pituitrin and Cushing-Syndrome

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

Cushing's syndrome is a consequence of primary or, more commonly, secondary oversecretion of cortisol. Cardiovascular disease is the major cause of morbidity and mortality in Cushing's syndrome, and excess risk remains even in effectively treated patients. The cardiovascular consequences of cortisol excess are protean and include, inter alia, elevation of blood pressure, truncal obesity, hyperinsulinemia, hyperglycemia, insulin resistance, and dyslipidemia. This review analyses the relationship of cortisol excess, both locally and at tissue level, to these cardiovascular risk factors, and to putative mechanisms for hypertension. Previous studies have examined correlations between cortisol, blood pressure, and other parameters in the general population and in Cushing's syndrome. This review also details changes induced by short-term cortisol administration in normotensive healthy men.

Topics: Blood Pressure; Cardiac Output; Cardiovascular Diseases; Cushing Syndrome; Female; Humans; Hydrocortisone; Hyperglycemia; Hyperlipidemias; Hypertension; Insulin Resistance; Male; Obesity; Plasma Volume; Renin-Angiotensin System; Risk Factors; Sympathetic Nervous System; Vascular Resistance; Vasodilation; Vasopressins

AIMAH is a clinical condition characterized by the presence of adrenal macronodules even in the absence of ACTH. Usually the clinical overt syndrome only becomes apparent after several decades of life; this is probably due to the low steroidogenic enzyme capacity of the hyperplastic tissue. However, in asymptomatic individuals in whom the AIMAH was incidentally discovered, the HHA axis is usually disrupted. In the great majority of AIMAH cases, cortisol secretion is aberrantly regulated by hormones such as GIP, AVP, beta-adrenergic agonists, LH/hCG and in some cases by serotonin, acting through their specific receptors. The molecular mechanisms responsible by ectopic expression of such hormone receptors and/or their aberrant coupling to steroidogenesis are still largely unknown. Although this aberrant expression may have an important role in the augmented cell proliferation initiation, as well as in the steroidogenesis, it is probable that additional genetic events involving cell cycle regulation, adhesion and transcription occur. In rare cases GNAS1 mutations not related to McCune-Albright syndrome may be found in this condition. In some patients, the presence of aberrant hormone receptors creates the possibility of specific pharmacological treatment, isolated or associated with unilateral adrenalectomy.

Topics: Adrenal Glands; Adrenocorticotropic Hormone; Chromogranins; Cushing Syndrome; GTP-Binding Protein alpha Subunits, Gs; Humans; Hyperplasia; Mutation; Signal Transduction; Vasopressins

Multiple alterations of G-protein-coupled receptors and G-proteins regulating intracellular transduction signal have been described in endocrine tumours. In Cushing's syndrome, aberrant or 'illicit' expression of membrane receptors (mainly G-protein-coupled receptors) has been observed in adrenal adenomas and adrenocorticotropic hormone (ACTH)-independent macronodular bilateral adrenal hyperplasia. The best characterized example to date is the aberrant expression of the gastric inhibitory polypeptide receptor that causes 'food-dependent hypercortisolism'. Aberrant expression of the luteinizing hormone, 2-adrenergic, interleukin receptors have also been reported. The level of expression of the vasopressin V1a receptor correlates with the direct (ACTH-independent) cortisol response to vasopressin.

Topics: Animals; Cushing Syndrome; Gastric Inhibitory Polypeptide; Humans; Hydrocortisone; Receptors, Adrenergic, beta; Receptors, Cell Surface; Receptors, Gastrointestinal Hormone; Receptors, LH; Receptors, Serotonin; Receptors, Serotonin, 5-HT4; Receptors, Vasopressin; Vasopressins

Cushing's disease remains a difficult diagnosis in spite of new technical procedures such as pituitary MRI, selective bilateral petrosal or cavernous sampling, (111)In pentreotide scan and 18 Flurodeoxyglucose pituitary PET scan. In this article, we review biological diagnostic procedures of Cushing's disease and corticotroph adenomas. According to our experience and the literature, we summarize the approach in medical treatment of Cushing's disease.

Topics: ACTH Syndrome, Ectopic; Adenoma; Adrenal Cortex Neoplasms; Adrenocortical Hyperfunction; Adrenocorticotropic Hormone; Adult; Algorithms; Carcinoid Tumor; Child; Corticotropin-Releasing Hormone; Cushing Syndrome; Dexamethasone; Diagnosis, Differential; Diagnostic Imaging; Dopamine Agonists; Female; Humans; Hypothalamo-Hypophyseal System; Magnetic Resonance Imaging; Male; Petrosal Sinus Sampling; Pituitary Neoplasms; Pituitary-Adrenal Function Tests; Pituitary-Adrenal System; Pregnancy; Pregnancy Complications, Neoplastic; Vasopressins

The diagnosis of Cushing's syndrome remains one of the most challenging tasks in clinical neuroendocrinology. The diagnostic procedure can be divided into two distinct steps: diagnosis of the neuroendocrine disorder and differential diagnosis of the precise aetiology. The goal of the first laboratory tests is to obtain biochemical proof of Cushing's syndrome. Patients with Cushing's syndrome are relatively insensitive to glucocorticoid feedback and exhibit an oversecretion of cortisol devoid of a circadian cycle. In our experience, a low-dose dexamethasone suppression test provides the most reliable confirmation of steroid resistance, a cortisol level of<50 nmol/l at 9 a.m. having 98% sensitivity. A cortisol level below 50 nmol/l at midnight rules out active Cushing's syndrome with, in our experience, 100% sensitivity and a specificity depending on numerous other variables. A very high level of free urinary corticol can be a useful sign. After having established the diagnosis of Cushing's syndrome, a persistently low level of ACTH (<10 pg/ml), or preferentially an undetectable level unresponsive to CRH (100 microgram iv), is suggestive of an ACTH-independent disorder, and consequently of primary adrenal disease. The precise location of the lesion can identified with CT or MRI imaging, generally prior to surgical cure. If the ACTH level is detectable, patients with pituitary Cushing's syndrome, or Cushing's disease, should be differentiated from those with ectopic ACTH secretion. The secreting tumour may be difficult to localise and diagnosis is never 100% sure with dynamic tests. Catheterisation of the petrosal sinus with CRH stimulation provides the best sensitivity for differentiating the two aetiologies. We consider a central to peripheral gradient of>3 to confirm the pituitary origin of the disorder with a 98% sensitivity. Chest or abdominal CT can be helpful to identify an ectopic tumour but very small tumours may go undetected. MRI can detect 60 or 70% of all pituitary adenomas but is virtually non-contributive to the diagnosis of Cushing's disease in children.

Topics: Adenoma; Adrenocorticotropic Hormone; Corticotropin-Releasing Hormone; Cushing Syndrome; Dexamethasone; Diagnosis, Differential; Diagnostic Imaging; Humans; Petrosal Sinus Sampling; Pituitary Neoplasms; Vasopressins

There are few challenges to an endocrinologist's diagnostic acumen greater than the diagnosis of Cushing's disease. In this article, we will review the main pitfalls in the diagnosis of Cushing's disease and discuss the value of techniques of biochemical and radiological diagnosis.

Topics: Circadian Rhythm; Corticotropin-Releasing Hormone; Cushing Syndrome; Dexamethasone; Diagnosis, Differential; Humans; Hydrocortisone; Magnetic Resonance Imaging; Metyrapone; Vasopressins

Recent studies from several groups have indicated that abnormal or ectopic expression and function of adrenal receptors for various hormones may regulate cortisol production in ACTH-independent hypercortisolism. Gastric inhibitory polypeptide (GIP)-dependent Cushing's syndrome has been described in patients with either unilateral adenoma or bilateral macronodular adrenal hyperplasia; this syndrome results from the large adrenal overexpression of the GIP receptor without any activating mutation. We have conducted a systematic in vivo evaluation of patients with adrenal Cushing's syndrome in order to identify the presence of abnormal hormone receptors. In macronodular adrenal hyperplasia, we have identified, in addition to GIP-dependent Cushing's syndrome, other patients in whom cortisol production was regulated abnormally by vasopressin, ss-adrenergic receptor agonists, hCG/LH, or serotonin 5HT-4 receptor agonists. In patients with unilateral adrenal adenoma, the abnormal expression or function of GIP or vasopressin receptor has been found, but the presence of ectopic or abnormal hormone receptors appears to be less prevalent than in macronodular adrenal hyperplasia. The identification of the presence of an abnormal adrenal receptor offers the possibility of a new pharmacological approach to control hypercortisolism by suppressing the endogenous ligands or by using specific antagonists for the abnormal receptors.

Topics: Adrenocorticotropic Hormone; Catecholamines; Cushing Syndrome; Female; Gastric Inhibitory Polypeptide; Humans; Hydrocortisone; Male; Pregnancy; Receptors, Cell Surface; Vasopressins

Cushing's syndrome is defined as the symptoms and signs of glucocorticoid excess, but the precise diagnosis may be difficult to establish and harder to localise. The clinicial, biochemical and imaging features of the syndrome are discussed in the light of our own extensive experience and the published literature. We describe the optimal diagnostic routines currently recommended in major centres, and analyse the sensitivities and specialities of the various tests employed. Only by means of establishing a precise diagnosis can the disorder be successfully treated.

