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)

An 18-month old infant with Cushing's disease due to an ACTH producing pituitary tumor is presented. The case showed typical clinical and morphological sings of hypercortisolism. The infant died of pulmonary thromboembolism after transsphenoidal partial adenomectomy. The adrenals were diffusely hyperplastic. The pituitary adenoma was classified as an undifferentiated mucoid cell adenoma with sparse granulation by light microscopy. Immunoenzymatic studies demonstrated ACTH not only in granulated adenoma cells. Ultrastructurally the cells were only differentiated as typical ACTH cells or so-called follicular cells in small areas. Most of them were undifferentiated, showing pleomorphism of the relatively sparse organelles. In-vitro experiments using suspensions of adenoma cells showed a distinct enhancement of ACTH secretion after arginine-vasopressin and a further decrease ultrastructurally in the number of secretory granules. No effect of ACTH levels and no alterations of the ultrastructure were observed after cortisol. The case is representative of typical hypothalamic-hypophyseal Cushing's disease with an undifferentiated pituitary adenoma secreting ACTH in part autonomously. This constellation of Cushing's syndrome is extremely rare at the age of one year. Our case is the second one reported in the literature.
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PMID:ACTH secreting pituitary adenoma in an infant of 18 months. Immunohistochemical, electron-microscopic, and in-vitro studies. 627 57

The effect of D-Ala2, MePhe4, Met-(0)enkephalinol (Sandoz FK 33-824; 0.5 mg, im) on pituitary hormone secretion was studied in 11 patients with Addison's disease and 11 patients with ACTH-dependent Cushing's disease. In patients with Addison's disease, a pronounced fall of plasma ACTH levels was observed (P less than 0.005). The ACTH response to FK 33--824 was partially reversed by naloxone (4 mg, iv). In patients with Cushing's disease, no unequivocal decrease in either ACTH or cortisol was seen. Moreover, FK 33--824 failed to influence the vasopressin-induced ACTH increase in 5 patients with Cushing's disease. In patients with cortisol deficiency due to either Addison's disease or bilateral adrenalectomy for Cushing's disease, FK 33--824 led to increases in PRL and GH similar to those described in normal subjects. However, in the presence of longstanding hypercortisolism, the PRL increase was significantly diminished, and the GH response to FK 33--824 was completely abolished. Our results suggest that in Addison's disease ACTH release is influenced by inhibitory opiate receptors. In patients with Cushing's disease, ACTH secretion is insensitive to FK 33-284, presumably because of an autonomous pituitary adenoma or hypothalamic derangement. The impairment of the PRL and GH responses to FK 33--824 in Cushing's syndrome seems to reflect a direct action of the elevated cortisol level, for it is not seen after bilateral adrenalectomy.
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PMID:Effects of a met-enkephalin analog on adrenocorticotropin (ACTH), growth hormone, and prolactin in patients with ACTH hypersecretion. 628 Dec 97

Neuron-specific enolase (NSE) was localized, using the immunoperoxidase technique, in the cytoplasm of the five adenohypophyseal hormone-secreting cell types, and in nerve fibers of the pars nervosa of the human pituitary. Crooke's hyaline material was negative. Neuron-specific enolase was found in all pituitary adenoma types; there was no correlation between degree of granularity or differentiation of tumor cells and intensity of NSE immunopositivity. One hypothalamic hamartoma was positive for NSE; a craniopharyngioma and a neurohypophyseal granular cell tumor were not. Neuron-specific enolase was present in peptide hormone-producing endocrine cells outside the pituitary and in their tumors; the majority of other tumors were negative for NSE, although one breast carcinoma, one ovarian cystadenocarcinoma, and one lymphoma were positive for NSE. In control studies, absorption of NSE antisera with growth hormone abolished immunoreactivity; there was no immunologic cross-reaction demonstrable by radioimmunoassay.
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PMID:Immunohistochemical localization of neuron-specific enolase in the human hypophysis and pituitary adenomas. 636 13

