; Male; Middle Aged; Prostaglandin Antagonists; Prostaglandins; Vasopressins; Water

From 1976 to 1980, 18 of the 250 patients (7%) seen with small cell carcinoma of the lung had clinically evident inappropriate secretion of antidiuretic hormone (ADH). Hyponatremia was usually severe (116 +/- 7 meq/l), and eight patients showed symptoms of water intoxication at the time of diagnosis. Of the eight patients who had plasma ADH measured at diagnosis, seven had elevated values (mean 52.0, range 16.1 - greater than 250 pg/ml). Intensive combination chemotherapy produced objective tumor responses in all patients, and syndrome of inappropriate ADH secretion (SIADH) resolved in 16 of 17 evaluable patients within three weeks of initiation of treatment. ADH values after therapy were normal, and all patients maintained a normal serum sodium during the period of tumor remission in spite of unrestricted fluid intake. All 17 evaluable patients have developed progressive cancer, but only 10 have manifested recurrent SIADH. Patient survival was similar to the overall population of small cell carcinoma patients without SIADH. The indirect methods of treatment for SIADH (fluid restriction, demeclocycline, lithium, urea) are frequently of transient value while awaiting a response to chemotherapy or in patients with resistant tumors. However, the initial treatment of choice for SIADH associated with small cell carcinoma of the lung is combination chemotherapy.

Topics: Adult; Aged; Antineoplastic Agents; Carcinoma, Small Cell; Drug Therapy, Combination; Female; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Middle Aged; Paraneoplastic Endocrine Syndromes; Recurrence; Retrospective Studies; Sodium; Uric Acid; Vasopressins

We report a patient who had an oat cell bronchogenic carcinoma in association with the syndrome of inappropriate antidiuresis. There was an unusually long interval between the onset of hyponatraemia and clinically evident malignant disease. Dynamic testing of vasopressin secretion showed preservation of baroregulated, but not osmoregulated, vasopressin release. Immunoreactive vasopressin was detected in pleural fluid, which co-eluted with synthetic vasopressin on gel chromatography.

Topics: Carcinoma, Bronchogenic; Carcinoma, Small Cell; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Middle Aged; Vasopressins

At diagnosis, 65% of 103 patients with small cell carcinoma of the lung were found to have elevated plasma concentrations of vasopressin-associated human neurophysin (VP-HNP), oxytocin-associated human neurophysin (OT-HNP), or both, which were thought to be related to tumor secretion of these proteins. The remainder of patients were designated as nonsecretors (24%) or possible secretors (11%), depending upon plasma concentration of the neurophysins prior to therapy. There was a significantly higher percentage of secretors among patients with extensive disease (82%) than among those with limited disease (40%) (P = 0.001). However, within each stage group, there was no correlation between secretory status and response to therapy, survival, or histologic subtype. In addition, patients who initially were nonsecretors or possible secretors maintained this status throughout the course of disease remission and subsequent relapse. These findings suggest the possibility of biochemical differences between tumors which present as limited disease and those which present as extensive disease. The syndrome of inappropriate antidiuretic hormone secretion (SIADH) was infrequent in limited disease but was present in 33% of patients with extensive disease. SIADH was not seen without VP-HNP elevation; however, with extensive disease, 49% of patients with elevated VP-HNP had SIADH. In contrast, elevated plasma concentrations of the neurophysins were seen in only 19.6% of 56 patients with non-small cell carcinoma of the lung. The levels were in general lower than those in patients with small cell carcinoma and were seen at approximately equal frequencies in each major cellular subtype.

Topics: Adenocarcinoma; Carcinoma, Small Cell; Carcinoma, Squamous Cell; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Neurophysins; Oxytocin; Prognosis; Vasopressins

The very rare occurrence of an ADH-producing small cell carcinoma of the lung in a 52 year old male patient with cranial diabetes insipidus since childhood is described. In this case diabetes insipidus disappeared concomitantly with development of lung cancer and re-appeared with shrinkage of the lung tumour by radiation therapy. Further progressive expansion of the primary and metastatic tumours induced the syndrome of inappropriate ADH secretion once again (SIADH). This deterioration in the clinical course was reflected in the plasma levels of ADH and neurophysins. The existence of vasopressin in the tumour tissue was also demonstrated by means of an immunohistochemical staining technique combined with anti-vasopressin serum.