Topics: Adrenocorticotropic Hormone; Corticotropin-Releasing Hormone; Cushing Syndrome; Dexamethasone; Diagnosis, Differential; Diagnostic Imaging; Humans; Hydrocortisone; Vasopressins

Topics: ACTH Syndrome, Ectopic; Adrenocorticotropic Hormone; Anti-Inflammatory Agents; Circadian Rhythm; Corticotropin-Releasing Hormone; Cushing Syndrome; Deamino Arginine Vasopressin; Dexamethasone; Diagnosis, Differential; Female; Growth Substances; Humans; Hydrocortisone; Magnetic Resonance Imaging; Male; Metyrapone; Oligopeptides; Petrosal Sinus Sampling; Renal Agents; Tomography, X-Ray Computed; Vasopressins

Topics: Acromegaly; Adrenocorticotropic Hormone; Animals; Blood Glucose; Calcitonin; Carcinoma, Small Cell; Cell Transformation, Neoplastic; Chorionic Gonadotropin; Corticotropin-Releasing Hormone; Cushing Syndrome; Dexamethasone; Female; Galactorrhea; Gene Expression Regulation; Growth Hormone; Humans; Hypercalcemia; Lymphokines; Nerve Tissue Proteins; Paraneoplastic Endocrine Syndromes; Parathyroid Hormone; Peptide Biosynthesis; Pregnancy; Pro-Opiomelanocortin; Prolactin; Prostaglandins; Transforming Growth Factors; Vasopressins; Vitamin D

The 41-amino acid CRF fulfils all the criteria for a corticotrophin releasing factor, although considerable evidence suggests that other factors, particularly VP, also play a physiologically significant role in controlling ACTH release. Although human CRF has now been identified as a 41-residue peptide, most studies to date have used oCRF-41 in their exploration of the physiology and pathology of the hypothalamic--pituitary--adrenal axis. Low doses of oCRF-41 appear to be safe, and for specific tests of the readily-releasable pool of ACTH and related peptides 100 micrograms is a practical dose for most purposes. Although serious side-effects have only been noted at doses above 100 micrograms, it is reasonable to monitor all patients administered CRF-41 with great care, and in particular to be alert to hypotension, especially in patients with corticosteroid deficiency. There is little doubt that, in combination with the standard insulin-tolerance test, the CRF test is a useful means of diagnosing hypothalamic or portal dysfunction in patients with secondary adrenal failure. However, in the diagnosis and differential diagnosis of Cushing's syndrome, the role of the CRF test remains unclear. In normal subjects, a high basal cortisol level usually inhibits the response to CRF, such that a greatly enhanced response is suggestive of pituitary-dependent Cushing's syndrome. In patients with diagnosed ACTH-dependent Cushing's syndrome, an absent response to CRF predisposes towards an ectopic source of ACTH. However, there are exceptions in all directions, and it is uncertain whether the CRF test will prove of greater value than the traditional procedures, such as the dexamethasone suppression test. The differential diagnosis of depression and Cushing's disease may be its greatest value. In terms of treatment, there are as yet few data on the usefulness of CRF in expediting recovery of the pituitary-adrenal axis following long-term suppression, such as in patients with Cushing's syndrome treated by removal of a unilateral adenoma or trans-sphenoidal microadenomectomy. It is possible that such treatment may eventually be a useful application of CRF, although data are not yet available.

Topics: Acetylcholine; Acromegaly; Adrenocorticotropic Hormone; Animals; Circadian Rhythm; Corticotropin-Releasing Hormone; Cushing Syndrome; Depressive Disorder; Diagnosis, Differential; Growth Hormone; Humans; Hypothalamo-Hypophyseal System; Immunologic Techniques; Kinetics; Models, Biological; Pituitary-Adrenal System; Stress, Physiological; Vasopressins

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; Chorionic Gonadotropin; Cushing Syndrome; Erythropoietin; Gastrointestinal Hormones; Hormones, Ectopic; Hypercalcemia; Hypoglycemia; Hyponatremia; Melanocyte-Stimulating Hormones; Neurologic Manifestations; Paraneoplastic Endocrine Syndromes; Parathyroid Hormone; Polycythemia; Prostaglandins E; Somatomedins; Vasopressins

A variety of cells found in the pituitary and pineal glands, sympathetic nervous system and adrenal glands, the gut, pancreas, thyroid (C-cells), chemoreceptors (type I-Cells), lungs (P-cells), skin (melanocytes) and the urogenital tract have a common origin from the neural crest. These cells are programmed for neuro-endocrine function and, as a group, can be regarded as one of the physiological control systems. They secrete a variety of amine and peptide hormones and have common cytochemical characteristics from which the term APUD cell is derived. Tumours of these cells are referred to as 'apudomas' and may synthesise not only their own hormones but also those which are normally produced by other APUD cells. The relevant physiological properties of some of the peptides which have been described relatively recently are discussed and the principal clinical syndromes produced by the APUDomas are described.

Topics: Adenoma, Islet Cell; APUD Cells; Apudoma; Cushing Syndrome; Endocrine System Diseases; Gastrointestinal Neoplasms; Hormones; Humans; Malignant Carcinoid Syndrome; Neoplasms, Nerve Tissue; Pancreatic Neoplasms; Paraneoplastic Endocrine Syndromes; Pheochromocytoma; Pituitary Neoplasms; Thyroid Neoplasms; Vasopressins; Zollinger-Ellison Syndrome

Topics: Adenocarcinoma; Adrenocorticotropic Hormone; Adult; Carcinoma; Carcinoma, Bronchogenic; Carcinoma, Small Cell; Carcinoma, Squamous Cell; Chorionic Gonadotropin; Cushing Syndrome; Dexamethasone; Gynecomastia; Humans; Hypercalcemia; Lomustine; Lung Neoplasms; Male; Mechlorethamine; Neoplasm Metastasis; Neostigmine; Parathyroid Hormone; Smoking; Vasopressins; Water-Electrolyte Balance

Topics: Adrenocortical Hyperfunction; Adult; Carcinoid Heart Disease; Cushing Syndrome; Endocrine System Diseases; Gynecomastia; Humans; Hypercalcemia; Hyperparathyroidism; Hyperthyroidism; Hyponatremia; Lung Neoplasms; Male; Middle Aged; Osmolar Concentration; Osteoarthropathy, Secondary Hypertrophic; Syndrome; Vasopressins

Topics: Adenocarcinoma; Adrenocorticotropic Hormone; Arginine; Biliary Tract Diseases; Bronchial Neoplasms; Carcinoma; Chorionic Gonadotropin; Colonic Neoplasms; Cushing Syndrome; Erythropoietin; Female; Follicle Stimulating Hormone; Growth Hormone; Gynecomastia; Hormones, Ectopic; Humans; Hypercalcemia; Lactation Disorders; Lung Neoplasms; Luteinizing Hormone; Models, Biological; Neoplasms; Paraganglioma; Paraneoplastic Endocrine Syndromes; Polycythemia; Pregnancy; Prolactin; Thyroid Neoplasms; Vasopressins

Topics: Adrenal Gland Diseases; Adrenal Glands; Adrenalectomy; Cushing Syndrome; Dexamethasone; Diagnosis, Differential; Humans; Hydrocortisone; Hyperaldosteronism; Hypertension; Hypokalemia; Kidney; Obesity; Pituitary-Adrenal Function Tests; Pituitary-Adrenal System; Vasopressins

Topics: Adolescent; Bronchial Neoplasms; Carcinoma, Small Cell; Child, Preschool; Cushing Syndrome; Diagnosis, Differential; Hormones, Ectopic; Humans; Hyperaldosteronism; Hypercalcemia; Hyperparathyroidism; Hyponatremia; Kidney Neoplasms; Paraneoplastic Endocrine Syndromes; Renin; Sodium Chloride; Syndrome; Vasopressins

Topics: Adrenocorticotropic Hormone; Bronchial Neoplasms; Carcinoid Tumor; Cushing Syndrome; Endocrine System Diseases; Female; Gonadotropins; Hormones, Ectopic; Humans; Islets of Langerhans; Male; Neoplasms; Parathyroid Hormone; Thymus Neoplasms; Thyroid Neoplasms; Vasopressins

Topics: 5-Hydroxytryptophan; Acanthosis Nigricans; Carcinoid Tumor; Carotid Body Tumor; Catecholamines; Cushing Syndrome; Dermatomyositis; Endocrine System Diseases; Gynecomastia; Hormones, Ectopic; Humans; Hypercalcemia; Hyperthyroidism; Hypoglycemia; Hyponatremia; Neoplasms; Neuromuscular Diseases; Osteoarthropathy, Secondary Hypertrophic; Peripheral Nervous System Diseases; Polycythemia; Puberty, Precocious; Syndrome; Toxins, Biological; Vascular Diseases; Vasopressins; Zollinger-Ellison Syndrome

Topics: Addison Disease; Adrenocorticotropic Hormone; Biological Assay; Blood Chemical Analysis; Circadian Rhythm; Cushing Syndrome; Hormones, Ectopic; Humans; Hyperplasia; Hypopituitarism; Insulin; Lysine; Metyrapone; Pituitary Neoplasms; Pyrogens; Radioimmunoassay; Vasopressins

Topics: Adenoma; Adrenal Gland Neoplasms; Adrenocorticotropic Hormone; Cushing Syndrome; Diabetes Insipidus; Diagnosis, Differential; Growth Hormone; Hormones, Ectopic; Humans; Hyperpituitarism; Hypopituitarism; Pituitary Diseases; Pituitary Function Tests; Pituitary Gland; Pituitary Gland, Posterior; Vasopressins

Topics: Acromegaly; Cushing Syndrome; Diabetes Insipidus; Gigantism; Humans; Hypopituitarism; Hypothalamo-Hypophyseal System; Pituitary Diseases; Pituitary Gland, Posterior; Vasopressins

Topics: Adrenocorticotropic Hormone; Androgens; Animals; Catecholamines; Cushing Syndrome; Estrogens; Glucagon; Glucocorticoids; Growth Hormone; Humans; Hyperthyroidism; Hypothyroidism; Insulin; Insulin Secretion; Iodine; Pituitary Gland; Pituitary Hormone-Releasing Hormones; Progesterone; Rats; Stress, Physiological; Thyroid Gland; Thyroid Hormones; Thyroxine; Vasopressins

Topics: Acromegaly; Addison Disease; Adrenocortical Hyperfunction; Cushing Syndrome; Diabetes Insipidus; Endocrine System Diseases; Humans; Hyperaldosteronism; Hyperparathyroidism; Hypopituitarism; Hypothyroidism; Kidney; Vasopressins; Water-Electrolyte Balance

