Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Synthetic ovine corticotropin-releasing factor (o-CRF) stimulated adrenocorticotropin (ACTH) release at the concentration of 10(-10) M or more in monolayer culture of rat anterior pituitary cells. Dexamethasone, 10(-7) M, inhibited this effect. In 5 healthy human subjects, o-CRF, 1 microgram/kg iv bolus, increased plasma ACTH levels from less than 10 pg/ml to 40.4 +/- 11.0 (mean +/- SD) after 30-60 min, and plasma cortisol from 12.8 +/- 2.8 micrograms/dl to 23.6 +/- 3.1 after 45-60 min. Of 7 patients with Cushing's disease (CD), five showed an exaggerated response of plasma ACTH and cortisol, one an exaggerated response of plasma ACTH but low response of plasma cortisol and the other no response of both hormones. The significant positive correlation between the inhibition of plasma cortisol by dexamethasone and the response of plasma ACTH and cortisol to o-CRF in CD was seen. No response of plasma ACTH and cortisol to o-CRF was seen in each one patient with Cushing's syndrome due to an adrenocortical adenoma, ectopic ACTH syndrome (but low response at retesting), isolated ACTH deficiency and Sheehan's syndrome. In one patient with Addison's disease an exaggerated response of plasma ACTH but no response of plasma cortisol was seen. In 4 of 5 healthy subjects and 5 of 7 patients with CD, plasma ACTH and cortisol levels showed a second peak at 120--210 min after o-CRF administration. To clarify the prolonged effect of o-CRF in human in vivo, the disappearance rates of injected o-CRF were evaluated by radioimmunoassay in 3 patients with cured Cushing's syndrome. A biexponential decay curve showed t1/2 values of 9.3 +/- 0.4 min and 79.6 +/- 0.7 min (mean +/- SE). From the chromatographic profile, a portion of injected o-CRF was thought to be bound to macromolecule (s). o-CRF, as a specific secretagogue of ACTH, is thought to be useful tool in evaluating patients with hypothalamo-pituitary-adrenal disorders.
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PMID:[Studies for clinical application of ovine corticotropin-releasing factor]. 298 91

A sensitive assay method for pituitary cell antibodies (PitCA) was established by a biotin/avidin system using rat pituitary. Results in 24 cases out of 81 insulin-dependent diabetic patients and 10 cases of 21 adrenocorticotropic hormone (ACTH) deficient patients were positive for autoantibodies to anterior pituitary cell cytoplasm. PitCA observed in the sera of insulin-dependent diabetic patients were suspected of being pituitary specific and independent with islet cell antibodies (ICA) and islet cell surface antibodies (ICSA). In the sera of ACTH deficient patients, PitCA were frequently absorbed with liver acetone powder. Populations of insulin-dependent diabetes mellitus (IDDM) are almost equal in males and females. A total of 16 cases out of 21 ACTH deficient patients were female. These results suggest that heterogenous PitCA are involved in the sera of those patients with IDDM and ACTH deficiency.
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PMID:Heterogeneity of anterior pituitary cell antibodies detected in insulin-dependent diabetes mellitus and adrenocorticotropic hormone deficiency. 301 44

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

Autoantibodies for anterior pituitary cell surface membrane (PitCSA) were assayed by immunofluorescence method using GH3 cells (rat GH and prolactin secreting cell) and AtT-20 cells (mouse adrenocorticotropic hormone secreting cell) as antigens. Out of 18 insulin dependent diabetic patients who were positive for antibodies to islet cell surface membrane (ICSA), 3 cases (16.7%) were positive for antibodies to GH3 cells and 12 cases (66.7%) were positive for antibodies to AtT-20 cells. Moreover, out of 18 insulin dependent diabetic patients who were negative for ICSA, 2 (11.1%) and 6 cases (33.3%) were positive for antibodies to GH3 cells and AtT-20 cells, respectively. Among 5 adrenocorticotropic hormone (ACTH) deficient patients, all of the sera were positive for antibodies to AtT-20 cells. These results suggested that PitCSA and ICSA have independent features, though both are closely related, and that PitCSA was one of the significant immunological markers often observed in the sera of the patients with insulin dependent diabetes mellitus (IDDM) and ACTH deficiency.
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PMID:Detection of antibodies to anterior pituitary cell surface membrane with insulin dependent diabetes mellitus and adrenocorticotropic hormone deficiency. 303 74

