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)

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.
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PMID:A sensitive bioassay for the determination of human plasma ACTH levels. 16 19

A 32-year-old man developed panhypopituitarism and diabetes insipidus shortly after sustaining a head injury. Hormonal investigation showed that basal prolactin levels were moderately elevated the first two years after the accident, but later returned to normal. There was no rise in prolactin after administration on chlorpromazine, and the response to thyrotropin-releasing hormone was attenuated. Basal luteinizing hormone and follicle-stimulating hormone levels were low and there was no change after administration of luteinizing-hormone-releasing hormone. There was also no growth hormone elevation following arginine infusion. On the other hand, there was a normal but delayed elevation of thyrotropin in response to thyrotropin-releasing hormone. Appropriate stimulation tests showed normal responsiveness of the thyroid, adrenals and testes. These findings are compatible with an injury to the pituitary stalk, damaging the neurohypophyseal tract and affecting the blood supply to the pituitary gland.
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PMID:Pituitary insufficiency following head injury. 35 6

Twelve patients (10 women and 2 men) with a primary empty sella turcica were studied. Endocrine function tests were performed as follows: growth hormone (GH) was measured after insulin-induced-hypoglycaemia, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) after LH-releasing hormone, thyrotrophin (TSH) and prolactin after thyrotrophin-releasing hormone; pituitary reserve of adrenocorticotrophin (ACTH) was determined by measurement of plasma cortisol after lysine-vasopressin and 11 deoxycortisol after metyrapone. Five of the patients (group A) had no endocrine disturbance. Seven patients (group B) had a hypothalamo-pituitary disorder. Two of them had panhypopituitarism which appeared in one case after meningoencephalitis and in the other after a severe cranial trauma. In two cases an amenorrhoea-galactorrhoea syndrome with increased prolactin level (68 and 230 ng/ml) led to a diagnosis of a prolactin producing adenoma, which was confirmed by surgery. Finally three cases of amenorrhoeagalactorrhoea, with normal prolactin level, and/or diabetes insipidus remained unexplained. However, no causal relationship could be demonstrated between the pituitary disturbance and the "empty sella". Primary empty sella turcica is therefore a neuroanatomical and neuroradiological entity with no endocrine implication. A pituitary disorder might suggest a microadenoma or an incidentally associated disease.
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PMID:The primary empty sella an endocrine study on 12 cases. 98 92

A 20-yr-old male was found to have diabetes insipidus is association with panhypopituitarism but without any focal neurological lesion being identified. He was initially treated with steroid supplements, the features of diabetes insipidus being controlled with a thiazide diuretic. Eighteen months later the patient lost thirst sensation and stopped treatment, subsequently being re-admitted with severe dehydration, oliguria and focal neurological signs. Further investigation, including brain biopsy, confirmed the presence of an atypical pinealoma which was considered inoperable. Measurements of plasma antidiuretic hormone (ADH) and angiotensin II (AII) concentrations during the severe dehydration showed very high levels of AII, but inappropriately low plasma ADH levels for the severity of dehydration. We consider that the evidence obtained from this case supports the view that the oliguria with hypertonic urine present during severe dehydration was due to a direct renal action of the very high AII levels, possibly supplemented by the residual ADH secretion.
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PMID:A case of hypopituitarism with diabetes insipidus and loss of thirst. Role of antidiuretic hormone and angiotensin II in the control of urine flow and osmolality. 117 97

We document a male infant with congenital panhypopituitarism as detected at birth, in whom the adenohypophysis was totally absent by magnetic resonance imaging and all the anterior pituitary hormones were undetectable. His neurohypophysis was, by contrast, identified ectopically at the median eminence and antidiuretic hormone was appropriately secreted.
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PMID:Isolated aplasia of the anterior pituitary as a cause of congenital panhypopituitarism. Case report. 181 46

Fourteen patients undergoing transsphenoidal extirpation of craniopharyngiomas or Rathke's cysts underwent endocrinological evaluation before and after surgery. One patient died during the procedure because of uncontrollable arterial bleeding. The other patients were followed for up to 16 years (average, 8.5 years). One patient had recurrence of tumor 12 years after surgery. Another patient, the only one operated on because of a recurrent craniopharyngioma after previous radiation therapy, died 2 years after the transsphenoidal operation. No patient recovered pituitary functions that had been lost before surgery. One patient, who had an isolated growth hormone deficiency, and another, who had panhypopituitarism with sustained antidiuretic hormone secretion, had no change postoperatively from their preoperative endocrine status. The other 11 patients lost pituitary function and required pharmacological replacement of one to four pituitary hormones.
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PMID:Results of transsphenoidal extirpation of craniopharyngiomas and Rathke's cysts. 201 Dec 23