Topics: Adenoma, Islet Cell; Adrenocortical Hyperfunction; Adrenocorticotropic Hormone; Alkalosis; Cushing Syndrome; Electrolytes; Endocrinology; Humans; Hypernatremia; Hypokalemia; Hyponatremia; Neoplasms; Pancreatic Neoplasms; Vasopressins; Water-Electrolyte Balance

Cortisol secretion in adrenal Cushing's syndrome can be regulated by the aberrant adrenal expression of receptors for gastric inhibitory polypeptide, vasopressin, catecholamines, LH/human CG (LH/hCG), or serotonin. Four patients with incidentally discovered bilateral macronodular adrenal hyperplasia without clinical Cushing's syndrome were evaluated for the possible presence of aberrant adrenocortical hormone receptors. Urinary free cortisol levels were within normal limits, but plasma cortisol levels were slightly elevated at nighttime and suppressed incompletely after dexamethasone administration. Plasma ACTH was partially suppressed basally but increased after administration of ovine CRH. A 51-yr-old woman had ACTH-independent increases of plasma cortisol after 10 IU AVP im (292%), 100 microg GnRH iv (184%), or 10 mg cisapride orally (310%); cortisol also increased after administration of NaCl (3%), hCG, human LH, and metoclopramide. In a 61-yr-old man, cortisol was increased by AVP (349%), GnRH (155%), hCG (252%), and metoclopramide (191%). Another 53-yr-old male increased plasma cortisol after AVP (171%) and cisapride (142%). Cortisol secretion was also stimulated by vasopressin in a 54-yr-old female. This study demonstrates that subclinical secretion of cortisol can be regulated via the aberrant function of at least V1-vasopressin, LH/hCG, or 5-HT4 receptors in incidentally identified bilateral macronodular adrenal hyperplasia.

Topics: Adrenal Hyperplasia, Congenital; Cisapride; Cushing Syndrome; Dopamine Antagonists; Female; Follicle Stimulating Hormone; Gonadotropin-Releasing Hormone; Hormones; Humans; Hydrocortisone; Male; Membranes; Metoclopramide; Middle Aged; Receptors, Cell Surface; 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

Bilateral macronodular adrenal hyperplasia (BMAH) is a rare cause of Cushing's syndrome (CS) and its familial clustering has been described previously. Recent studies identified that ARMC5 mutations occur frequently in BMAH, but the relation between ARMC5 mutation and the expression of aberrant G-protein-coupled receptor has not been examined in detail yet.. We studied a large French-Canadian family with BMAH and sub-clinical or overt CS. Screening was performed using the 1-mg dexamethasone suppression test (DST) in 28 family members. Screening for aberrant regulation of cortisol by various hormone receptors were examined in vivo in nine individuals. Sequencing of the coding regions of ARMC5 gene was carried out.. Morning ambulating cortisol post 1 mg DST were >50 nmol/l in 5/8 members in generation II (57-68 years old), 9/22 in generation III (26-46 years old). Adrenal size was enlarged at different degrees. All affected patients increased cortisol following upright posture, insulin-induced hypoglycemia and/or isoproterenol infusion. β-blockers led to the reduction of cortisol secretion in all patients with the exception of two who had adrenalectomies because of β-blockers intolerance. We identified a heterozygous germline variant in the ARMC5 gene c.327_328insC, (p.Ala110Argfs*9) in nine individuals with clinical or subclinical CS, in four out of six individuals with abnormal suppression to dexamethasone at initial investigation and one out of six individuals with current normal clinical screening tests.. Systematic screening of members of the same family with hereditary BMAH allows the diagnosis of unsuspected subclinical CS associated with early BMAH. The relation between the causative ARMC5 mutation and the reproducible pattern of aberrant β-adrenergic and V1-vasopressin receptors identified in this family remains to be elucidated.

Topics: Adrenal Glands; Adrenal Hyperplasia, Congenital; Adrenalectomy; Adrenergic beta-Agonists; Adrenergic beta-Antagonists; Adult; Aged; Armadillo Domain Proteins; Cushing Syndrome; Dexamethasone; Germ-Line Mutation; Humans; Hydrocortisone; Insulin; Isoproterenol; Middle Aged; Pedigree; Posture; Propranolol; Quebec; Receptors, Adrenergic, beta; Receptors, Vasopressin; Tomography, X-Ray Computed; Tumor Suppressor Proteins; Vasopressins

Topics: Adrenalectomy; Arginine Vasopressin; Catecholamines; Cushing Syndrome; Humans; Hydrocortisone; Male; Middle Aged; Vasopressins

We herein present the case of a 53-year-old patient with adrenocorticotropin-independent macronodular adrenocortical hyperplasia (AIMAH), which is a rare form of Cushing syndrome. He had hypercortisolemia and bilateral macronodular adrenal glands with a left side predominance. The administration of vasopressin significantly increased the plasma cortisol level (1.9-fold). Following left adrenalectomy, the patient's hypercortisolemia significantly improved and vasopressin responsiveness was lost, suggesting that the responsiveness originated from the resected left adrenal gland. The marked difference in vasopressin responsiveness between the adrenals corresponded with their asymmetrical size and function. Evaluating the differences in the vasopressin sensitivity may therefore be helpful for understanding the progression of AIMAH.

Topics: Adenoma; Adrenal Cortex; Adrenal Cortex Neoplasms; Adrenalectomy; Adrenocorticotropic Hormone; Cushing Syndrome; Deamino Arginine Vasopressin; Dexamethasone; Diabetes Mellitus, Type 2; Glucose Tolerance Test; Gonadotropin-Releasing Hormone; Humans; Hydrocortisone; Hypertriglyceridemia; Laparoscopy; Male; Middle Aged; Organ Size; Receptors, Vasopressin; Thyrotropin-Releasing Hormone; Vasopressins

Cushing's syndrome due to familial ACTH-independent macronodular adrenal hyperplasia (AIMAH) has been reported in small kindreds. In vasopressin-sensitive AIMAH (VPs-AIMAH), VP stimulates an aberrant, ACTH-independent increase in cortisol. The aims of this study were to (i) delineate the preclinical phenotype of VPs-AIMAH in a three-generation kindred (AIMAH-01) and two smaller kindreds (AIMAH-02 and AIMAH-03) and (ii) investigate the aetiology of VP sensitivity in AIMAH-01.. Clinical studies of three kindreds for adrenal tumours or early Cushing's and molecular studies of adrenal tumours (AIMAH-01).. Thirty-three individuals, from three kindreds, were screened for perturbations of the hypothalamic-pituitary-adrenal axis or adrenal tumours.. Patients underwent clinical, biochemical and adrenal imaging investigations. Evaluation included low-dose (1 IU/70 kg) VP stimulation. Adrenal VP receptor (AVPR1A, AVPR1B, AVPR2) expression (AIMAH-01) was assessed using RT-PCR and immunohistochemistry (IHC). IHC for VP was also performed.. AIMAH-01 had three siblings with Cushing's, and four individuals with suppressed ACTH/aberrant VP responses and/or adrenal nodules. In AIMAH-02, a father and son were affected. AIMAH-03 had three siblings with Cushing's. RT-PCR showed adrenal overexpression of AVPR1A and AVPR1B. IHC detected AVPR1A. The adrenal tumour from one patient also stained weakly for VP and AVPR2.. Adrenal nodules, suppressed ACTH and increased VP sensitivity may represent preclinical disease, allowing early detection, and treatment, of affected individuals. In AIMAH-01, increased VP sensitivity may be due to adrenal VP receptor overexpression. In these kindreds, VPs-AIMAH is familial, and autosomal dominant inheritance is most likely.

Topics: Adrenal Gland Neoplasms; Adrenal Hyperplasia, Congenital; Adrenocorticotropic Hormone; Adult; Aged; Cushing Syndrome; Female; Gene Expression; Humans; Male; Middle Aged; Pedigree; Receptors, Vasopressin; Vasopressins; Young Adult

Bilateral adrenalectomy is the standard treatment for Cushing's syndrome (CS) related to ACTH-independent bilateral macronodular hyperplasia (AIMAH), although it imposes life-long adrenal insufficiency. This study reports a clinical case in order to discuss the clinical interest of pharmacological beta-blockade of illegitimate membrane receptors and unilateral adrenalectomy as alternatives to bilateral adrenalectomy for treatment of CS due to AIMAH. Evidence for cortisol stimulation by upright posture and insulin-induced hypoglycemia in a patient with CS related to AIMAH led us to try beta-blockers as a therapeutic test and then as a first line treatment. Thus, a 3-day beta-blocker test (320 mg/d propranolol) induced normalization of cortisol secretion, with return of hypercortisolism at the end of the test. A long term treatment with 320 mg/d propranolol allowed sustained normalization of cortisol secretion and progressive disappearance of Cushingoid features but after 8 months the patient complained of Raynaud's syndrome and fatigue. Lowering propranolol dosage or switching to atenolol was less efficient to reduce cortisol levels. Unilateral adrenalectomy was then performed as a second line treatment, leading to normalisation of the 24h urinary cortisol without adrenal insufficiency. Long term control of blood pressure and glycemia were observed during a 7-year follow-up without beta-blocker. In conclusion, a 3-day propranolol test may identify patients with AIMAH who can benefit from a long term beta-blocker treatment. In case of intolerance to beta-blocking agents, unilateral adrenalectomy may allow for long term control of Cushing's syndrome related to AIMAH without adrenal insufficiency.

