Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adrenocortical insufficiency causes difficulty in diagnosis and morbidity out of proportion to its rarity, because of the non-specific, multi-system nature of the clinical features. Most of these are due to cortisol deficiency. Prominent features are well-known ones such as weight loss and asthenia, and hypoglycaemia. Less prominent in recent accounts are those due to failure of cellular sodium export and to vasopressin excess, which are frequent and clinically significant. For this reason, the clinical features of isolated ACTH deficiency, isolated glucocorticoid deficiency and Addison's disease overlap greatly. In addition, cortisol deficiency has secondary endocrine effects, e.g. glucocorticoid-reversible hypothyroidism, hyperprolactinaemia and hypercalcaemia. Further overlap between the various steroid insufficiency syndromes occurs because of the association of various organ-specific autoimmune endocrinopathies with Addison's disease. Over 80% of Addison's disease is of the autoimmune type, though almost any systemic destructive process can cause similar steroid insufficiency. Demonstration of adrenal insufficiency requires various combinations of tetracosactrin adrenal stimulation tests, and hypoglycaemia or equivalent tests, if the cause is ACTH deficiency but the correct test can only be chosen to suit a firm clinical diagnosis. The treatment of adrenocortical insufficiency is described.
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PMID:Adrenocortical insufficiency. 300 80

The primary lesion site in isolated ACTH deficiency was studied in three patients by examining the responses of immunoreactive ACTH to insulin-induced hypoglycemia, lysine vasopressin, and synthetic ovine corticotropin-releasing hormone (CRH). In all patients, no significant changes in immunoreactive ACTH followed insulin-induced hypoglycemia or lysine vasopressin. Fifty micrograms (greater than or equal to 1 microgram/kg BW) of CRH administered as an iv bolus dose daily for 6 consecutive days elicited no significant increase in plasma immunoreactive ACTH, beta-lipotropin, or cortisol levels in all patients. Eight iv bolus injections of 0.63 microgram/kg BW CRH at 4-h intervals also failed to induce a significant response of immunoreactive ACTH to an iv bolus dose of 1 microgram/kg CRH at 36 h in one patient. In contrast, a single bolus dose of 50 micrograms CRH induced a response of plasma immunoreactive ACTH in a patient with Cushing's disease and a patient with Addison's disease. The present results suggest that the primary lesion of isolated ACTH deficiency is not the hypothalamus, but, rather, is located in pituitary ACTH-secreting cells.
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PMID:Responsiveness of hypophyseal-adrenocortical axis to repetitive administration of synthetic ovine corticotropin-releasing hormone in patients with isolated adrenocorticotropin deficiency. 301 17

A 65-year-old female with general malaise, anorexia and marked emaciation was studied by secretion stimulation tests on 6 anterior pituitary hormones. Only ACTH showed no response and the other 5 hormones responded normally. The basal value of antidiuretic hormone was normal. She was found to be suffered from primary hypothyroidism. Though neither antithyroid antibodies nor other autoantibodies were found, Hashimoto's thyroiditis was confirmed by a thyroid open biopsy. Neoplastic lesions of the hypophysis were ruled out by various X-ray and CT examinations of the sella turcica as well as the brain. The case was concluded to be isolated ACTH deficiency associated with Hashimoto's thyroiditis. The substitution therapy using small doses of adrenocortical hormone and thyroid hormone has kept her well and she has been living normally for these five years.
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PMID:Isolated ACTH deficiency associated with Hashimoto's thyroiditis: report of a case. 608 96

A 28 year old woman presented with symptoms and biochemical findings suggesting hypoglycemia. Detailed endocrine investigations indicated secondary adrenocortical insufficiency with no rise in plasma ACTH or plasma cortisol following insulin-induced hypoglycemia or vasopressin infusion. The adrenal glands however produced cortisol normally following prolonged stimulation with depot tetracosactrin. Other anterior pituitary hormones were released normally following appropriate stimulation tests. The literature on isolated ACTH deficiency is briefly reviewed, and this case represents one of the few reports in which the diagnosis has been substantiated by ACTH radioimmunoassays.
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PMID:Isolated ACTH deficiency confirmed by ACTH radioimmunoassay. 624 62

Isolated adrenocorticotropin (ACTH) deficiency is a rare cause of secondary adrenocortical insufficiency. This review summarizes the clinical and laboratory features of 39 previously reported cases plus 4 new patients. The clinical manifestations of isolated ACTH deficiency are variable, nonspecific and similar to those seen in adrenocortical insufficiency of any cause. The diagnosis of isolated ACTH deficiency due to intrinsic pituitary disease is made unequivocally when all the following criteria are met: 1) low basal urinary 17-hydroxycorticosteroid (17-OHCS) levels with or without low basal plasma cortisol, 2) low or normal basal plasma ACTH, 3) stimulation of cortisol, 17-OHCS or both during prolonged ACTH administration, 4) lack of 17-OHCS elevation in response to metyrapone and 5) normal secretory indices of other pituitary hormones. Isolated ACTH deficiency secondary to suprapituitary (e.g., hypothalamic) dysfunction is also based upon the above criteria, but, in addition, is associated with stimulation of cortisol and ACTH secretion following vasopressin administration.
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PMID:Isolated ACTH deficiency: a heterogeneous disorder. Critical review and report of four new cases. 627 46