Methionine-enkephalin-like substance was measured in CSF by the radioreceptor-assay established by Furui et al. Samples were obtained from preoperative 20 cases, in which were included 11 cases of pituitary adenoma, 3 cases of craniopharyngioma, 2 cases of pseudtumor cerebri and 4 normal cases, by lumbar puncture. Also postoperative measurement of this substance and pre- and postoperative measurement of ACTH in plasma were performed in 5 cases of Cushing's disease. Five ml of CSF was chromatograpied on two successive columns, lyophilized and assayed for opiate receptor affinity against 3H-dihydromorphine. Measured values were expressed as methionine-enkaphalin equivalents using the displacement curve run in parellel. Methionine-enkephalin-like substance level ranged from less than 0.5 to 20.0 pmoles/ml in all cases and mean value was 2.6 pmoles/ml (+/- 1.0 S.E.) in normal subjects. In Cushing's disease the level was not elevated preoperatively (2.1 +/- 0.3) and did not significantly decrease postoperatively (1.6 +/- 0.4 pmoles/ml) in contrast to the decrease of ACTH in plasma. It is suggested that methionine-enkephalin-like substance in CSF is not derived from ACTH producing cells of pituitary gland. One case of craniopharyngioma showed very high value. This case revealed diabetes insipidus at sampling. The possibility of participation of methionine-enkephalin in secretion of antidiuretic hormone was discussed.
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PMID:[Measurement of methionine-enkephalin-like substance in CSF from normal subjects and patients with pituitary adenoma (author's transl)]. 737 Jan 37

A case of choristoma of the posterior lobe of the pituitary is presented. The clinical presentation suggested chromophobe pituitary adenoma and the true diagnosis was only established on histological esamination. Despite the patient's advanced age her-operative course was satisfactory, but the disturbances of endocrine and visual function remained virtually unchanged. Perusal of the literature shows that this is the twentieth case of suprasellar or neurohypophyseal choristoma so far published. It provides an opportunity to review the clinical presentation, radiology and treatment, as well as to discuss the histiogenesis and nature of this rare pituitary tumor.
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PMID:Suprasellar choristoma. 746 79

Hyponatremia, usually attributed to the syndrome of inappropriate secretion of antidiuretic hormone, typically occurs in a delayed fashion following transsphenoidal removal of a pituitary adenoma. In a series of 99 consecutive patients who underwent transsphenoidal surgery for pituitary adenoma, nine patients developed delayed hyponatremia, seven of whom were symptomatic. Of these seven patients, four had been discharged from the hospital and required readmission on postoperative Day 7 to 9. In the nine patients who developed hyponatremia, on the average, serum sodium levels began to fall on Day 4 and reached a nadir on Day 7 (mean serum sodium nadir 123 mmol/L). The development of delayed hyponatremia was associated with the presence of a macroadenoma in eight of the nine patients. Seven of the nine patients had serum sodium levels less than 130 mmol/L and required treatment. One patient was treated with fluid restriction alone and six were treated with both fluid restriction and intravenous urea therapy. Twenty-four and 48 hours after urea administration, serum sodium levels rose by an average of 6 and 10 mmol/L, respectively, and at discharge, levels averaged 136 mmol/L. Intravenous administration of urea provides a rapid yet safe means of correcting symptomatic hyponatremia when fluid restriction alone is inadequate. In this article, the authors discuss the pathogenesis of delayed hyponatremia.
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PMID:Delayed hyponatremia after transsphenoidal surgery for pituitary adenoma. Report of nine cases. 889 58

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.
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PMID:Isolated hyponatremia after transsphenoidal pituitary surgery. 782 44