Topics: Adrenal Glands; Adrenalectomy; Adrenergic beta-Antagonists; Atenolol; Cushing Syndrome; Female; Humans; Hydrocortisone; Hyperplasia; Middle Aged; Posture; Propranolol; Treatment Outcome; Vasopressins

Hyper-responsiveness of plasma cortisol to vasopressin has been demonstrated in ACTH-independent bilateral macronodular adrenocortical hyperplasia (AIMAH) and some adrenal adenomas with Cushing's syndrome (CS). However, the clinical significance of hyper-responsiveness of plasma cortisol to vasopressin has not been investigated systematically in adrenal nodule(s). The aim of this study was to clarify the prevalence of hyper-responsiveness of plasma cortisol to vasopressin (vasopressin responder) and their clinical characteristics in terms of hormonal secretion using vasopressin-loading test in the patients with adrenal nodule(s) except pheochromocytomas. A vasopressin-loading test was performed on 61 consecutive patients with adrenal nodules (CS: 33, aldosterone-producing adenoma: 10, non-functional tumor: 18). Vasopressin responders were observed in 36.1% of adrenal nodule(s), 42.4% of CS and 28.5% of non-CS. In responders with CS, eight patients had bilateral nodules that were diagnosed as AIMAH, and the remaining six patients had a unilateral nodule. These patients had lower plasma cortisol than non-responders at both morning (P<0.01) and midnight (P<0.05), as well as the morning following overnight dexamethasone suppression at 1mg (P<0.05) and 8mg (P<0.05). Hyper-responsiveness of the adrenal gland to vasopressin resulting in enhanced plasma cortisol was frequently observed among patients with adrenal nodule(s). The vasopressin responders among the patients with adrenal nodule(s) frequently had CS with low autonomous cortisol secretion.

Topics: Adrenal Gland Neoplasms; Adrenal Glands; Adult; Aged; Cushing Syndrome; Dexamethasone; Female; Glucocorticoids; Humans; Hydrocortisone; Male; Middle Aged; Vasopressins

Vasopressin was reported to stimulate secretion of both cortisol and aldosterone through eutopic V1a receptors in adrenal gland. Recently, adrenal hyper-responsiveness of plasma cortisol to vasopressin with eutopic overexpession of V1a receptors has been reported in Cushing's syndrome, such as a majority of cases of ACTH-independent macronodular adrenal hyperplasia and some cases of Cushing's adenomas. There were a few reports regarding the aldosterone response to vasopressin in aldosterone-producing adenoma. The aim of our study was to investigate the aldosterone response to vasopressin and its pathophysiological roles in the patients with aldosterone-producing adenoma. Vasopressin-loading test was performed in 10 patients with aldosterone-producing adenoma, and in 16 patients with non-functioning adrenal tumors. The roles of the aldosterone response to vasopressin were analyzed in terms of hormonal secretion and the expression of V1a receptor mRNA on the operated adrenal gland in aldosterone-producing adenoma. We found that (1) a varying aldosterone response to vasopressin was observed, (2) absolute response of plasma aldosterone in aldosterone-producing adenoma was significantly higher than that in non-functioning tumor, (3) aldosterone response rate to vasopressin was significantly and negatively correlated with the decline rate (%) in plasma aldosterone from morning to evening in aldosterone-producing adenoma, (4) V1a receptor mRNA was expressed at various values in aldosterone-producing adenoma, and (5) surgical removal of aldosterone-producing adenoma eliminated the aldosterone response to vasopressin observed in patients with aldosterone-producing adenoma. These findings indicated that vasopressin might be involved in the coordination of aldosterone secretion through eutopic expression of V1a receptor in aldosterone-producing adenoma.

Topics: Adenoma; Adrenal Glands; Aged; Aldosterone; Circadian Rhythm; Cushing Syndrome; Female; Humans; Male; Middle Aged; Pituitary Neoplasms; Prospective Studies; Receptors, Vasopressin; RNA, Messenger; Vasopressins

Although Cushing's syndrome arises from various neuroendocrine tumors secreting adrenocorticotropin (ACTH) ectopically, ovarian carcinoma rarely causes this syndrome.. A 66-year-old woman presented with facial swelling and skin pigmentation. She manifested hypercortisolemia, high plasma ACTH, and lack of dexamethasone suppression. MRI showed a solid ovarian tumor and resection of the tumor led to normalization of ACTH and cortisol levels. In addition, elevated serum vasopressin (ADH) and alpha-fetoprotein (AFP) were found, which were also normalized after removal of tumors. Pathological diagnosis was serous adenocarcinoma with neuroendocrine and hepatoid features. Immunohistochemistry detected immunoreactivity of chromogranin A, ACTH, ADH, and AFP in tumor cells.. This is a very rare case of successful treatment of Cushing's syndrome arising from an ovarian adenocarcinoma secreting multiple endocrine substances.

Topics: Adrenocorticotropic Hormone; Aged; alpha-Fetoproteins; Cushing Syndrome; Cystadenocarcinoma, Serous; Dehydroepiandrosterone Sulfate; Estradiol; Female; Humans; Immunohistochemistry; Neurophysins; Ovarian Neoplasms; Parathyroid Hormone; Protein Precursors; Vasopressins

Both pituitary surgery and radiotherapy for Cushing's disease can lead to growth hormone (GH) deficiency. Studies to date have, however, described the incidence of impaired GH secretion and not the incidence of severe GH deficiency following treatment of Cushing's disease. Furthermore, following cure of Cushing's disease and resolution of hypercortisolaemia, recovery of GH secretory status is seen, thus creating uncertainty as to the persistence of any documented GH deficiency. This study has two aims; to determine the incidence of severe persistent GH deficiency following treatment of Cushing's disease and to assess the time scale of any recovery of GH secretory status following surgical cure of Cushing's disease.. The case notes of 37 patients either cured or in clinical and biochemical remission following treatment for Cushing's syndrome were reviewed to determine the incidence of severe GH deficiency. Of 34 patients with Cushing's disease, 20 were treated by pituitary surgery, and 14 with radiotherapy. Three patients with adrenal adenomas underwent unilateral adrenalectomy.. GH secretory status was assessed by provocative testing using an insulin tolerance test (ITT, 85% of all tests), glucagon stimulation test (GST) or arginine stimulation test (AST).. Thirty-six percent (5/14) of radiotherapy treated patients demonstrated severe GH deficiency at a mean time of 99 months following remission. Fifty-nine percent (10/17) of surgically treated patients assessed in the two years following remission demonstrated severe GH deficiency, whilst only 22% (2/9) of patients assessed beyond two years following remission demonstrated severe GH deficiency. This latter cohort is biased, with patients in whom severe GH deficiency had been demonstrated on earlier tests being over-represented. It is more accurate to estimate the incidence of persistent severe GH deficiency following surgically induced remission of Cushing's disease by incorporating data from patients in whom original testing demonstrated adequate GH reserve. Collating such data, 13% (2/15) of patients had persistent severe GH deficiency. Across all time periods five surgically treated patients demonstrated recovery of GH secretory status over a median time course of 19 months. In the surgically treated cohort, seven (35%) patients had anterior pituitary hormone deficits other than GH deficiency: 14% (2/14) of patients with normal GH secretory status at the last assessment, 83% (5/6) of patients with severe GHD at the last assessment. Of the 5 patients who demonstrated recovery of GH secretory status 40% (2) had additional anterior pituitary hormone deficits. Within the radiotherapy treated cohort 14% (2/14) of patients demonstrated additional anterior pituitary hormone deficits: 11% (1/9) of patients with normal GH secretory status and 20% (1/5) of patients with severe GH deficiency. None of the patients with adrenal adenomas treated by unilateral adrenalectomy demonstrated any abnormality of GH secretory status. The incidence of severe persistent GH deficiency following surgically induced or radiotherapy induced remission of Cushing's disease is lower than has been suggested by previous studies, although these latter studies have assessed GH insufficiency and not severe GH deficiency. In the presence of additional pituitary hormone deficits severe GHD is common and is likely to be persistent. Recovery of GH secretory status is seen in a high proportion of patients reassessed, at a median time of 19 months following surgically induced remission of Cushing's disease. Thus, we recommend that definitive assessment of GH secretory status is delayed for at least two years following surgical cure of Cushing's disease. This has important implications for patients in whom GH replacement therapy is being considered.

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Arginine; Child; Cushing Syndrome; Female; Follicle Stimulating Hormone; Follow-Up Studies; Glucagon; Growth Hormone; Humans; Incidence; Insulin; Luteinizing Hormone; Male; Middle Aged; Retrospective Studies; Stimulation, Chemical; Thyrotropin; Time Factors; Vasopressins

We studied the putative role of the vasopressin receptors in the phenotypic response of steroid-secreting adrenocortical tumors. A retrospective analysis of a series of 26 adrenocortical tumors responsible for Cushing's syndrome (19 adenomas and 7 carcinomas) showed that vasopressin (10 IU, i.m., lysine vasopressin) induced an ACTH-independent cortisol response (arbitrarily defined as a cortisol rise above baseline of 30 ng/mL or more) in 7 cases (27%). In comparison, 68 of 90 patients with Cushing's disease (76%) had a positive cortisol response. We then prospectively examined the expression of vasopressin receptor genes in adrenocortical tumors of recently operated patients (20 adenomas and 19 adrenocortical carcinomas). We used highly sensitive and specific quantitative RT-PCR techniques for each of the newly characterized human vasopressin receptors: V1, V2, and V3. The V1 messenger ribonucleic acid (mRNA) was detected in normal adrenal cortex and in all tumors. Its level varied widely between 2.0 x 10(2) and 4.4 x 10(5) copies/0.1 microgram total RNA, and adenomas had significantly higher levels than carcinomas, although there was a large overlap. Among the 6 recently operated patients who had been subjected to the vasopressin test in vivo, the tumor V1 mRNA levels were higher in the 4 responders (9.5 x 10(3) to 5.0 x 10(4)) than in the 2 nonresponders (2.0 x 10(2) and 1.8 x 10(3)). One adenoma that had a brisk cortisol response in vivo, also had in vitro cortisol responses that were inhibited by a specific V1 antagonist. In situ hybridization showed the presence of V1 mRNA in the normal human adrenal cortex where the signal predominated in the compact cells of the zona reticularis. A positive signal was also present in the tumors with high RT-PCR V1 mRNA levels; its distribution pattern was heterogeneous and showed preferential association with compact cells. RT-PCR studies for the other vasopressin receptors showed a much lower signal for V2 and no evidence for V3 mRNA. We could not establish whether the V2 mRNA signal observed in normal and tumoral specimens was present within adrenocortical cells or merely within tissue vessels. We conclude that the vasopressin V1 receptor gene is expressed in normal and tumoral adrenocortical cells. High, and not ectopic, expression occurs in a minority of tumors that become directly responsive to vasopressin stimulation tests.