Topics: Carcinoma, Small Cell; Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Middle Aged; Neurophysins; Remission, Spontaneous; Vasopressins

Transplantable human oat cell carcinoma cells of the lung with ectopic vasopressin production were incubated with labeled amino acids and immunoreactive neurophysins in cell extracts were analyzed by isoelectric focusing. When the cells were incubated with L-(35S)-cysteine for 20 h, one major peak (isoelectric point; pI=5.3) and several minor peaks (pI=6.1, 5.7, 5.1, 4.9 and 4.7) of labeled proteins were observed. On sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the relative molecular mass (Mr) of the pI 5.7 protein was estimated to be 20,000 and that of the pI 6.1 species to be 19,000, while the remainder had a Mr of approximately 10,000. The result of the pulse-labeling experiment has clearly shown that the pI 5.7 and 6.1 proteins, which have affinity for concanavalin A, are biosynthetic precursors for the smaller form of neurophysin with a pI 5.3. When subjected to limited proteolysis with trypsin, the pI 5.7 protein generated a Mr 10,000 protein and a smaller peptide. The Mr 10,000 protein thus produced was identified as neurophysin on the basis of its pH-dependent affinity for vasopressin and the migration pattern on isoelectric focusing. The smaller peptide coeluted with synthetic arginine vasopressin and bound to neurophysin suggesting that it possesses a cysteine-tyrosyl sequence at its N-terminus. Similarly, the pI 6.1 protein liberated neurophysin and vasopressin-like peptide after incubation with trypsin. These results suggests that the glycosylated protein with a pI of 5.7 and a Mr of 20,000 is the common precursor to vasopressin and neurophysin in human oat cell carcinoma of the lung with ectopic vasopressin production. The pI 6.1 protein may be an intermediate in the conversion of the precursor to vasopressin and neurophysin.

Topics: Carcinoma, Small Cell; Cysteine; Hormones, Ectopic; Humans; In Vitro Techniques; Inappropriate ADH Syndrome; Isoelectric Focusing; Lung Neoplasms; Male; Middle Aged; Molecular Weight; Neurophysins; Vasopressins

A case of tuberculous Addison's disease presenting with psychosis, profound hyponatraemia, and detectable plasma antidiuretic hormone is reported. Clinical and biochemical improvement after corticosteroid replacement was followed by relapse with further psychosis and inappropriate antidiuretic hormone secretion: both were promptly reversed by demethylchlortetracycline. The association of psychological symptoms with Addison's disease, the role of anti-diuretic hormone secretion in Addison's disease, and the inter-relationship between Addison's disease, psychosis and anti-diuretic hormone secretion are discussed.

Topics: Addison Disease; Body Weight; Demeclocycline; Fludrocortisone; Humans; Hydrocortisone; Inappropriate ADH Syndrome; Male; Middle Aged; Psychotic Disorders; Vasopressins; Water Intoxication

Topics: Adult; Aged; Arginine Vasopressin; Body Water; Female; Furosemide; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Prostaglandins E; Vasopressins

Topics: Adolescent; Aged; Diuresis; Ethacrynic Acid; Female; Furosemide; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Potassium; Sodium; Sodium Chloride; Urea; Vasopressins; Water Deprivation

ADH imbalance may occur in patients after pituitary surgery. Two cases are presented that demonstrate the problems associated with the disturbance of water metabolism. The medical management of these patients is discussed, with emphasis on the importance of the correct choice of pharmacological agents to control the manifestations of ADH imbalance.

Topics: Aged; Carbamazepine; Chlorpropamide; Clofibrate; Diuretics; Female; Fluid Therapy; Humans; Hypophysectomy; Inappropriate ADH Syndrome; Male; Pituitary Gland; Postoperative Complications; Time Factors; Vasopressins; Water-Electrolyte Balance

Topics: Humans; Hyponatremia; Hypotension, Orthostatic; Inappropriate ADH Syndrome; Infusions, Parenteral; Osmolar Concentration; Rocky Mountain Spotted Fever; Sodium Chloride; Vasopressins

A patient with a four-year history of unexplained hyponatremia was seen with recurrent nasal discharge and was found to have a typical olfactory neuroblastoma. The clinical laboratory diagnostic studies suggested that the patient's sodium deficiency was secondary to the syndrome of inappropriate antidiuretic hormone. Subsequent resection of the neoplasm led to resolution of the hyponatremia, suggesting that a (tumor-associated) humoral factor, such as vasopressin or a vasopressinlike substance, was responsible for the electrolyte disturbance. A search of the literature disclosed one previous case of vasopressin-secreting nasal neuroblastoma.

