pituitrin and Addison-Disease

Osmotic demyelination of the brain (ODS) is a dreaded complication that typically occurs several days after aggressive therapy for chronic hyponatraemia, but is eminently avoidable. In this teaching exercise, Professor McCance, an imaginary consultant, is asked to explain how he would have treated a 28-year-old female who had hyperkalaemia, hypoglycaemia, hypotension and hyponatraemia (118 mM) to prevent the development of ODS. He begins with a review of the physiology, including his own landmark work on chronic hyponatraemia associated with a contracted extracellular fluid volume. Adding quantitative analysis, the cause of the excessive rise in plasma sodium concentration is revealed, and a better plan for therapy is proposed.

Topics: Addison Disease; Adult; Brain Diseases; Demyelinating Diseases; Female; Humans; Hyperkalemia; Hypoglycemia; Hyponatremia; Hypotension; Renal Agents; Syndrome; Vasopressins; Water-Electrolyte Imbalance

The osmoregulation of arginine-8-vasopressin (AVP) was investigated in 14 patients with primary hypothyroidism, in 6 with Addison's disease, and in 21 with central diabetes insipidus (CDI). In the latter disease the effect of histamine stimulus was also evaluated. Plasma AVP was measured by radioimmunoassay (RIA). Patients with primary hypothyroidism were classified into subgroups with elevated or normal basal levels of plasma AVP. A decreased osmotic threshold was found in hypothyroid patients with augmented basal AVP levels. Patients with Addison's disease exhibited an increased basal level of plasma AVP and a decreased osmotic threshold. CDI patients according to their AVP responses on osmotic stimulus fell into two groups: CDI I gave no response at all, while CDI II responded subnormally. CDI II exhibited blunted AVP release to histamine. The AVP reactions of the CDI I patients fell into two subgroups: CDI I/A had undetectable plasma AVP, whereas histamine evoked AVP release in CDI I/B. Patients with CDI II suffer from a partial CDI, while those with CDI I/A represent a complete form of the disease and CDI I/B presumably have an osmoreceptor failure.

Topics: Addison Disease; Adult; Arginine; Diabetes Insipidus; Female; Humans; Hypothyroidism; Male; Middle Aged; Saline Solution, Hypertonic; Vasopressins; Water-Electrolyte Balance

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: Addison Disease; Ascites; Edema; Extracellular Space; Heart Failure; Humans; Hyponatremia; Intestinal Secretions; Kidney Failure, Chronic; Liver Cirrhosis; Potassium; Sodium; Vasopressins; Water-Electrolyte Balance

Topics: Addison Disease; Adrenal Cortex Hormones; Adrenal Glands; Adrenocorticotropic Hormone; Anti-Inflammatory Agents; Asthma; Corticotropin-Releasing Hormone; Facial Paralysis; Glucocorticoids; Granulomatosis with Polyangiitis; Hepatitis; Humans; Hypothalamus; Melanocyte-Stimulating Hormones; Myasthenia Gravis; Pituitary Gland; Pulmonary Edema; Retroperitoneal Fibrosis; Shock, Septic; Vasopressins

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: Addison Disease; Animals; Calcitonin; Glucocorticoids; Growth Hormone; Hormones; Humans; Hyperaldosteronism; Hyperparathyroidism; Hyperthyroidism; Hypoparathyroidism; Insulin; Intestinal Absorption; Magnesium; Parathyroid Hormone; Rats; Vasopressins; Vitamin D

Topics: Acromegaly; Addison Disease; Adult; Central Nervous System Diseases; Diabetes Insipidus; Humans; Hyperthyroidism; Hypothyroidism; Kidney; Lung Diseases; Male; Neoplasms; Pituitary Diseases; Thyroid Diseases; 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: Addison Disease; Child; Diabetes Mellitus, Type 1; Humans; Hyponatremia; Male; Natriuresis; Polyendocrinopathies, Autoimmune; Rhabdomyolysis; Vasopressins