Topics: Adenoma; Adrenal Cortex Hormones; Adrenal Cortex Neoplasms; Carcinoma; Cushing Syndrome; Gene Expression; Humans; Hydrocortisone; In Situ Hybridization; Lypressin; Phenotype; Polymerase Chain Reaction; Receptors, Vasopressin; Retrospective Studies; RNA-Directed DNA Polymerase; RNA, Messenger; Vasopressins

A retrospective analysis was performed to study the fluid and sodium status of patients undergoing transsphenoidal surgery (TS) for Cushing's disease. We evaluated the time of onset, duration, and relative incidence of isolated hyponatremia and identified possible factors associated with it. Of 58 patients that underwent TS over 1 yr, 52 without postoperative diabetes insipidus or volume depletion were studied. Isolated hyponatremia after TS for Cushing's disease occurred in 21%, and symptomatic hyponatremia (plasma sodium, < or = 125 mmol/L) with new onset headache, nausea, and emesis occurred in 7.0% of all operated. These later patients escaped monitoring and intervention for 24 h. The development of hyponatremia began early in the postoperative period and progressed slowly over 7 days. Maximum antidiuresis occurred on postoperative day 7. Vasopressin levels measured in two patients while hypoosmolar suggested that unregulated vasopressin release contributed to the hyponatremia. Cortisol levels, glucocorticoid replacement, and pituitary adenoma size were similar in normonatremic and hyponatremic patients. Patients combining a history of an estrogenic milieu and documented posterior pituitary trauma at surgery experienced lower nadir plasma sodium. All hyponatremic patients were fluid restricted, and none developed progressive neurological symptoms, morbidity, or mortality. We speculate that the mild degree and slow rate of development of hyponatremia and/or active monitoring and intervention contributed to the good outcome.

Topics: Adolescent; Adult; Cushing Syndrome; Female; Humans; Hyponatremia; Incidence; Male; Pituitary Gland; Postoperative Complications; Retrospective Studies; Sodium; Sphenoid Bone; Time Factors; Vasopressins

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

We describe a case of Cushing's syndrome caused by a phaeochromocytoma secreting corticotrophin-releasing hormone (CRH) and corticotrophin (ACTH). A 49-year-old white woman presented with a 1-month history of lower limb oedema, polydipsia and polyuria. Physical examination revealed a patient with plethoric facies, lanugo-type facial hair, central obesity, red abdominal striae, lower limb oedema, and blood pressure of 210/115 mmHg. Laboratory studies showed high plasma ACTH and markedly elevated urinary cortisol excretion that suppressed more than 50% with high-dose dexamethasone administration. Computed tomographic scan of the abdomen showed a 4-cm left adrenal tumour. Catecholamines and metabolites were markedly increased in a 24-hour urine collection. Results of venous catheterization studies showed that CRH and ACTH were secreted by the tumour. In addition, with ovine CRH administration, inferior petrosal sinus sampling showed pituitary secretion of ACTH. Left adrenalectomy resulted in complete remission of Cushing's syndrome. Light microscopic and immunohistochemical studies revealed a phaeochromocytoma that produced CRH, ACTH and vasopressin. RNA studies showed that this tumour, in contrast to normal adrenal and other reported phaeochromocytomas, transcribed a lone pituitary-sized (1200 nucleotide) pro-opiomelanocortin mRNA. This is the second reported case of a CRH-secreting phaeochromocytoma.

Topics: Adrenal Gland Neoplasms; Adrenocorticotropic Hormone; Blotting, Northern; Corticotropin-Releasing Hormone; Cushing Syndrome; Female; Humans; Middle Aged; Pheochromocytoma; Pro-Opiomelanocortin; RNA; Vasopressins

We have studied the diurnal rhythm of pars distalis and pars intermedia-type immunoreactive (IR)-POMC peptides and cortisol in 3 normal dogs and 1 dog with Cushing's syndrome and have documented the responses to a variety of agents in 42 dogs with Cushing's disease, 2 of which were known or presumed to have pars intermedia tumors and another of which had both pars distalis and pars intermedia adenomas, and in 20 dogs with adrenocortical adenomas causing Cushing's syndrome. The normal dogs did not have a diurnal plasma POMC peptide rhythm; the dog with Cushing's disease appeared to have a similar number of secretory episodes of increased amplitude. Plasma POMC peptides and cortisol in animals with Cushing's disease did not suppress normally with low dose dexamethasone. Five animals with Cushing's disease did suppress with high dose dexamethasone, the dog with dual adenomas suppressed only partially, and 1 dog with a pars intermedia adenoma did not suppress at all. The response to insulin-induced hypoglycemia was similar in normal dogs and 4 dogs with Cushing's disease, but 3 animals with adrenal tumors did not respond. The response to metyrapone was normal in 6 dogs with Cushing's disease and, surprisingly, in 1 with adrenal tumor. Arginine vasopressin stimulated POMC peptide secretion in normal and 6 Cushing's dogs, as well as alpha MSH, a pars intermedia-type POMC peptide, in a dog presumed to have a pars intermedia tumor. Ovine CRF stimulated pars distalis-type POMC peptide secretion in normal dogs and 17 dogs with Cushing's disease, but not in 15 dogs with adrenal tumor; IR-alpha MSH was unaffected. TRH appeared to stimulate IR-ACTH in normal animals, but not in those with Cushing's disease. Dopamine had no apparent effect in 2 normal and 1 Cushing's dogs. Initial plasma disappearance t1/2 values of IR-ACTH and lipotropin were 22-27 min. In summary, responses in normal and Cushing's dogs were generally what would be predicted from previous human and animal studies, but some of those in animals with pars intermedia tumors and even in normal dogs were different from what had been anticipated. Canine Cushing's syndrome provides an interesting model for an uncommon human disorder.

Topics: Animals; Blood Glucose; Circadian Rhythm; Cushing Syndrome; Dexamethasone; Dogs; Dopamine; Female; Hydrocortisone; Insulin; Male; Metyrapone; Pro-Opiomelanocortin; Thyrotropin-Releasing Hormone; Vasopressins

Topics: Adrenocorticotropic Hormone; Animals; Circadian Rhythm; Corticotropin-Releasing Hormone; Cushing Syndrome; Depressive Disorder; Drug Synergism; Humans; Hydrocortisone; Peptides; Pro-Opiomelanocortin; Vasopressins

The response of pituitary adenomas obtained surgically from patients with Cushing's disease of Nelson's syndrome to synthetic ovine corticotropin-releasing factor (CRF), vasopressins, somatostatin-28, dexamethasone, 3-isobutylmethylxanthine or high [K+] was examined in vitro by measuring the amount of pro-opiomelanocortin (POMC)-derived peptides secreted into the culture medium. CRF did not stimulate the secretion of adrenocorticotropin-, beta-endorphin-, or gamma 3-melanotropin-like peptides from the pituitary adenomas at concentrations ranging from 1 x 10(-13) M to 1 x 10(-7) M whereas vasopressins, 3-isobutyrl-methylxanthine and high [K+] increased, while somatostatin-28 and dexamethasone suppressed, the secretion of these POMC-derived peptides. These findings suggest that either the pituitary ACTH-producing tumors have lost their receptors to CRF or their post-receptor mechanism to CRF is not functional.

Topics: Adenoma; Adolescent; Adrenocorticotropic Hormone; Adult; beta-Endorphin; Cells, Cultured; Corticotropin-Releasing Hormone; Cushing Syndrome; Dexamethasone; Endorphins; Female; Humans; Male; Melanocyte-Stimulating Hormones; Nelson Syndrome; Pituitary Neoplasms; Somatostatin; Somatostatin-28; Vasopressins

Topics: Adrenocorticotropic Hormone; Cushing Syndrome; Erythropoietin; Gonadotropins; Hormones, Ectopic; Humans; Hypercalcemia; Hypoglycemia; Hyponatremia; Insulin; Melanocyte-Stimulating Hormones; Paraneoplastic Endocrine Syndromes; Parathyroid Hormone; Pigmentation Disorders; Vasopressins

Topics: Bronchial Neoplasms; Cushing Syndrome; Hormones, Ectopic; Humans; Hypercalcemia; Paraneoplastic Endocrine Syndromes; Vasopressins

A cyclic excess of cortisol secretion was detected in a patient with diabetes insipidus and diabetes mellitus. The cycles of hypercortisolism were of 7 days' duration, but during the nadir of these cycles urinary excretion of corticosteroids and 17-ketosteroids was within the normal range. The radiological appearance of the sella turcica was normal; however, computerized axial tomography of the head revealed a small tumor immediately superior to the sella turcica. At operation a small chromophobe adenoma superior to the diaphragma sellae and involving the hypophysial stalk was partially resected. Postoperatively, the patient continued to have 7-day cycles of increased corticosteroid excretion, but the amounts excreted were less than they had been preoperatively. Other patients have been described in whom Cushing's disease has been due to cyclic hypercortisolism. These cycles have been remarkably regular in individual patients, but of variable duration in different patients. Furthermore, cyclic hormonogenesis probably occurs in a variety of endocrinopathies. (Neurosurgery, 5: 598--603, 1979).