Topics: Adult; Female; Hormones, Ectopic; Humans; Hyponatremia; Inappropriate ADH Syndrome; Neuroectodermal Tumors, Primitive, Peripheral; Nose Neoplasms; Vasopressins

Topics: Child; Child, Preschool; Female; Humans; Inappropriate ADH Syndrome; Infant; Male; Meningoencephalitis; Sodium; Vasopressins

The syndrome of inappropriate antidiuretic hormone secretion (SIADH) as a cause of hypotonic hyponatremia is well recognized. The syndrome is commonly associated with cranial and thoracic infectious disease or malignancy. An idiopathic form of the syndrome has been reported, but poorly documented. Our patient, an 88-year-old man without any associated disease, had SIADH confirmed by a standard water load test. The pattern of antidiuretic hormone release corresponded to the "vasopressin leak" pattern. A review of ten cases of "idiopathic" SIADH showed that each of these cases has been associated with neuropsychiatric or other medical disturbances. We conclude that idiopathic inappropriate antidiuresis does exist and is a discrete category of SIADH. Data suggest that advanced age may be a risk factor for this disease. This syndrome may account for the increased susceptibility to hyponatremia among older patients.

Topics: Adolescent; Aged; Child, Preschool; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Mental Disorders; Middle Aged; Osmolar Concentration; Vasopressins

The endocrine status of 106 patients with undifferentiated small cell carcinoma of the lung was evaluated before treatment was begun. Almost one half of the patients had evidence of abnormal control of the secretion of adrenal cortical steroids, manifested by loss of diurnal rhythmicity or dexamethasone suppressibility. Only two had the clinical syndrome of ectopic ACTH secretion. Evidence of inappropriate secretion of vasopressin was found in 38% of the patients, most of whom also had abnormalities of corticosteroid secretory pattern. About one half of the patients had evidence of abnormal glucose tolerance, and many also had a paradoxical rise of plasma growth hormone concentration after glucose administration. The levels of the other hormones studies were normal. The pattern of hormone abnormality observed in these patients appears to be relatively specific for small cell undifferentiated carcinoma, and is different from that observed in other pulmonary tumors. Patients with abnormal control of plasma cortisol had a worse prognosis than those with normal adrenal function, largely because of decreased response rates to chemotherapy. Other endocrine abnormalities were of no prognostic significance.

Topics: 11-Hydroxycorticosteroids; Adrenal Cortex; Adrenocorticotropic Hormone; Blood Glucose; Carcinoma, Small Cell; Cyclophosphamide; Female; Humans; Hydrocortisone; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Methotrexate; Middle Aged; Prognosis; Sodium; Vasopressins

Two cases of Schwartz-Bartter syndrome are reported. Both were due to malignant anaplasic tumours of the APUD type with multiple abnormal endocrine secretion, and both were accompanied with hypouricaemia of uncertain significance. The authors believe that the association of hypernatraemia with hypouricaemia should alert clinicians to the possibility of a syndrome of inappropriate antidiuretic hormone secretion (SIADH) of malignant origin.

Topics: Apudoma; Carcinoma, Small Cell; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Uric Acid; Vasopressins

Topics: Drinking; Humans; Inappropriate ADH Syndrome; Vasopressins

Topics: Acute Disease; Albuterol; Asthma; Female; Humans; Inappropriate ADH Syndrome; Middle Aged; Vasopressins

Topics: Arginine Vasopressin; Body Water; Chlorpropamide; Deamino Arginine Vasopressin; Diabetes Complications; Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Polyuria; Time Factors; Vasopressins

A 45-year-old woman with myxedema coma due to primary hypothyroidism manifested hyponatremia, impaired water excretion, and elevated urine osmolarity as well as natriuresis suggestive of a syndrome of inappropriate antidiuretic hormone secretion. However, plasma vasopressin was undetectable or very low and plasma aldosterone levels were suppressed in the presence of hyponatremia. Subsequent replacement therapy with levothyroxine caused a rapid decline in sodium clearance which was independent of the change in glomerular filtration rate, and corrected the impaired water excretion and hyponatremia. Plasma vasopressin levels returned to the normal range after the correction of hyponatremia. Thus, the results indicate that neither vasopressin nor aldosterone plays a dominant role in the pathogenesis of the hyponatremia in this patient. It appears that thyroid hormone deficiency itself caused the derangement of tubular cell function, which resulted in the development of the impaired water excretion and hyponatremia.

Topics: Coma; Female; Glomerular Filtration Rate; Humans; Hyponatremia; Hypothyroidism; Inappropriate ADH Syndrome; Middle Aged; Myxedema; Osmolar Concentration; Sodium; Thyroxine; Vasopressins

Various clinical disorders of water and electrolytes metabolism were reported in relation to decrease or increase of the plasma anti-diuretic hormone (ADH), however, the estimated ADH value was not infrequently found inconsistent with clinical features. In order to determine the influence from surgical intervention to the hypophyseo-hypothalamic system, continuous estimation of the urinary secretion and specific gravity was performed with computerized analyzer, and it was found that there were at least 5 patterns of postoperative change in rhythmicity of ADH secretion. Most interesting finding was that the ADH was discharged in phasic pattern and irregularly intermingled oligo- and polyuric phases were observed quite in early stage of postoperative observation. Forty cases were examined and this method of examination was found useful in the prognostic view point for the postoperative water and electrolytes disorders.