Galanin is colocalized with adrenocorticotrophin (ACTH) in the human pituitary and with corticotrophin releasing hormone, arginine, vasopressin, and oxytocin in the hypothalamus. Galanin, vasopressin, and oxytocin influence the secretion of pituitary ACTH. The aim of this study was to investigate if the endogenous stimulation of ACTH release in Addison's disease was reflected in plasma galanin, vasopressin, and oxytocin. ACTH, galanin, vasopressin, and oxytocin were measured in plasma from 14 patients with Addison's disease, one patient with Nelson's syndrome, and 14 healthy controls. Eight patients had elevated plasma ACTH whereas six patients and all controls had ACTH levels within the reference-range. There was no difference in galanin or vasopressin between patients and controls or between samples with low or high ACTH concentrations. In contrast, oxytocin was higher in patients with elevated plasma ACTH compared to patients and controls with normal or low ACTH. No relation was found between galanin or oxytocin and age or sex. A tendency towards lower vasopressin with increasing age was found among the men (p=0.057). The highest ACTH and galanin levels were found in the patient with Nelson's syndrome. In conclusion, increased plasma ACTH was not reflected in elevated plasma galanin or vasopressin. In contrast, elevated ACTH levels were accompanied by higher oxytocin levels.

Topics: Addison Disease; Adrenocorticotropic Hormone; Adult; Aged; Aged, 80 and over; Case-Control Studies; Female; Galanin; Humans; Male; Middle Aged; Oxytocin; Vasopressins

Topics: Addison Disease; Adrenal Glands; Humans; Hyponatremia; Male; Middle Aged; Tuberculosis; 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

A 50-yr-old woman with Addison's disease from the age of 14 yr was diagnosed as empty sella turcica in 1974 (Rev Clin Esp 139: 183, 1975). She subsequently continued with hyperpigmentation in spite of adequate hormone substitution therapy which permitted her to lead a normal life. When studied she showed an extreme elevation of plasma ACTH (1500--2000 pg/ml), and with dexamethasone (2 and 8 mg/day) continued to have levels of 900 pg/ml. With 60 mg hydrocortisone daily, effects of overdosage were observed (swelling and Cushingoid facies) associated with depigmentation. However, she continued to manifest levels of plasma ACTH of 700 pg/ml and an absence of circadian rhythm. It seems likely that this patient represents a case of pituitary ACTH secretory adenoma (corticotropinoma) secondary to the preexisting Addison's disease. The circulating levels of other pituitary hormones were normal.

Topics: Addison Disease; Adenoma; Adrenocorticotropic Hormone; Adult; Dexamethasone; Female; Humans; Hydrocortisone; Male; Middle Aged; Pituitary Neoplasms; Somatostatin; Vasopressins

We report on two children with both Addison's disease and diabetes mellitus, a rare occurrence in children. One of the children first developed Addison's disease and later developed diabetes mellitus, while the other had the onset of diabetes mellitus first and later Addison's disease. In the latter patient a direct relationship was shown between the insulin dose and adrenal cortical hormone. Organ-specific antibody studies are reported and the diagnosis and management of these combined endocrinopathies are discussed.

Topics: Addison Disease; Adrenal Cortex; Adrenocorticotropic Hormone; Autoantibodies; Child; Diabetes Mellitus, Type 1; Female; Humans; Insulin; Male; Organ Specificity; Thyroid Gland; Vasopressins

Studies were designed to determine whether angiotensin II has a direct stimulatory effect on arginine-vasopressin in man and to determine the role, if any, played by angiotensin II in the control of vasopressin release in physiological and pathological conditions. Acute infusion of angiotensin II in normal volunteers produced small but definite increases in plasma levels of arginine-vasopressin (5-4+/-0-3(S.E.M.) to 6-4+/-0-2 pg/ml) only when plasma angiotensin II levels were supraphysiological. Concurrent measurements of plasma arginine-vasopressin and angiotensin II were made during acute changes in fluid balance and posture in normal volunteers and in clinical conditions characterized by high plasma levels of angiotensin II (Addison's disease and Bartter's syndrome). The results of these studies allow us to conclude that there is little to suggest a direct effect of angiotensin II which is likely to be relevant to the normal physiological control of arginine-vasopressin in man.

