Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 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 43 year old man with diabetes insipidus who showed panhypopituitarism and marked hypergammaglobulinemia due to histiocytosis X is reported. His low basal plasma adrenocorticotropin (ACTH) and growth hormone (GH) failed to respond to insulin-induced hypoglycemia. His basal serum thyroid hormone level was below normal and normal basal plasma thyrotropin (TSH) showed a delayed response with normal peak value to TSH-releasing hormone (TRH). Normal basal plasma pituitary gonadotropin also showed a delayed response with normal peak value to luteinizing hormone-releasing hormone (LH-RH). Suppression of plasma prolactin (PRL) by levodopa (l-dopa) was impaired and elevation of basal plasma PRL was noted at the second admission. These results, combined with diabetes insipidus, suggested that the panhypopituitarism in these patients was hypothalamic in origin. The polyclonal hypergammaglobulinemia was characterized by elevated serum IgG and IgE levels which returned to normal after corticosteroid treatment with concomitant clinical improvement. Elevated serum IgE levels, tissue and peripheral eosinophilia, and the effectiveness of corticosteroid therapy support the hypothesis that some allergic mechanism may be involved in the pathogenesis of this disease.
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PMID:A case of histiocytosis X associated with panhypopituitarism and hyperimmunoglobulinemia G and E. 22 67

A patient with a pituitary adenoma secreting adrenocorticotropin hormone manifested panhypopituitarism after an episode of pituitary apoplexy. The previously elevated urinary levels of 17-ketogenic steroids dropped sharply, and plasma cortisol became undetectable. The apoplexy also resulted in a partially empty sella on which the dorsum sellae collapsed. Recurrent Cushing's disease developed and was cured by transsphenoidal resection of a microadenoma.
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PMID:Cushing's disease with pituitary apoplexy leading to hypopituitarism, empty sella, and spontaneous fracture of the dorsum sellae. Case report. 22 16

A sensitive and specific radioimmunoassay for human beta-lipotropin (betah-LPH) in unextracted plasma was developed using pur betah-LPH as tracer and standard and an antiserum not cross-reacting with human beta-MSH and hACTH. In healthy volunteers plasma betah-LPH ranged from less than 20 to 150 pg/ml at 8:00 a.m. and rose after metyrapone administration. betah-LPH was very low in panhypopituitarism, normal in most patients with untreated Cushing's disease, elevated in acromegaly and extremely high in Nelson's syndrome.
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PMID:Radioimmunoassay of human beta-lipotropin in unextracted plasma. 92 35

The effect of acute administration of human growth hormone (HGH) and of alpha-melanocyte stimulating hormone (alpha-MSH) on plasma aldosterone, cortisol, corticosterone and growth hormone has been studied in normal man and in patients with panhypopituitarism. There is no acute effect of exogenous HGH on plasma levels of aldosterone, cortisol and corticosterone in normal man and in patients with panhypopituitarism. The plasma level of immunoreactive HGH measured during acute HGH infusion in man does not seem to be proportional to the dose administred in our study. Alpha-MSH raises the concentartion of plasma HGH, BYT THIS STIMULATION IS NOT DOSE-DEPENDENT. Aldosterone, cortisol and corticosterone concentrations are not influenced by the elevation of HGH mediated by alpha-MSH in normal man. Although in some patients with panhypopituitarism an elevation of plasma aldosterone concenntration following alpha-MSH infusion is observed, it is unlikely that MSH is directly involved in the acute regulation of aldosterone secretion in healthy subjects.
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PMID:Influence of acute administration of human growth hormone and alpha-MSH on plasma concentrations of aldosterone, cortisol, corticosterone and growth hormone in man. 117 3