Topics: Adenoma; Circadian Rhythm; Humans; Hydrocortisone; Hypophysectomy; Hypothalamus; Inappropriate ADH Syndrome; Pituitary Neoplasms; Postoperative Period; Vasopressins

Topics: Adult; Ethanol; Female; Humans; Inappropriate ADH Syndrome; Pituitary Gland; Pregnancy; Pregnancy Complications; Tuberculosis, Meningeal; Vasopressins

A 58-year-old man with bronchogenic oat cell carcinoma developed a typical syndrome of inappropriate secretion of antidiuretic hormone. The tumor tissue obtained at autopsy had been serially transplanted in nude mice for more than four years with 20 passages. The levels of vasopressin were remarkably increased in the plasma of nude mice bearing this tumor [24.4 +/- 18.3 (S.D.) pg/ml, n = 3] as well as in the tumor tissues ]134.3 +/- 72.2 ng/g, n = 3]. Furthermore, human nicotine-stimulated neurophysin was detected in both plasma and tumor tissues (7.4 +/- 3.7 ng/ml, n = 3, and 2.28 +/- 0.90 micrograms/g, n = 3, respectively). On ad libitum intake of water, nude mice bearing this tumor excreted significantly less urine with higher sodium concentration than did controls, but serum sodium concentrations did not differ from those of controls. When tumor-bearing mice were hydrated with 2 ml of water twice a day i.p., their diuretic response was found to be suppressed in parallel with the tumor size. However, these mice did not become hyponatremic because they drank less water. When a larger amount of water was loaded which could not be compensated by restriction of water drinking, serum sodium concentrations were markedly decreased. On the basis of these results, the lung cancer, when transplanted into nude mice, produced and secreted its own antidiuretic hormone, which induced inappropriate secretion of antidiuretic hormone in the mice. These mice may provide a useful experimental model for the study of excessive secretion of antidiuretic hormone and associated pathophysiological disorders.

Topics: Animals; Carcinoma, Bronchogenic; Carcinoma, Small Cell; Drinking; Female; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Mice; Mice, Nude; Middle Aged; Natriuresis; Neoplasm Transplantation; Sodium; Transplantation, Heterologous; Vasopressins

Hypouricaemia has been observed in patients with the syndrome of inappropriate secretion of antidiuretic hormone (IADH). Accordingly, 69 patients with untreated bronchogenic small cell carcinoma were examined for IADH. Serum urate was also measured. IADH was proven in 25 (35%) of the 69 patients. The median serum concentration of urate in these patients was 0.26 mmol/l (range 0.13-0.50), compared to 0.36 mmol/l (0.21-0.60) in the 44 patients without IADH. The difference is statistically significant (p less than 0.01), but serum urate--when used alone--is lacking in both sensitivity and specificity for the diagnosis of IADH.

Topics: Carcinoma, Bronchogenic; Carcinoma, Small Cell; Female; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Uric Acid; Vasopressins

Topics: ACTH Syndrome, Ectopic; Adrenocorticotropic Hormone; Aged; Carcinoma, Small Cell; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Paraneoplastic Endocrine Syndromes; Vasopressins

Topics: Aged; Carbamazepine; Demeclocycline; Female; Glucocorticoids; Humans; Inappropriate ADH Syndrome; Lung Diseases; Lung Neoplasms; Male; Phenytoin; Vasopressins

The role of antidiuretic hormone in maintaining normal water balance is review. The diagnosis of inappropriate secretion of antidiuretic hormone is done when a patient presents hyponatremia with no evidence of volume depletion, urine osmolality that is inappropriately high for serum tonicity, and absence of intrinsic renal or adrenal disease. Among the various possible etiology, the most frequent corresponds to disorders of the central nervous system, particularly bacterial meningitis. The various methods of treatment, fluid restriction, Hantman method and lithium salts are discussed.