Topics: Addison Disease; Angiotensin II; Arginine Vasopressin; Bartter Syndrome; Gastrointestinal Hemorrhage; Humans; Male; Osmolar Concentration; Posture; 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

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

Topics: Addison Disease; Angiotensin II; Feedback; Humans; Hyperaldosteronism; Renin; Sodium; Vasopressins; Water-Electrolyte Balance

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: 17-Hydroxycorticosteroids; 17-Ketosteroids; Addison Disease; Adrenal Insufficiency; Humans; Vasopressins

Topics: Addison Disease; Adolescent; Adult; Blood Glucose; Diethylstilbestrol; Female; Growth Hormone; Humans; Hypopituitarism; Insulin; Male; Middle Aged; Physical Exertion; Pituitary Gland; Vasopressins

Trichloroacetic acid extracts of plasma were fractionated on a CG-50 resin column and the 50% acetic acid eluents chromatographed on silicic acid-impregnated glass paper in butanol-acetic acid-water. The specific arginine vasopressin (AVP) zone was eluted and assayed for antidiuretic activity in the diuretic rat. Thioglycolate inactivation was used to confirm AVP activity. Recovery of as little as 4 muU AVP per ml plasma ranged between 80 and 90%. In normal subjects after an overnight fast, plasma AVP ranged between 2.5 and 10.0 muU per ml. AVP secretion was inhibited by hemodilution and stimulated with nicotine and hypertonic saline. Plasma AVP was absent in patients with diabetes insipidus even after neurohypophyseal stimulation. Plasma AVP was abnormally elevated during mild dehydration and remained above the normal range despite hemodilution in patients with untreated adrenocortical insufficiency demonstrating a delayed water diuresis. Glucosteroid therapy lowered plasma AVP to normal in dehydrated patients. A normal diuretic response to hydration was accompanied by a fall in plasma AVP to zero in steroid-treated patients. These findings suggest that hypersecretion of AVP may play an important role in the abnormal water metabolism of adrenocortical insufficiency and that the glucosteroids promote normal water diuresis by inhibiting the secretion of AVP from the neurohypophysis.

Topics: Addison Disease; Adrenal Insufficiency; Adult; Animals; Arginine; Chromatography, Paper; Diuresis; Female; Glucose; Glycolates; Humans; Hydrocortisone; Hypopituitarism; Hypothalamo-Hypophyseal System; Male; Middle Aged; Nicotine; Rats; Sodium Chloride; Steroids; Thioglycolates; Trichloroacetic Acid; Vasopressins

Topics: Addison Disease; Adolescent; Adrenalectomy; Adult; Aldosterone; Creatine; Dextroamphetamine; Diabetes Insipidus; Edema; Ethanol; Female; Humans; Kidney Tubules; Middle Aged; Natriuresis; Posture; Spironolactone; 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: Addison Disease; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diuresis; Diuretics; Humans; Hyperglycemia; Kidney Tubules; Osmosis; Physiology; Polyuria; Syndrome; Vasopressins

Topics: Addison Disease; Adrenalectomy; Adrenocorticotropic Hormone; Aldosterone; Arginine Vasopressin; Blood Chemical Analysis; Creatine; Creatinine; Glucose; Humans; Natriuresis; Potassium; Sodium; Sodium, Dietary; Vasopressins; Water; Water-Electrolyte Balance

Topics: Addison Disease; Adrenal Cortex; Adrenal Insufficiency; Humans; Hypoadrenocorticism, Familial; Pituitary Gland; Pituitary Gland, Posterior; Vasopressins

Topics: Addison Disease; Adrenal Cortex; Adrenal Cortex Hormones; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Humans; Hydrocortisone; Vasopressins