Topics: 17-Hydroxycorticosteroids; 17-Ketosteroids; Adenoma, Chromophobe; Adrenal Cortex; Adult; Cushing Syndrome; Dexamethasone; Diabetes Insipidus; Humans; Hydrocortisone; Male; Periodicity; Pituitary Neoplasms; Vasopressins

The response of plasma ACTH and/or cortisol concentrations to thyrotropin-releasing-factor (TRF), vasopressin, and insulin administration was determined in 5 patients with Nelson's syndrome and 12 patients with untreated Cushing's disease. TRF administration was associated with a mean increment of 267 pg/ml in plasma ACTH concentrations in patients with Nelson's syndrome, and of 42 pg/ml in patients with Cushing's disease. The increment in plasma cortisol concentrations in the latter group was 12 mug%. No ACTH or cortisol response was observed in normal subjects. Patients with Cushing's disease or Nelson's syndrome exhibited significantly greater increments in plasma ACTH concentrations in response to vasopressin administration (P less than .05, P less than .02 respectively) than did normal subjects; the increment in cortisol concentration was also greater, (P less than .05), in patients with Cushing's disease than in normal subjects. No significant difference was present between patients with Cushing's disease and Nelson's syndrome with regard to the magnitude of the ACTH response to vasopressin administration. In contrast, the increment in plasma cortisol and plasma ACTH concentrations following insulin induced hypoglycemia was significantly less in patients with Cushing's disease than seen in normal subjects, (P less than .001, P less than .05 respectively); while this stimulus was associated with a significantly greater increment in plasma ACTH concentrations in patients with Nelson's syndrome as compared to that seen in normal subjects, (P less than .01) and in patients with Cushing's disease (P less than .01). These findings indicate that pituitary function in patients with Nelson's syndrome is not autonomous and suggest the possibility that altered central nervous regulatory mechanism might play a role in the etiology of the pituitary tumors which are frequently associated with this syndrome. The TRF induced rise in plasm cortisol and ACTH concentrations in patients with Cushing's disease and Nelson's syndrome suggests the possibility of altered hypothalamic or pituitary receptors in such patients.

Topics: Adolescent; Adrenocorticotropic Hormone; Adult; Cushing Syndrome; Female; Growth Hormone; Humans; Hydrocortisone; Hypoglycemia; Insulin; Klinefelter Syndrome; Male; Middle Aged; Prolactin; Thyrotropin; Thyrotropin-Releasing Hormone; Vasopressins

While pituitary tumors are not as rare as was once thought, it is difficult to assess how many are of clinical significance. Trans-sphenoidal pituitary exploration is a technique which can be performed with low operative morbidity and mortality, and when instituted early can prevent subsequent visual and endocrine impairment from an expanding lesion. Thus early recognition has increased importance.

Topics: Acromegaly; Adenoma; Adenoma, Chromophobe; Adrenocorticotropic Hormone; Adult; Cushing Syndrome; Female; Follicle Stimulating Hormone; Growth Hormone; Humans; Luteinizing Hormone; Male; Middle Aged; Pituitary Neoplasms; Prolactin; Thyrotropin; Vasopressins

The effect of metergoline, a specific antiserotoninergic drug, on ACTH secretion was investigated in 29 normal volunteers and in 4 patients with increased ACTH production (3 with Addison's disease, 1 with Cushing's disease). In 15 normal subjects, a 4-day treatment with 10 mg daily of metergoline significantly blunted the ACTH response to insulin hypoglycemia. Mean peak ACTH values before and after treatment were, respectively, 333 +/- 39.2 (SE) and 235 +/- 38.8 pg/ml (P less than 0.05). The corresponding values of plasma cortisol were 29.6 +/- 2.96 and 20.5 +/- 2.67 mug/100 ml (P less than 0.05). In contrast, metergoline failed to affect the ACTH response to lysine-vasopressin (LVP) administered iv (8 subjects studied) and im (6 subjects studied). In 3 patients suffering from Addison's disease, an appreciable although not statistically significant lowering of the plasma ACTH levels was noted during metergoline administration. The mean pre- and post-treatment values of plasma ACTH in these patients were, respectively, 1116 +/- 192.2 and 666 +/- 100.8 pg/ml, 4240 +/- 50.0 and 3398 +/- 368.0 pg/ml, and 431 +/- 44.0 and 352 +/- 23.9 pg/ml. In one patient with Cushing's disease caused by a pituitary adenoma, metergoline did not appreciably modify plasma ACTH levels. Taken together, these results lend support to the concept of a physiological stimulating effect of serotonin on ACTH secretion. Moreover, they are compatible with the view that serotonin exerts its action chiefly at the hypothalamic level while LVP promotes ACTH release by a primary action on the pituitary.

Topics: Addison Disease; Adrenocorticotropic Hormone; Adult; Cushing Syndrome; Ergolines; Female; Humans; Hydrocortisone; Hypoglycemia; Hypothalamo-Hypophyseal System; Insulin; Lypressin; Male; Metergoline; Middle Aged; Serotonin; Serotonin Antagonists; Vasopressins

The development of a sensitive and specific radioimmunoassay for vasopressin is described. Antibodies were successfully produced following the coupling of synthetic arginine vasopressin with bovine serum albumin carried out with carbodiimide. In order to standardize the assay, the labelled hormone has to be separated twice using a DEAE-Sephadex-A-25 column and thin layer chromatography with cellulose plates. A further condition to obtain a reproducible standard curve is the use of a pure arginine vasopressin checked by cellulose chromatography. Most of the vasopressin batches available do not fulfil this requirement of purity. With the method described, vasopressin can be determined in unextracted human urine. The lower limit of detection is 2 pg/ml. Normal values are in the range of 67.5 +/- 34.3 ng/24 h (kappa +/- SD, n =45). No significant difference of AVP excretion was found between men and women. The usefulness of the assay is demonstrated in patients with hypothalamic or pituitary disorders.

Topics: Acromegaly; Adolescent; Adult; Aged; Arginine Vasopressin; Breast Neoplasms; Child; Chromatography, Thin Layer; Cushing Syndrome; Diabetes Insipidus; Female; Humans; Immune Sera; Immunodiffusion; Lypressin; Male; Middle Aged; Prostatic Neoplasms; Radioimmunoassay; Vasopressins

A case of a 21-year-old woman with Cushing's disease due to a pituitary tumor is described. The patient was treated with cyprohepatadine for 4 weeks immediately following pituitary alpha-particle irradiation. A standard vasopressin test to measure ACTH-mediated cortisol release was performed four times: prior to pituitary irradiation, after irradiation, after 4 weeks of cyproheptadine therapy, and off cyproheptadine for 2 weeks. Cyproheptadine failed to modify vasopressin-stimulated cortisol release in the patient described. This study suggests that cyproheptadine, which has previously been shown to decrease ACTH secretion, probably acts principally at the hypothalamic, rather than at the pituitary level.

Topics: Adult; Cushing Syndrome; Cyproheptadine; Female; Humans; Hydrocortisone; Insulin; Pituitary Gland; Time Factors; Vasopressins

Among the malignant tumors of nonendocrine origin that are capable of producing polypeptide hormones and of manifesting as different endocrine syndromes discussed here are ectopic ACTH syndrome, SIADH, and ectopic gonadotropin-producing tumors.

Topics: Adrenocorticotropic Hormone; Carcinoma, Hepatocellular; Carcinoma, Small Cell; Chorionic Gonadotropin; Cushing Syndrome; Diagnosis, Differential; Erythropoietin; Follicle Stimulating Hormone; Gynecomastia; Hormones, Ectopic; Humans; Hyperthyroidism; Hypoglycemia; Hyponatremia; Liver Neoplasms; Lung Neoplasms; Luteinizing Hormone; Male; Paraneoplastic Endocrine Syndromes; Polycythemia; Puberty, Precocious; Thyrotropin; Vasopressins; Water Intoxication

Plasma ACTH (normal value: 0.16 plus or minus mU/100 ml) was measured in 116 patients with Cushing's syndrome, using a bioassay including dynamic tests and sequential determinations. In 10 patients with adrenal tumors ACTH levels were nondetectable (ND) or low, and usually nonstimulatable. In 10 patients with ectopic ACTH secretion high levels (0.42 plus or minus 0.07 mU/100 ml) were measured. The extracts of 6 tumors yielded an ACTH-like substance. Forty-three patients with Cushing's disease (without pituitary tumor) had, before treatment, a mean ACTH level of 0.18 plus or minus 0.01 mU/100 ml, accompanied by high levels of plasma cortisol (32.1 plus or minus 1.9 mug/100 ml). Irregular nycthemeral variations occurred. ACTH rose to 0.30 mU/100 ml after incomplete adrenalectomy (20 patients) and to 1.14 mU/100 ml after total adrenalectomy (21 patients). Dexamethasone (8 mg per day) suppressed ACTH levels. Metyrapone induced a normal ACTH rise, but at abnormal times. Lysine-vasopressin (LVP) induced an ACTH mean relative increase of 120% before, and of 140% after adrenalectomy (i.e., within the normal range). Six nonadrenalectomized patients with pituitary tumors showed similar abnormalities of ACTH regulation. However, the ACTH rise after LVP was above 500%. When pituitary tumors occurred after adrenalectomy (12 patients) the mean basal ACTH level was 18 mU/100 ml. Dexamethasone induced a 90% decrease, and LVP a 416% increase in ACTH levels. In 6 patients with nodular adrenal hyperplasia, ACTH was undetectable before treatment. After adrenalectomy, ACTH rose to 0.4 mU/100 ml (11 patients) and the increase after LVP was 90%. Five additional patients developed pituitary tumors. These data confirm the abnormalities of ACTH feedback regulation in Cushing's disease. However, even when pituitary tumors occur, ACTH levels can be altered by metyrapone, dexamethasone and LVP. This last test is of particular interest for the detection of pituitary tumors. The follow-up pattern of treated nodular adrenal hyperplasia appears to be very similar to that of Cushing's disease.