Topics: Child; Furosemide; Hormones, Ectopic; Humans; Hypothalamus; Inappropriate ADH Syndrome; Lithium; Lithium Carbonate; Vasopressins; Water-Electrolyte Balance

We studied 29 patients with malignant hypertension and 28 patients with the syndrome of inappropriate antidiuretic hormone secretion to assess the relation of plasma vasopressin to blood pressure in states of acute and chronic vasopressin excess. In the patients with malignant hypertension, vasopressin levels were elevated (13 +/- 2 pg per milliliter. [+/- S.E.M.]) but did not correlate with arterial pressure; however, in normal volunteers, blood pressure did not rise when vasopressin was increased beyond these levels through infusion of the peptide. In the patients with inappropriate antidiuretic hormone secretion, blood pressure was not elevated, but vasopressin was raised (39 +/- 7 pg per milliliter) and did not correlate with systolic or diastolic pressure. These data do not support the concept that an acute or chronic excess of vasopressin makes an important contribution to the regulation of blood pressure.

Topics: Adult; Blood Pressure; Female; Humans; Hypertension, Malignant; Inappropriate ADH Syndrome; Male; Middle Aged; Vasopressins

Topics: Adrenal Insufficiency; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Vasopressins

Serum osmolality and antidiuretic hormone (ADH) levels were determined for 17 patients with cerebral infarction, 4 with subarachnoid hemorrhage, and 12 controls. The ADH levels were elevated significantly in the stroke patients. Hyponatremia was not observed. Stroke patients are at risk for developing electrolyte disturbances; thus, fluid intake and electrolyte levels should be closely observed.

Topics: Cerebral Infarction; Humans; Inappropriate ADH Syndrome; Subarachnoid Hemorrhage; Vasopressins; Water-Electrolyte Imbalance

Topics: Hormones, Ectopic; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Oxytocin; Pharyngeal Neoplasms; Sarcoma; Vasopressins

Topics: Arginine Vasopressin; Body Water; Deamino Arginine Vasopressin; Diabetes Insipidus; Humans; Hypernatremia; Hypoglycemia; Hyponatremia; Inappropriate ADH Syndrome; Pharmacology; Radioimmunoassay; Vasopressins; Water-Electrolyte Imbalance

Topics: Animals; Body Fluids; Dendrites; Diabetes Insipidus; Haplorhini; Hypothalamus; Inappropriate ADH Syndrome; Macaca mulatta; Osmolar Concentration; Sensory Receptor Cells; Vasopressins; Water-Electrolyte Balance

Topics: Demeclocycline; Female; Humans; Hyponatremia; Hypothyroidism; Inappropriate ADH Syndrome; Middle Aged; Vasopressins; Water-Electrolyte Imbalance

Topics: Humans; Hypothalamus; Inappropriate ADH Syndrome; Pituitary Gland; Vasopressins

Topics: Humans; Hyponatremia; Inappropriate ADH Syndrome; Urea; Vasopressins

Topics: Anuria; Diabetes Insipidus; Edema; Humans; Inappropriate ADH Syndrome; Oliguria; Syndrome; Vasopressins; Water-Electrolyte Balance

A 20-year-old patient was evaluated because of polydipsia and polyuria; by means of the dehydration test a partial defect in the secretion of antidiuretic hormone (ADH) was demonstrated, since the urinary osmolality after the administration of exogenous vasopressin was superior by 25 percent to the maximum spontaneous urinary osmolality reached after a period of fluid restriction. Nevertheless, there was also a component of psychogenic polydipsia because the daily basal fluid intake was superior to 15 liters, and in view of the fact that the urinary osmolality could reach 600 mOsm/kg, the endocrine defect cannot totally be responsible for the enormous volume of fluid intake. This is the first case in the world literature in which the association between potomania and deficiency in the secretion of ADH is reported. Since ADH is one of the factors which regulate the behaviour of various animal species it is possible that its deficiency may be directly responsible for the psychic disorder which led to the potomania. It is also possible that an anatomical hypothalamic lesion, too small to be demonstrated, might have a simultaneous effect on the centers regulating thirst and the neurons producing vasopressin.

Topics: Adult; Clofibrate; Female; Humans; Inappropriate ADH Syndrome; Osmolar Concentration; Polyuria; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Adult; Aged; Diuretics; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Sodium; Sodium Chloride; Vasopressins; Water-Electrolyte Balance

A radioimmunoassay of ADH has been applied to the study of plasma ADH levels in various conditions. The validity of the assay has been evaluated by the usual quality control parameters of RIA and by the measure of plasma levels in 12 upright water deprived normal volunteers (mean 9.5 pg/ml, SEM +/- 1.5) in 8 resting and hydrated normal volunteers (1.3 +/- 0.4 pg/ml), in a case of diabetes insipidus (1.6 pg/ml), in 8 cases of SIADH Syndrome (range 13-77 pg/ml) and in 4 anesthetized dogs before (33.7 +/- 9.2 pg/ml) and after acute haemorrhage (66 +/- 9.5 pg/ml, p less than 0.02). The osmotoic challenge to ADH secretion has been studied in 8 patients with no overt endocrine pathology by salt perfusion and showed a significant rise (p less than 0.05) of plasma ADH from 6.3 +/- 3.1 pg/ml before, to 20.6 +/- 7.9 pg/ml during salt infusion corresponding to the significant (p less than 0.0001) rise of plasma osmolality from 273 +/- 2.8 to 288.2 +/- 1.1 m Osm/kg.