We report here three patients with hypopituitarism accompanied by primary empty sella, whose first manifestations were various mental symptoms. Endocrine studies revealed that two patients showed panhypopituitarism and the other had isolated adrenocorticotropin (ACTH) deficiency. Although several different types of pituitary dysfunctions have been described in a mild form, empty sella is usually asymptomatic. Their first manifestations were mental symptoms; consciousness disturbance, psychomotor agitation, visual hallucination and delusion. Isolated ACTH deficiency is an uncommon disease which etiology is still undetermined. A case with isolated ACTH deficiency associated with an empty sella has been reported before. It is suggested that empty sella might have a role in pathogenesis of isolated ACTH deficiency. The empty sella was confirmed by metrizamide cisternography and magnetic resonance imaging (MRI). These imaging studies are good tools to disclose empty sella. Replacement with cortisone and levothyroxine resulted in an improvement in the mental symptoms in two patients with panhypopituitarism. No alteration was observed following cortisone administration in the patient with isolated ACTH deficiency. Delusion and visual hallucination in this patient poorly responded to treatment with neuroleptics.
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PMID:[Three patients with hypopituitarism accompanied by primary empty sella presenting mental symptoms]. 259 26

This survey deals with disorders caused by genetically disturbed function of the anterior pituitary gland. Genetic Dwarfism may be caused by isolated growth hormone deficiency (IGHD) or panpituitary diseases, such as congenital absence of the pituitary or familial panhypopituitarism. Genetic disturbances of isolated pituitary hormone secretion without dwarfism may occur as isolated gonadotropin deficiency (IGD), isolated luteinizing hormone deficiency ("fertile eunuch"), Kallmann syndrome (olfactogenital dysplasia), isolated thyrotropin deficiency (ITD) and isolated corticotropin deficiency (ICD). Pituitary dysfunction may also be associated with other genetic disease entities.
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PMID:Genetic disorders of the anterior pituitary gland. 300 77

One woman (patient 1), aged 27 years, and one man (patient 2), aged 26 years, had pituitary surgery for pituitary-dependent Cushing's syndrome. An adenoma was identified and removed in both patients. Persistence of hypercortisolism characterized the response of patient 2 to surgery; transient hypoadrenalism, the response of patient 1. Patient 1 subsequently underwent a relapse. At the second surgery (total hypophysectomy for both patients), hyperplasia was demonstrated in patient 1, and scattered nests of adrenocorticotropic hormone (ACTH)-secreting cells were demonstrated in patient 2. Postoperatively, Cushing's syndrome persisted in both patients. Inferior petrosal sampling for ACTH during corticotropin releasing hormone stimulation verified a pituitary source of ACTH in patient 1. A decrease in cortisol secretion following hypophysectomy and subsequent cure by pituitary irradiation constitutes the evidence for pituitary origin in patient 2. Dexamethasone suppression and corticotropin releasing hormone-stimulation tests consistently suggested a pituitary cause throughout the clinical course of both patients. Computed tomographic scans after hypophysectomy revealed postoperative changes only. In both patients, panhypopituitarism, except for cortisol and ACTH, followed hypophysectomy. It may be concluded that patients with diffuse pituitary ACTH hyperplasia cannot, at present, be identified preoperatively by conventional clinical testing. Surgery for such patients may not be the therapy of choice.
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PMID:Failure of hypophysectomy to correct pituitary-dependent Cushing's disease in two patients. 319 Mar 83

A patient developed reversible panhypopituitarism due to an adrenal adenoma causing Cushing's syndrome. After removal of the adrenal adenoma, thyroid-stimulating hormone, corticotropin, growth hormone, follicle-stimulating hormone, luteinizing hormone, and prolactin responses to various stimuli recovered completely. The reversible panhypopituitarism of this patient may have occurred at the level of the pituitary gland as a result of hypercortisolemia.
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PMID:Reversible panhypopituitarism due to Cushing's syndrome. 337 19

A 32-year-old woman had seizures and coma due to severe hypoglycemia (26 mg/dL) in the 32nd week of an otherwise uncomplicated pregnancy. She responded dramatically to the administration of cortisol. Initial endocrine evaluation disclosed prolactin (PRL), corticotropin, and thyrotropin (TSH) deficiencies. The patient recovered completely with cortisol and thyroid hormone therapy and was delivered of a healthy male child at term. Endocrine reevaluations one week and six months postpartum disclosed luteinizing hormone, follicle-stimulating hormone, growth hormone, PRL, corticotropin, and probable TSH deficiencies. The cause of this panhypopituitarism has not been determined. This case suggests that the appropriate initial treatment for spontaneous symptomatic hypoglycemia in pregnancy, while awaiting further endocrine evaluation, is the administration of cortisol.
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PMID:Spontaneous hypoglycemic seizures in pregnancy. A manifestation of panhypopituitarism. 669 58


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