In a 20-year-old woman, a complicated full-term delivery was followed by a 14-month history of galactorrhea, amenorrhea, and symptoms of hypocortisolism. Evaluation revealed the presence of an empty sella, hyperprolactinemia, and an isolated pituitary deficiency of ACTH, resulting in secondary adrenal insufficiency. The defect in ACTH secretion was apparently due to intrinsic pituitary rather than hypothalamic disease, because administration of lysine vasopressin did not stimulate ACTH release. An empty sella with hyperprolactinemia has been described before. However, to the authors' knowledge, isolated ACTH deficiency as a complication of postpartum hypopituitarism (atypical Sheehan's syndrome) in association with an empty sella and hyperprolactinemia has not previously been reported.
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PMID:Primary empty sella, hyperprolactinemia, and isolated ACTH deficiency after postpartum hemorrhage. 630 Dec 77

A 55 year old man with isolated ACTH deficiency is reported. The lesion would appear to be located in the pituitary gland since plasma ACTH and cortisol did not respond to lysine vasopressin and corticotrophin releasing factor (CRF). A fall in T4, a rise in basal values of TSH, prolactin (Prl), LH and FSH, excessive responses of TSH and Prl to TRH, and hyperreactive responses of LH and FSH to LRH were observed. These hormonal changes were examined before and after administration of cortisol. The abnormality in these hormones might be caused by deficiency of long-term glucocorticoid.
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PMID:Isolated ACTH deficiency accompanied by 'primary hypothyroidism' and hyperprolactinaemia. 631 88

A 64-year-old woman presented with recurrent episodes of confusion and nonspecific abdominal symptoms associated with hyponatraemia, which prompted a provisional diagnosis of the syndrome of inappropriate antidiuretic hormone secretion. Further investigation revealed evidence of hypocortisolaemia secondary to isolated adrenocorticotrophic hormone (ACTH) deficiency, which was successfully treated with steroid therapy. The clinical spectrum and aetiological associations of isolated ACTH deficiency are reviewed.
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PMID:Isolated adrenocorticotrophic hormone deficiency in the absence of polyglandular endocrinopathy. A case report. 632 Apr 78

A case of ACTH deficiency and partial GH deficiency associated with neurohypophyseal ectopy is described. A 42-year-old woman of short stature was admitted for hypoglycemic coma. The patient had hypocortisolemia, an increase in urinary 17-OHCS after consecutive injections of ACTH-Z, and a low plasma ACTH level which showed no response to corticotropin-releasing factor. This indicated the presence of ACTH deficiency. The plasma GH level showed a blunted response to insulin-induced hypoglycemia, but its response to GRF was preserved. Other hypothalamo-pituitary axes were intact. T1-weighted magnetic resonance imaging demonstrated ectopic neurohypophyseal tissue and a tiny anterior pituitary remnant. ACTH deficiency and partial GH deficiency might have developed as a consequence of pituitary stalk injury and inadequate regeneration of the anterior lobe.
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PMID:An adult case of neurohypophyseal ectopy presenting ACTH deficiency and partial GH deficiency. 759 3

We studied the incidence of postoperative hyponatremia in 91 consecutive patients (44 males and 47 females; age, 45 yr; range, 12-76) operated on transsphenoidally for pituitary tumors. A postoperative serum sodium concentration less than 135 mmol/L (the lowest, 109 mmol/L) was observed in 32 (35%) patients. Hyponatremia occurred most commonly in patients operated on for Cushing's disease (11 of 18 patients; 61%). Hyponatremia was symptomatic in 18 (56%) of the patients. Neither the size nor the operability of the tumor or transient postoperative polyuria predicted the development of hyponatremia. Hyponatremia was first observed on the sixth or seventh postoperative day. The patients were treated with water restriction and by increasing the hydrocortisone replacement dose in the case of ACTH deficiency, and recovery took place, on the average, within 5 days. High urinary osmolality and plasma arginine vasopressin concentration during hyponatremia in a subgroup of study patients with these measurements indicated that inappropriate vasopressin secretion was involved in the pathogenesis of hyponatremia. In conclusion, postoperative hyponatremia after transsphenoidal surgery is common and may put the patients at increased risk of severe hyponatremic symptoms. Therefore, all patients should be screened for serum electrolytes for 1 week after transsphenoidal surgery.
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PMID:Hyponatremia after transsphenoidal surgery for pituitary tumors. 796 34


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