Topics: Adrenal Gland Diseases; Adrenalectomy; Adrenocorticotropic Hormone; Animals; Biological Assay; Cushing Syndrome; Dexamethasone; Hormones, Ectopic; Humans; Hydrocortisone; Hyperplasia; Metyrapone; Pituitary Function Tests; Pituitary Gland; Pituitary Gland, Anterior; Pituitary Neoplasms; Rats; Vasopressins

A sensitive bioassay for the measurement of plasma ACTH is presented. The use of silicic acid adsorption of plasma, with a subsequent acid wash and aqueous acetone desorption, was successful in removing those substances which had interfered with the steroidogenic response of dispersed adrenal cells when unextracted plasma was employed. This extraction procedure extracted 72-76% of ACTH present in plasma. Two pg ACTH1-39 could be consistently detected. Alpha-hACTH1-39 and alpha-pACTH1-39 exhibited equal potencies. Beta-MSH was ineffective at dosage levels up to 2 x 10(8) pg. One x 10(8) pg of ACTH1-10, ACTH4-10, or alpha-MSH had a steroidogenic effect equivalent to that of 40 pg ACTH1-39. ACTH 17-39 and ACTH 11-24 were incapable of stimulating steroid production at doses of 1 x 10(8) pg. Excesses of the latter, but not of the former appeared to be able to antagonize the steroidogenic effect of ACTH1-39. Plasma from normal subjects, bioassayed by this extraction procedure, contained 12-186 pg/ml ACTH at 0400-0800: 14-93 pg/ml ACTH at 1000-1300, and less than 10-34 pg/ml ACTH at 1600-2200. Hypoglycemia and vasopressin administration were followed by increases in plasma ACTH concentratrations. Plasma ACTH concentrations in untreated patients with Cushing's disease (sampled over the period 0900-1300) ranged from 65-220 pg/ml. Three patients with Addison's disease (untreated or 12 h following replacement steroid withdrawal) had ACTH concentrations of 223, 370 and 1226 pg/ml. Markedly elevated ACTH concentrations were observed in a patient with Nelson's syndrome (391 and 835 pg/ml). Bioassayable ACTH was not detected in 2 patients with panhypopituitarism.

Topics: Acetone; Addison Disease; Adrenal Glands; Adrenocorticotropic Hormone; Adsorption; Animals; Biological Assay; Blood Glucose; Cushing Syndrome; Humans; Hypopituitarism; Melanocyte-Stimulating Hormones; Radioimmunoassay; Rats; Silicic Acid; Time Factors; Vasopressins

Topics: Adolescent; Adult; Circadian Rhythm; Cushing Syndrome; Diencephalon; Female; Humans; Hydrocortisone; Lypressin; Male; Middle Aged; Pituitary Gland; Propranolol; Vasopressins

The exact prevalence of the humoral syndromes associated with neoplasm is not known but it seems clear that they exist more commonly than is realized. Hormonal syndromes are very often seen in patients with carcinoma of the lung. Awareness of the large number of ectopic hormonal syndromes in patients with tumors can lead to early diagnosis, treatment, and herald recurrence. They may be responsible for new signs and symptoms which can be life-shortening. Hormonal causes of clinical deterioration must be considered before concluding that symptoms are due to metastases in patients with neoplastic disease. Tumors are chemically active and the important concept which has had great impact on the diagnosis, treatment, and basic understanding of mechanisms, which are important to endocrinologists and oncologists has been stated by Liddle: "Certain tumors of nonendocrine tissue can produce hormones that are similar to normal hormones except that their production is not appropriately controlled by normal physiologic mechanisms." Survival and quality of life can be reduced in patients with the metabolic complications of these humors. The list of humoral substances released by tumors is growing as technologic advances lead to their detection. Other chemical substances produced by neoplastic tissue may have biologic activity which impacts on the patient's clinical condition and which we cannot recognize, at this time, because the techniques to detect them have not been developed. If there are signs or symptoms of overproduction of a hormone, search for a tumor; if a patient has a tumor, search for biologically active substances.

Topics: Cushing Syndrome; Erythropoietin; Hormones; Hormones, Ectopic; Humans; Hypercalcemia; Hypoglycemia; Neoplasms; Paraneoplastic Endocrine Syndromes; Vasopressins

Topics: Acromegaly; Addison Disease; Adrenalectomy; Blood Glucose; Cushing Syndrome; Diabetes Insipidus; Dwarfism; Dwarfism, Pituitary; Female; Glucagon; Growth Hormone; Humans; Hyperthyroidism; Hypogonadism; Hypopituitarism; Insulin; Lysine; Male; Pyrogens; Radioimmunoassay; Vasopressins

Topics: 17-Hydroxycorticosteroids; Adenoma, Basophil; Adenoma, Chromophobe; Adolescent; Adrenal Gland Neoplasms; Blood Glucose; Cushing Syndrome; Female; Humans; Lysine; Male; Middle Aged; Stimulation, Chemical; Vasopressins

Topics: Adenoma; Adrenal Gland Neoplasms; Adrenocorticotropic Hormone; Circadian Rhythm; Cushing Syndrome; Electroencephalography; Female; Growth Hormone; Humans; Hydrocortisone; Insulin; Middle Aged; Secretory Rate; Sleep; Sleep, REM; Vasopressins

Topics: Addison Disease; Adrenalectomy; Adrenocorticotropic Hormone; Cushing Syndrome; Humans; Lysine; Methods; Metyrapone; Perfusion; Radioimmunoassay; Secretory Rate; Silicon Dioxide; Stimulation, Chemical; Time Factors; Vasopressins

Topics: Adrenocorticotropic Hormone; Adult; Cushing Syndrome; Diagnosis, Differential; Female; Follicle Stimulating Hormone; Growth Hormone; Hormones, Ectopic; Humans; Hyperthyroidism; Hypocalcemia; Hypoglycemia; Hyponatremia; Insulin; Luteinizing Hormone; Mediastinal Neoplasms; Middle Aged; Osmolar Concentration; Parathyroid Hormone; Pigmentation Disorders; Syndrome; Thymus Neoplasms; Thyrotropin-Releasing Hormone; Vasopressins

Topics: 17-Hydroxycorticosteroids; 17-Ketosteroids; Adult; Circadian Rhythm; Corticotropin-Releasing Hormone; Cushing Syndrome; Dexamethasone; Dihydroxyphenylalanine; Drug Evaluation; Female; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Methyldopa; Stimulation, Chemical; Vasopressins

Topics: 17-Hydroxycorticosteroids; Adrenocorticotropic Hormone; Cushing Syndrome; Dexamethasone; Dihydroxyphenylalanine; Female; Humans; Hydrocortisone; Metyrapone; Middle Aged; Periodicity; Pituitary-Adrenal System; Vasopressins

Topics: Adrenocorticotropic Hormone; Cushing Syndrome; Gynecomastia; Hormones, Ectopic; Hypercalcemia; Melanocyte-Stimulating Hormones; Paraneoplastic Endocrine Syndromes; Vasopressins

Topics: Adrenocorticotropic Hormone; Cell Transformation, Neoplastic; Cushing Syndrome; Humans; Hypercalcemia; Hyponatremia; Neoplasms; Parathyroid Hormone; Precancerous Conditions; Vasopressins

Topics: Adrenalectomy; Adrenocorticotropic Hormone; Circadian Rhythm; Cushing Syndrome; Dexamethasone; Diagnosis, Differential; Humans; Hydrocortisone; Immune Sera; Injections, Intramuscular; Injections, Intravenous; Insulin; Iodine Radioisotopes; Lysine; Pituitary Neoplasms; Prognosis; Radioimmunoassay; Vasopressins

Topics: Adenocarcinoma; Adenoma; Adrenal Cortex Hormones; Adrenal Gland Neoplasms; Adrenocortical Hyperfunction; Adrenocorticotropic Hormone; Arginine; Carbon Isotopes; Cushing Syndrome; Growth Hormone; Humans; Hydroxycorticosteroids; Hypoglycemia; Insulin; Luteinizing Hormone; Lysine; Pituitary Irradiation; Stimulation, Chemical; Vasopressins

Topics: 17-Hydroxycorticosteroids; Adolescent; Adrenal Gland Neoplasms; Adrenal Glands; Adrenal Insufficiency; Adrenalectomy; Adrenocorticotropic Hormone; Adult; Child; Cortisone; Cushing Syndrome; Female; Humans; Hydrocortisone; Hypothalamus; Male; Metyrapone; Middle Aged; Pituitary Gland; Pituitary-Adrenal Function Tests; Postoperative Complications; Prednisone; Stress, Physiological; Time Factors; Vasopressins

Topics: Adrenal Glands; Adrenocortical Hyperfunction; Adult; Circadian Rhythm; Cushing Syndrome; Dexamethasone; Electroencephalography; Female; Growth Hormone; Humans; Hydrocortisone; Hydroxycorticosteroids; Hypoglycemia; Hypothalamus; Insulin; Male; Middle Aged; Pituitary Gland; Pituitary-Adrenal Function Tests; Polysaccharides, Bacterial; Sleep Stages; Vasopressins

Topics: Addison Disease; Adolescent; Adrenal Gland Diseases; Adrenal Glands; Adrenalectomy; Adrenocorticotropic Hormone; Adult; Aged; Child; Cushing Syndrome; Dexamethasone; Female; Fluorometry; Humans; Hydrocortisone; Hyperplasia; Hypopituitarism; Hypothalamo-Hypophyseal System; Injections, Intramuscular; Lysine; Male; Metyrapone; Middle Aged; Pituitary Neoplasms; Pituitary-Adrenal Function Tests; Vasopressins

Topics: Adrenal Cortex Hormones; Adrenal Gland Neoplasms; Cushing Syndrome; Diagnosis, Differential; Humans; Lysine; Vasopressins

Topics: Adrenal Glands; Adrenocorticotropic Hormone; Cushing Syndrome; Diagnosis, Differential; Growth Hormone; Humans; Hypothalamus; Insulin; Lysine; Pituitary Gland; Pituitary-Adrenal Function Tests; Vasopressins