A 58-yr-old woman had frequent hypoglycemic attacks, undetectable levels of plasma cortisol, ACTH, and beta-lipotropin, and deficient responses of these hormones after insulin induced-hypoglycemia and metyrapone. Her GH responses to arginine infusion were normal as were her gonadotropin responses to LRH. Her TSH and PRL responses to TRH were abnormally high. Anaphylactic shock occurred after the injection of either synthetic ACTH-Z-(1-24) (Cortrosin-Z) or ACTH-(1-18) (Acthormone). She had received two prior injections of synthetic ACTH-Z-(1-24) 2 months earlier. Circulating anti-ACTH antibody was found in her plasma by radioimmunological methods, but this antibody did not prevent corticosterone production by ACTH in an in vitro ACTH bioassay system. The pathogenic significance of this antibody in the ACTH deficiency is doubtful, and the etiology of the isolated ACTH and beta-LPH deficiency is not clear.
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PMID:Anaphylactic shock after synthetic adrenocorticotropin-(1-18) in a patient with isolated adrenocorticotropin and beta-lipotropin deficiency. 625 32

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

A dose of 1.5 micrograms/kg of MCI-028, human corticotropin-releasing hormone (hCRH), was administered intravenously to 38 children with non-endocrine short stature with normal function in the hypothalamo-pituitary-adrenocortical axis and to 71 children with a disorder in the same axis. Blood levels of adrenocorticotropic hormone (ACTH) and cortisol were determined to evaluate the axis. The 95% confidence limits of peak responses of ACTH and cortisol in non-endocrine short stature were between 17.2 and 135.3 pg/ml, and between 13.1 and 35.6 micrograms/dl, respectively, and were used as standards for children. When compared with these standards, the hormonal responses in children with various disorders in the hypothalamo-pituitary-adrenocortical axis were as follows: in two children with Cushing's syndrome caused by adrenal tumor, ACTH values were decreased and were not responsive to hCRH, while cortisol values, though within the normal limit, were not responsive; in children with primary adrenal insufficiency or congenital adrenal hyperplasia, cortisol values were decreased and not responsive, whereas ACTH values tended to be increased and ACTH response high except for 21 alpha-hydroxylase deficiency of congenital adrenal hyperplasia. In two cases of pituitary dwarfism complicated with ACTH deficiency, both ACTH and cortisol values were decreased and poorly responsive; and in children who were receiving glucocorticoid, both ACTH and cortisol values tended to be decreased and to respond poorly to hCRH. As for side effects, hot flushing was observed among 8.0% of the subjects after administration of hCRH. But this symptom was not severe and no other side effects of clinical importance were observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of hypothalamo-pituitary-adrenocortical function in children by human corticotropin-releasing hormone (MCI-028) test. 795 24