Cushing's syndrome occurs rarely; in analyzing 50 cases studied at our institution we discuss the following aspects: syndromatic diagnosis, etiologic differentiation into the 3 categories of the syndrome, and therapeutic strategies for each variety. We postulate that non-endocrinologists should be responsible for the syndromatic diagnosis, easily done by using 2 simple tools: the measurement of basal free urinary cortisol and the performance of an overnight suppression of the adrenal axis with 1 mg of dexamethasone (Nugent's test). In contrast, the etiologic diagnosis and the therapeutic interventions should be strictly restricted to highly specialized institutions having well seasoned endocrinologists, a reliable endocrine laboratory, easy access to computed tomographies of the brain and abdomen as well as to nuclear resonance imaging of the brain. The usefulness of our in-house devised vasopressin challenge following overnight dexamethasone suppression for the etiologic diagnosis is highlighted. Neurosurgical expertise in the transsphenoidal approach to the pituitary gland as well surgeons well experienced in adrenal surgery are a must to offer a reasonable chance of success to patients with the syndrome. Forty one (82%) of the series were female patients, 78% were pituitary-dependent and 22% pituitary-independent Cushings. Six out of 8 (75%) of the adrenal tumors were carcinomas. Only 3 patients (6%) qualified as ectopic ACTH syndromes. The easiest variety to diagnose and treat was the adrenal adenoma (2 cases); adrenal carcinomas were always incurable. The ectopic ACTH syndrome was amenable to successful medical treatment with ketoconazole or surgical resolution with complete resection of the offending tumor (1 of 3 cases) or bilateral adrenalectomy (2 of 3 cases) Pituitary-dependent Cushings are quite tricky to diagnose and difficult to treat. Transsphenoidal resection of the offending microadenoma was successful in only 43.5% (10/23) of cases and we experienced 3 recurrences of the syndrome even after 8 years of successful removal of the pituitary adenoma. The remainder had to be cured by bilateral adrenalectomy. Seven out of 39 patients with Cushing's disease (18%) ultimately died for a variety of reasons; six out of 6 patients (100%) with adrenal carcinoma died of dissemination; two out of 2 adrenal adenomas cured and 1 out of the 3 ectopic ACTH syndromes died of dissemination of a malignant thymic carcinoma. We conclude that Cushing's syndrome is a serious, underdiagnosed disorder, which should be suspected and diagnosed by the non specialized physician and then referred to a specialized center for expert etiologic diagnosis and surgical therapy.
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PMID:[Cushing's syndrome: review of a national caseload]. 852 77

Hyponatremia is rarely reported as a delayed complication of transsphenoidal resection of pituitary adenoma. Usually attributed to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), hyponatremia causes nonspecific symptoms, often after hospital discharge. To clarify the frequency, presentation, and outcome of this poorly understood complication, we reviewed our database of 2297 patients who underwent transsphenoidal pituitary surgery between February 1971 and June 1993. Of 53 patients (2.3%) treated for symptomatic hyponatremia, 11 were excluded (2 received arginine vasopressin within 24 hours, 1 had untreated hypothyroidism, 4 had untreated adrenal insufficiency, and 4 had incomplete records). The remaining 42 patients (1.8%), 11 men and 31 women aged 21 to 79 years, presented 4 to 13 days (mean, 8 d) postoperatively with nausea and vomiting (20 patients), headache (18 patients), malaise (12 patients), dizziness (4 patients), anorexia (2 patients), and seizures (1 patient). Hyponatremia was unrelated to sex, age, adenoma type, tumor size, or glucocorticoid tapering. Although the clinical picture in our patients is consistent with SIADH, this was not supported by the antidiuretic hormone levels, which were normal or low-normal in the two patients in whom they were measured, suggesting the possibility that low serum sodium may not reflect SIADH. In all patients, hyponatremia resolved within 6 days (mean, 2 d); treatment consisted of salt replacement and mild fluid restriction in 37 patients and fluid restriction only in 4 (treatment unknown in 1). Delayed hyponatremia after transsphenoidal resection of pituitary adenoma is not as rare as previously thought, nor is it necessarily associated with SIADH or with hypoadrenalism during glucocorticoid tapering.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Delayed onset of hyponatremia after transsphenoidal surgery for pituitary adenomas. 855 92

Diabetes insipidus (DI) is an uncommon but important complication in the neurosurgical population. This retrospective study aimed to determine the incidence, profile and outcome of patients admitted to an 18-bedded neurosurgical intensive care unit who developed DI. The overall incidence was 3.7% (29/792 admissions). Aetiologies included subarachnoid haemorrhage (12/29), severe head injury (11/29), post-surgical excision of craniopharyngioma or pituitary adenoma (5/29) and acute haemorrhagic stroke (1/29). All patients were treated with a regime of fluid replacement, electrolyte correction, parenteral or intranasal desmopressin (DDAVP), or parenteral pitressin. Overall mortality was 72.4%. There were no deaths in the patients who underwent excision of tumours. Complications included acute pulmonary oedema, hypernatremia and hypokalaemia. The development of DI was found to be associated with impending brain death and mortality in the majority of patients with subarachnoid haemorrhage and severe head injury. However, careful diagnosis and management of DI after hypothalamo-neurohypophyseal surgery did not result in any permanent neurological sequelae.
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PMID:Diabetes insipidus in neurosurgical patients. 977 76


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