Topics: 17-Hydroxycorticosteroids; Adrenocorticotropic Hormone; Carcinoma, Bronchogenic; Cushing Syndrome; Diagnosis, Differential; Female; Gonadotropins; Hormones, Ectopic; Humans; Hypopituitarism; Lung Neoplasms; Male; Parathyroid Hormone; Vasopressins

Topics: Adrenalectomy; Adrenocorticotropic Hormone; Alkalosis; Autoimmune Diseases; Bone Diseases; Carcinoma, Bronchogenic; Cushing Syndrome; Endocrine System Diseases; Hypercalcemia; Hyperparathyroidism; Hyponatremia; Lung Neoplasms; Metabolic Diseases; Neoplasm Metastasis; Neurologic Manifestations; Neuromuscular Diseases; Skin Diseases; Skin Manifestations; Vascular Diseases; Vasopressins

Topics: 17-Hydroxycorticosteroids; 17-Ketosteroids; Adrenal Cortex Hormones; Adrenal Glands; Adrenal Insufficiency; Adrenocorticotropic Hormone; Cushing Syndrome; Humans; Hypothalamo-Hypophyseal System; Pituitary-Adrenal Function Tests; Prednisone; Stress, Physiological; Vasopressins

Topics: 17-Hydroxycorticosteroids; Adrenal Gland Diseases; Adrenocorticotropic Hormone; Circadian Rhythm; Cushing Syndrome; Dexamethasone; Humans; Hydrocortisone; Hyperplasia; Insulin; Metyrapone; Pituitary-Adrenal Function Tests; Pyrogens; Vasopressins

Topics: 17-Hydroxycorticosteroids; 17-Ketosteroids; Adolescent; Adult; Carbon Isotopes; Circadian Rhythm; Cushing Syndrome; Diagnosis, Differential; Fasting; Female; Humans; Hydrocortisone; Hypothalamo-Hypophyseal System; Male; Middle Aged; Obesity; Pituitary-Adrenal System; Secretory Rate; Steroids; Vasopressins

In an unselected series of 185 patients with histologically confirmed bronchial carcinoma 16 had endocrine disturbances attributable to the tumour (excluding pulmonary osteoarthropathy). Of these, 11 patients had hypercalcaemia; three inappropriate secretion of antidiuretic hormone; one Cushing's disease; three hypertrophic osteoarthropathy; and one gynaecomastia. Cushing's disease and inappropriate antidiuresis are specifically associated with oat-cell tumours, and hypercalcaemia occurs most frequently with squamous carcinoma. A negative correlation exists between gynaecomastia and osteoarthropathy on the one hand and oat-cell carcinoma on the other.

Topics: Adenocarcinoma; Bronchial Neoplasms; Carcinoid Tumor; Carcinoma, Bronchogenic; Carcinoma, Squamous Cell; Chlorides; Cushing Syndrome; Endocrine System Diseases; Gynecomastia; Humans; Hydrocortisone; Hypercalcemia; Osteoarthropathy, Primary Hypertrophic; Sodium; Urea; Vasopressins

Topics: Adrenal Gland Neoplasms; Adrenalectomy; Adult; Cushing Syndrome; Diagnosis, Differential; Female; Humans; Hydrocortisone; Injections, Intramuscular; Lysine; Male; Metyrapone; Middle Aged; Pituitary Diseases; Pituitary Gland; Vasopressins

Topics: Adrenal Gland Neoplasms; Adrenocortical Hyperfunction; Adrenocorticotropic Hormone; Cushing Syndrome; Hormones, Ectopic; Humans; Hydrocortisone; Pituitary-Adrenal Function Tests; Vasopressins

Topics: Adrenal Gland Neoplasms; Adrenocortical Hyperfunction; Adrenocorticotropic Hormone; Cushing Syndrome; Hormones, Ectopic; Hydrocortisone; Vasopressins

Topics: 17-Hydroxycorticosteroids; Adenoma; Adolescent; Adrenal Gland Neoplasms; Adrenocorticotropic Hormone; Adult; Circadian Rhythm; Cushing Syndrome; Dexamethasone; Diagnosis, Differential; Female; Humans; Hydrocortisone; Hyperplasia; Hypoglycemia; Hypothalamo-Hypophyseal System; Male; Metyrapone; Middle Aged; Pituitary-Adrenal Function Tests; Pituitary-Adrenal System; Secretory Rate; Vasopressins

Topics: Acromegaly; Adrenal Glands; Adult; Aged; Cushing Syndrome; Female; Fever; Glucocorticoids; Growth Hormone; Humans; Hypothalamus; Insulin; Male; Metyrapone; Middle Aged; Pituitary Diseases; Pituitary Gland; Pituitary-Adrenal Function Tests; Vasopressins

Topics: 17-Hydroxycorticosteroids; Adolescent; Adrenal Cortex Hormones; Adrenal Glands; Adrenalectomy; Adrenocortical Hyperfunction; Adrenocorticotropic Hormone; Adult; Aged; Cushing Syndrome; Female; Growth Hormone; Humans; Hypothalamo-Hypophyseal System; Insulin; Male; Metyrapone; Middle Aged; Pituitary-Adrenal System; Pyrogens; Vasopressins

Topics: Adrenocorticotropic Hormone; Circadian Rhythm; Cushing Syndrome; Dexamethasone; Humans; Hydrocortisone; In Vitro Techniques; Ion Exchange Resins; Lysine; Pituitary Function Tests; Pituitary-Adrenal Function Tests; Prednisolone; Protein Binding; Transcortin; Tritium; Vasopressins

Topics: Adrenocorticotropic Hormone; Adult; Cushing Syndrome; Female; Gastrins; Glucagon; Humans; Male; Melanocyte-Stimulating Hormones; Middle Aged; Neoplasms; Norepinephrine; Parathyroid Hormone; Serotonin; Vasopressins

Topics: 17-Hydroxycorticosteroids; Adrenal Gland Diseases; Adrenal Insufficiency; Adrenocorticotropic Hormone; Adult; Arginine; Corticotropin-Releasing Hormone; Cushing Syndrome; Female; Humans; Hypothalamo-Hypophyseal System; Insulin; Lysine; Male; Metyrapone; Middle Aged; Pituitary Gland; Pituitary-Adrenal Function Tests; Pyrogens; Stimulation, Chemical; Vasopressins

Topics: Acromegaly; Adenoma; Adolescent; Adrenal Gland Neoplasms; Adrenocorticotropic Hormone; Adult; Anorexia Nervosa; Brain Diseases; Brain Neoplasms; Cushing Syndrome; Endocrine System Diseases; Female; Humans; Hydrocortisone; Hypothalamus; Injections, Intramuscular; Lysine; Male; Metyrapone; Middle Aged; Pituitary Neoplasms; Pituitary-Adrenal Function Tests; Vasopressins

Topics: Adrenocortical Hyperfunction; Adult; Cushing Syndrome; Diagnosis, Differential; Female; Humans; Hydrocortisone; Lysine; Male; Middle Aged; Pituitary-Adrenal Function Tests; Vasopressins

Topics: Adrenocorticotropic Hormone; Cushing Syndrome; Female; Humans; Hydrocortisone; Insulin; Liver Diseases; Metyrapone; Myxedema; Obesity; Pituitary-Adrenal Function Tests; Pregnancy; Vasopressins

Topics: Acromegaly; Adult; Aged; Breast Neoplasms; Cushing Syndrome; Diabetes Insipidus; Diabetic Retinopathy; Female; Humans; Male; Middle Aged; Pituitary Gland; Polyuria; Prostatic Neoplasms; Ultrasonic Therapy; Vasopressins

Topics: Afibrinogenemia; Autonomic Nervous System Diseases; Bone Diseases; Carcinoma, Bronchogenic; Collagen Diseases; Cushing Syndrome; Endocrine System Diseases; Fibrinolysis; Hematologic Diseases; Humans; Hypercalcemia; Lung Neoplasms; Muscular Diseases; Neurologic Manifestations; Osteoarthropathy, Secondary Hypertrophic; Pathology; Peripheral Nervous System Diseases; Spinal Cord; Thrombophlebitis; Vascular Diseases; Vasopressins

Topics: 5-Hydroxytryptophan; Carcinoid Tumor; Carcinoma, Hepatocellular; Carotid Body Tumor; Catecholamines; Cushing Syndrome; Endocrine System Diseases; Female; Fibrosarcoma; Humans; Hyperthyroidism; Hypoglycemia; Hyponatremia; Liver Neoplasms; Lung Neoplasms; Male; Neoplasms; Polycythemia Vera; Puberty, Precocious; Vasopressins

Topics: Addison Disease; Arginine Vasopressin; Avena; Bronchial Neoplasms; Carcinoma, Small Cell; Cushing Syndrome; Gynecomastia; Humans; Hypercalcemia; Hyperthyroidism; Hyponatremia; Hypotension; Liver Cirrhosis; Male; Metabolism; Pathology; Physiology; Small Cell Lung Carcinoma; Sodium; Vasopressins

Topics: Carcinoid Tumor; Cushing Syndrome; Humans; Hyperthyroidism; Hypoglycemia; Neoplasms; Pheochromocytoma; Polycythemia; Puberty; Puberty, Precocious; Sexual Maturation; Vasopressins

Topics: Adrenocorticotropic Hormone; Cushing Syndrome; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diabetic Nephropathies; Endocrine Glands; Endocrine System Diseases; Hormones; Humans; Hypercalcemia; Hypothyroidism; Liver Diseases; Lung Neoplasms; Neoplasms; Nephrosis; Polycythemia; Pseudopseudohypoparathyroidism; Vasopressins

Topics: Adrenal Glands; Adrenalectomy; Adrenocorticotropic Hormone; C-Reactive Protein; Cushing Syndrome; Dexamethasone; Diabetes Insipidus; Diencephalon; Humans; Physiology; Pituitary Gland; Pyrogens; Stress, Physiological; Vasopressins