Topics: Animals; Dehydration; Diabetes Insipidus; Dogs; Hemorrhage; Humans; Inappropriate ADH Syndrome; Osmolar Concentration; Radioimmunoassay; Saline Solution, Hypertonic; Vasopressins

Forty-one patients with newly diagnosed small cell anaplastic lung cancer were evaluated for abnormalities in water homeostasis. Each patient underwent a standard water load (SWL) test. Overall, 68% had abnormalities in the SWL test. Abnormalities were found in 47% of the patients with carcinoma clinically limited to one hemithorax and in 86% of the patients with more extensive carcinoma. The determination of urinary antidiuretic hormone levels was available for 27 patients. Abnormally elevated levels were found in 44% of those patients. Forty-six patients had clinically detectable syndrome of the inappropriate secretion of antidiuretic hormone (SIADH); in 12% of patients water restriction was necessary. The incidence of detectable abnormalities in water homeostasis in this study was higher than has been previously recognized. The SWL test is a sensitive and useful means of determining the presence of impaired water handling in patients with small cell carcinoma of the lung.

Topics: Blood Urea Nitrogen; Carcinoma; Carcinoma, Bronchogenic; Drug Therapy, Combination; Female; Homeostasis; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Methods; Vasopressins; Water; Water-Electrolyte Balance

The low serum concentration of ADH requires extraction prior to assay. Various methods are compared (direct extraction by acetone, adsorption on talcum powder. Florisil, silicilic acid, Fuller's earth, QUSO, carbon-dextran, adsormone, then elution with hydrochloric acetone). The technic finally used was extraction with Florisil. The antibody used was commercially accessible. The separation of bound from free hormone required a second antibody fixed on Sephadex (DASP). The usual values found in 31 normal subjects from 22 to 89 years were: 7,4 . 4,1 pmol/l (M 2 sigma) 1 pmol/l = 1,08 pg/ml. These assays were carried out on tissue extracts prepared by mashing tumour fragments or lymph nodes removed from a patient with the Schwartz Bartter syndrome. They showed the existence in these tissues of high concentrations of ADH immunologically identical with that present in the serum of normal subjects.

Topics: Adsorption; Adult; Aged; Humans; Inappropriate ADH Syndrome; Methods; Middle Aged; Radioimmunoassay; Reference Values; Vasopressins

A double paraneoplasic syndrome with hypersecretion of ADH and ACTH revealed the presence of a small cell bronchial cancer in a man aged 62 years. Water and electrolyte anomalies due to the hypersecretions were of such a degree that an occlusive syndrome occurred. Very high levels of ADH and ACTH were found in the tumoral tissue. The measurement of these levels is rarely conducted at the present time but was able to define the mechanism of abnormal secretion of these two hormones in this case.

Topics: Adrenocortical Hyperfunction; Adrenocorticotropic Hormone; APUD Cells; Carcinoma; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Middle Aged; Paraneoplastic Syndromes; Vasopressins; Water-Electrolyte Imbalance

Known physiologic mechanisms explain the elevated blood ADH levels observed in most patients with the syndrome of inappropriate ADH. Therefore the word "inappropriate" is a misnomer. It implies that the mechanisms that regulate ADH release are not functioning normally--which is not true. The term misleads the physician who, ideally, should determine why a patient has an excessive blood ADH level and initiate appropriate treatment. Patients with ectopic production of ADH and hyponatremia should be so labeled: "Hyponatremia due to ectopic ADH production." The term SIADH, if used at all, should be reserved for the rare patient with CNS injury or disease that causes increased ADH release and in which the hypothalamic center does not respond normally to afferent peripheral stimuli.