To assess the diagnostic usefulness of a synthetic human corticotropin-releasing hormone (CRH) formulation (Code No. MCI-028), we administered 100 micrograms of the peptide intravenously to 183 patients with hypothalamo-pituitary-adrenocortical (HPA) disorders, and obtained the following findings. Among the 183 patients, data from 125 patients were suitable for analyzing the effects of the test. In patients with Cushing's disease, high plasma adrenocorticotropic hormone (ACTH) and cortisol levels increased further in response to MCI-028, while in patients with adrenal Cushing's syndrome, low ACTH and high cortisol values remained unchanged. In patients with pituitary-type hypopituitarism or isolated ACTH deficiency, low ACTH and cortisol levels responded poorly or insignificantly to MCI-028, whereas those with hypothalamic hypopituitarism showed delayed and considerable degree of responses of plasma ACTH and little increase in plasma cortisol levels. In Addison's disease, high plasma ACTH increased further in response to MCI-028, but low cortisol levels did not change. In patients with Cushing's syndrome soon after successful surgical treatment, plasma ACTH responsiveness was low or different depending on the clinical course of the patient. Patients treated with high doses of glucocorticoids for non-endocrine diseases tended to show impaired ACTH and cortisol responsiveness to MCI-028. Side effects, including the transient flushing which was observed most frequently in this study, did not cause any clinical problems.
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PMID:Human corticotropin-releasing hormone test in patients with hypothalamo-pituitary-adrenocortical disorders. 795 26

We compared the responses of ACTH and cortisol (F) to corticotropin-releasing hormone (CRH) administration (ovine 1 microgram/kg i.v. bolus) with the responses of urinary 17-OH corticosteroids (17-OHCS) and serum deoxycorticosterone (DOC) to metyrapone administration (450 mg/m2/dose every 4 h x seven doses) in 16 hypopituitary patients. Glucocorticoid therapy for these patients was withheld for a minimum of 3 wk before testing. The CRH test was performed 3 d before or 3 wk after the metyrapone test was used to diagnose the ACTH reserve status. In nine ACTH-intact hypopituitary patients (post-metyrapone 17-OHCS > 12.2 mumol/m2/d; DOC > or = 11.5 nmol/L), the peak F (497-773 nmol/L) and ACTH (5.2-22 pmol/L) responses to CRH stimulation were similar to those of normal subjects (F peak = 554-993 nmol/L and ACTH peak = 6-25 pmol/L at 15-60 min). In one patient with partial ACTH deficiency (postmetyrapone 17-OHCS = 10.5 mumol/m2/d; DOC = 6 nmol/L), the peak F response was low and delayed (246 nmol/L at 180 min) and the peak ACTH response was normal (7 pmol/L). Six severely ACTH-deficient patients (postmetyrapone 17-OHCS < 5.4 mumol/m2/d; DOC < or = 3.4 nmol/L) had a low F response at 15-90 min in all, with a delayed rise in three at 120-180 min in response to CRH administration, whereas ACTH responses were variable: absent or low, normal, delayed, or persistently exaggerated. In conclusion, the CRH-stimulated F response pattern in hypopituitary patients was comparable to the urinary 17-OHCS and serum DOC response to metyrapone administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of adrenocorticotropin and adrenal steroid responses to corticotropin-releasing hormone versus metyrapone testing in patients with hypopituitarism. 797 Sep 37

The pro-opiomelanocortin (POMC) gene encodes adrenocorticotrophin (ACTH) which is derived from precursors by proteolytic cleavage. Congenital, isolated ACTH deficiency is rare but may be familial and fatal. The aetiology is unknown though defects at both hypothalamus and adenohypophysis have been postulated. We have studied a female presenting with hypoglycaemia in the neonatal period. When studied at 6 weeks of age, ACTH was unmeasurable even after injection of corticotrophin releasing hormone (CRH1-41). ACTH precursors, quantitated by two-site immunoradiometric assay, were clearly measurable prior to treatment and were stimulated by CRH1-41 and suppressed by glucocorticoid administration. Concentrations of POMC, N-terminal pro-opiocortin (N-POC) and beta-endorphin (beta-EP) were within the normal adult range during glucocorticoid replacement therapy; ACTH and beta-lipotrophin remained undetectable. The secretion of glucagon, measured by radioimmunoassay, in response to hypoglycaemia was normal. By sequencing polymerase chain reaction products from the patient's genomic DNA, the entire coding region of the POMC gene was established to be normal. The results are compatible with a cleavage enzyme defect.
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PMID:Isolated congenital ACTH deficiency: a cleavage enzyme defect? 822 2


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