As endogenous opiates are known to be involved in regulation of appetite, an obese patient with panhypopituitarism and frequent episodes of ravenous hunger was treated with the oral opiate antagonist naltrexone for 13 months. This resulted in loss of body weight and attacks of severe hunger. The increased serum prolactin concentration and the dose of vasopressin required for substitution could be reduced. Long-term application of opiate antagonists may be useful in related cases.
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PMID:Long-term opiate receptor antagonism in a patient with panhypopituitarism: effects on appetite, prolactin and demand for vasopressin. 204 62

A 64-year-old woman was admitted for evaluation of hyponatremia. She was maintained on hypertonic saline administration. Without this therapy, the serum Na concentration decreased progressively to 127 mEq/L and the plasma osmolality to 254 mOsm/Kg H2O, on Day 3. At that time, the concentration of antidiuretic hormone (ADH) was as high as 3.5 pg/ml. A skull radiogram revealed an enlarged sella turcica. Computed tomography (CT) revealed a low density in the sella, and magnetic resonance imaging revealed equal intensity of the sella turcica and the cerebrospinal fluid. A diagnosis of empty sella syndrome was made by metrizamide cisternography in conjunction with CT scanning. A diagnosis of panhypopituitarism was made by endocrine function tests. 123I-thyroidal uptake was 6% when her serum TSH was 10.9 microU/ml, suggesting that she might also have primary hypothyroidism. When this patient was given glucocorticoid before levothyroxine replacement, her serum Na concentration rose up to about 140 mEq/L and a normal relationship between her plasma ADH level (2.4 pg/ml) and plasma osmolality (281 mOsm/kg H2O) was restored. Therefore, it was suggested that ADH hypersecretion induced by the glucocorticoid deficiency might in part contribute to the development of hyponatremia. This is the case of primary empty syndrome associated with panhypopituitarism, in whom initial symptom was caused by hyponatremia.
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PMID:A case of hyponatremia in panhypopituitarism caused by the primary empty sella syndrome. 304 Mar 85

A 29-year-old woman with evidence of a craniopharyngioma and documented panhypopituitarism is described. Clinical and laboratory evaluation revealed deficiencies of follicle-stimulating hormone, luteinizing hormone, thyroid-stimulating hormone, growth hormone, prolactin, adrenocorticotropic hormone and antidiuretic hormone. Prompt release of several pituitary hormones was noticed after administration of the hypothalamic releasing hormones FSH/LH-RF and thyrotropin-releasing hormone, whereas insulin-induced hypoglycemia, levodopa, chlorpromazine and clomiphene citrate, all of which act at the level of the hypothalamus, did not alter basal pituitary secretion. The patient's height of 60 inches, despite panhypopituitarism, and the interpretation of the above data are discussed in the light of current concepts regarding the dynamics of the hypothalamic-hypophyseal system.
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PMID:Survival and growth in a woman with untreated hypothalamic panhypopituitarism of 21 years' duration. 437 Apr 18

A complete endocrinological exploration was performed in a 23 year old male patient who presented clinical signs of an acquired panhypopituitarism which appeared two months after a severe head trauma, in order to determine whether the deficit lay in the hypothalamus or in the pituitary. TSH had normal basal levels, but presented a delayed rise after TRH administration. PRL rose normally after TRH administration, but presented a blunted response to both metoclopramide and insulin tolerance test. Cortisol rose significatively after lysine vasopressin, but failed to rise during insulin hypoglycaemia. These results are consistent with a hypothalamic defect. Extensive endocrinological data are often lacking in the few similar cases reported in the literature. Prl and TSH were usually found to have normal basal levels while other pituitary hormones were profoundly lowered. This was interpretated as a pituitary defect with some intact areas of the anterior lobe. However, this may also suggest a hypothalamic defect which could have been assessed by mor discriminative tests.
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PMID:Panhypopituitarism secondary to head trauma: evidence for a hypothalamic origin of the deficit. 624 99


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