Topics: Blood; Demeclocycline; Furosemide; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lithium; Osmolar Concentration; Pressoreceptors; Saline Solution, Hypertonic; Vasopressins

The hypothalamic-neurohypophyseal system functions to maintain plasma osmolality within narrow limits. It also is an important mechanism in maintaining normal body fluid volume. The system exerts its influence via release or inhibition of vasopressin (antidiuretic hormone, ADH) which acts on the kidney to decrease water excretion. Deficiency of ADH is usually due to hypothalamic-neurohypophyseal lesions (central diabetes insipidus) or insensitivity of the kidney to ADH (nephrogenic diabetes insipidus). These patients, if untreated, have the predictable result of dehydration, hyperosmolality, hypovolemia, and eventual death in severe cases. On the other hand, ADH excess of the syndrome of inappropriate ADH secretion due to a variety of causes promotes water retention, hypoosmolality and hyponatremia which, if untreated, may progress to convulsions, coma, and death. It is obviously important to diagnose accurately these pathologic states of hydration. Not only is initiation of treatment in general dependent upon recognition of the disease, but each type of pathologic hydration state has specific treatment which rewards both patient and physician with effective correction of the problem.

Topics: Demeclocycline; Diabetes Insipidus; Humans; Inappropriate ADH Syndrome; Kidney; Pituitary Gland, Posterior; Vasopressins

One the basis of two special typical cases, the authors detail the symptoms and signs and consider the physiopathology of inappropriate secretion of antidiuretic hormone related to vincristine. Urinary ADH was measured in both cases. ADH levels could be studied on ten consecutive occasions during the course of one of the cases (obs. n 1). Eleven similar cases have been found in the literature. ADH was measured in only three of them. Methods of treatment are considered, with particular emphasis on the role of demeclocycline.

Topics: Child; Demeclocycline; Humans; Inappropriate ADH Syndrome; Leukemia, Lymphoid; Vasopressins; Vincristine

A 72-year-old woman with the syndrome of inappropriate secretion of antidiuretic hormone of unknown cause during more than one year of observation is reported. Plasma vasopressin levels were excessively elevated, even during a water load test. Her serum electrolyte abnormalities and general state were ameliorated after fluid restriction. During treatment with demeclocycline the patient was able to increase fluid without deterioration.

Topics: Aged; Demeclocycline; Electrolytes; Female; Humans; Inappropriate ADH Syndrome; Osmolar Concentration; Vasopressins; Water

Topics: Aged; Demeclocycline; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Osmolar Concentration; Osmotic Pressure; Sodium; Vasopressins

Topics: Humans; Inappropriate ADH Syndrome; Vasopressins

Topics: Creatinine; Glomerular Filtration Rate; Growth Hormone; Humans; Inappropriate ADH Syndrome; Neurophysins; Pituitary Gland, Posterior; Postoperative Complications; Potassium; Sella Turcica; Sodium; Vasopressins; Water-Electrolyte Balance

Use of vasopressin injection (Pitressin) as an adjunct in the treatment of various types of gastrointestinal hemorrhage also produces an antidiuretic hormone effect of free water retention. This produces difficulties in fluid and electrolyte management and in the interpretation of changes in mental and hemodynamic status. This effect and its management are directly related to the total dose of the drug administered.

Topics: Gastrointestinal Hemorrhage; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Vasopressins

Topics: Child, Preschool; Face; Female; Humans; Hyponatremia; Hypothalamus; Inappropriate ADH Syndrome; Osmolar Concentration; Vasopressins

We have reviewed 14 cases of water intoxication in psychiatric patients. In these cases the possibility of the syndrome of inappropriate antidiuretic hormone secretion (SIADH) was suspected or diagnosed. The SIADH should be suspected in psychotic patients who drink water excessively, develop seizures, disorientation and deterioration of mental status.

Topics: Adult; Compulsive Behavior; Drinking; Female; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Neurocognitive Disorders; Psychotic Disorders; Psychotropic Drugs; Sodium; Vasopressins; Water Intoxication

Topics: Humans; Inappropriate ADH Syndrome; Infant; Male; Sodium; Vasopressins

Topics: Cognition Disorders; Consciousness Disorders; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Middle Aged; Osmolar Concentration; Vasopressins

Topics: Adult; Body Water; Diabetes Insipidus; Diuresis; Extracellular Space; Humans; Hypernatremia; Hyponatremia; Inappropriate ADH Syndrome; Intracellular Fluid; Kidney Concentrating Ability; Kidney Failure, Chronic; Osmolar Concentration; Sodium; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Topics: Humans; Inappropriate ADH Syndrome; Vasopressins; Water

Serum potassium concentration was normal (greater than or equal to 3.6 mmol/l) in 29 of 32 patients with the syndrome of inappropriate antidiuretic hormone excess (SIADH) associated with a bronchogenic carcinoma. In 11 of the patients there was no significant change in serum potassium concentration after correction of the syndrome, by fluid restriction. Hypokalaemia is thus an uncommon finding in SIADH due to bronchogenic carcinomas.

Topics: Aged; Carcinoma, Bronchogenic; Female; Humans; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Middle Aged; Osmolar Concentration; Potassium; Vasopressins

A patient with the syndrome of inappropriate antidiuretic hormone release (SIADH) following head injury and meningitis was studied during treatment with demeclocycline, a drug known to produce a reversible nephrogenic diabetes insipidus. No changes were observed during six days of demeclocycline 1200 mg/24 hr but urine output increased significantly, with the production of a dilute urine, when the dose was increased to 2400 mg/24 hr. The patient lost weight, and all biochemical features of the syndrome were rapidly corrected despite an unchanged fluid intake and despite the persistence of high plasma levels of ADH. The rise in serum sodium was accompanied by mild sodium retention, as measured by external balance and exchangeable sodium. A complication of treatment was the development of acute renal failure possibly induced by a nephrotoxic effect of high circulating levels of demeclocyline. On stopping demeclocyline renal function returned to normal and, after some delay, SIADH returned, and was still present 9 months after initial presentation. This confirms earlier reports of the efficacy of demeclocycline in SIADH; but the authors advise caution against increasing the dose above 1200 mg/24 hr.

Topics: Demeclocycline; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Sodium; Time Factors; Vasopressins

A systematic study has been undertaken to improve the understanding of water regulation in premature babies who are artificially ventilated. Thirty nine premature babies, 16 normal (Group N, GA 31.4 weeks, B/W 1622 g) and 23 with respiratory distress syndrome who were ventilated with or without continuous positive pressure (Group V, GA 31 weeks, BW 1505 g) have been studied. Plasma osmolalities were the same in both groups (284 and 282 mosM/Kg H2O) but there were significant differences (p less than 0.001) between the urine osmolalities N = 150.6 +/- 19.6 V = 294 +/- 25.9 mosM/Kg H2O) and the plasma ADH levels of the two groups (N = 2.9 +/- 0.4 pg/ml, V = 12.2 +/- 2.4 pg/ml). There was a significant correlation between the urine osmolality and the plasma ADH level but not between plasma osmolality and the plasma ADH level. Several hypotheses can be proposed but none are satisfactory.

Topics: Humans; Inappropriate ADH Syndrome; Infant, Newborn; Infant, Premature; Positive-Pressure Respiration; Respiratory Distress Syndrome, Newborn; Vasopressins

Topics: Adolescent; Adult; Aged; Animals; Diabetes Insipidus; Diuresis; Female; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Osmolar Concentration; Rats; Vasopressins; Water-Electrolyte Balance

The maintenance of osmolar constancy of the body fluids is dependent upon the recognition of osmolar disequilibrium and its correction by modifying the ingestion and excretion of fluid and solute. Osmolar changes are sensed by the hypothalamus which regulates the secretion of antidiuretic hormone to modify the renal excretion of water. The integrity of the system depends upon the renal ability to vary the solute concentration of urine.

Topics: Adult; Body Fluids; Diuresis; Humans; Inappropriate ADH Syndrome; Infant, Newborn; Kidney; Kidney Medulla; Osmolar Concentration; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Child; Craniopharyngioma; Female; Humans; Hyponatremia; Inappropriate ADH Syndrome; Infant; Male; Pituitary Neoplasms; Postoperative Care; Postoperative Complications; Sodium; Time Factors; Vasopressins; Water-Electrolyte Imbalance

Topics: Bronchopneumonia; Cerebrovascular Disorders; Humans; Inappropriate ADH Syndrome; Lithium; Male; Middle Aged; Vasopressins

Topics: Blood Proteins; Humans; Inappropriate ADH Syndrome; Porphyrias; Radioimmunoassay; Vasopressins

Topics: Brain Neoplasms; Breast Neoplasms; Diuresis; Female; Humans; Inappropriate ADH Syndrome; Neoplasms; Vasopressins

Topics: Arginine Vasopressin; Bronchial Neoplasms; Carcinoma, Bronchogenic; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lymphatic Metastasis; Natriuresis; Neoplasms; Physiology; Urine; Vasopressins

Topics: Craniocerebral Trauma; Diagnosis; Endocrine System Diseases; Humans; Hyponatremia; Inappropriate ADH Syndrome; Pathology; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Arginine Vasopressin; Carcinoma; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lung Neoplasms; Metabolism; Vasopressins; Water-Electrolyte Balance

Topics: Aldosterone; Brain Neoplasms; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lung Neoplasms; Natriuresis; Neoplasm Metastasis; Physiology; Vasopressins

Topics: Arginine Vasopressin; Clinical Laboratory Techniques; Encephalitis; Encephalitis, Herpes Simplex; Herpes Simplex; Humans; Hyponatremia; Inappropriate ADH Syndrome; Physiology; Vasopressins; Water-Electrolyte Balance