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)

In vivo and in vitro studies were carried out in a 37-year old female with cyclical Cushing's disease. Preoperative studies revealed periodic secretions of urinary corticosteroids occurring with a cyclicity of 2-3 weeks. On transsphenoidal surgery, a microadenoma was visualized in the anteroinferior portion of the anterior pituitary. Gel filtration analyses of the adenoma and surrounding tissues revealed increased concentrations of beta-endorphin and an activated conversion of beta-lipotropin to beta-endorphin in the adenoma compared with the surrounding tissues. These findings were in agreement with the characteristics previously reported for corticotroph adenomas. However, unexpectedly, concentrations of ACTH and beta-lipotropin in the adenoma were only slightly higher than those in the surrounding tissues. Precise mechanisms underlying this unusual finding were elusive, but it may have been due to the periodic nature of her hypercortisolism. In addition, this patient was reproducibly responsive to bromocriptine (2.5 mg, per os) with a reduction of the plasma cortisol level. Although this may suggest an intermediate lobe subtype of Cushing's disease as proposed by Lamberts' group, our case did not have any other characteristic suggestive of this proposed variant. However, it is tempting to speculate that cyclical changes in the central dopaminergic tone may have been at least a partial trigger for the periodic hormonogenesis in this patient.
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PMID:In vivo and in vitro studies in a patient with cyclical Cushing's disease showing some responsiveness to bromocriptine. 166 81

Eight surgical and one autopsy specimen of pituitary adenomas (six cases of Cushing's disease, two of Nelson's syndrome, and one of hypopituitarism) were studied by histochemical, immunohistocytological, and ultrastructural methods. Eight tumors showed the characteristic histochemical profile of corticotroph adenoma--amphophilic to basophilic, and periodic acid-Schiff-positive to some extent. In all tumors, immunohistochemical studies revealed adrenocorticotropic hormone (ACTH) and alpha-subunit in the cytoplasm of some adenoma cells. By electron microscopy, seven tumors were found to be monomorphous; six were typical corticotroph adenomas and one was a subtype II silent corticotroph adenoma. One unique lesion was bimorphous--i.e., composed of corticotrophs as well as cells resembling glycoprotein cells. Immunoelectron microscopy by the double-labeling immunogold technique, performed on one corticotroph adenoma, demonstrated the presence of ACTH and alpha-subunit not only within the same adenoma cells but also within the same secretory granules. The cytogenesis of ACTH alpha-subunit tumors, a rare form of plurihormonal adenoma, remains to be elucidated. The duration of disease associated with these tumors exceeded the duration in patients with ordinary corticotroph adenomas. Given the low frequency with which increases in serum alpha-subunit are detectable in patients with such tumors--13% in this series--hormone production is not recognized at preoperative evaluation.
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PMID:Pituitary adenomas that produce adrenocorticotropic hormone and alpha-subunit: clinicopathological, immunohistochemical, ultrastructural, and immunoelectron microscopic studies in nine cases. 169 Aug 66

Bilateral, selective, and simultaneous catheterization of the inferior petrosal sinus is not only a valuable tool in the differential diagnosis of Cushing's syndrome, but may also provide new insights into paracrine interactions at the pituitary level. We have investigated whether CRH (1 microgram/kg BW) has any effect on the release of PRL, GH, TSH, or the alpha-subunit of hCG during this procedure. Sixteen patients under evaluation for Cushing's syndrome (Cushing's disease, n = 12; ectopic ACTH syndrome, n = 2; glucocorticoid resistance, n = 1; hormonally inactive adenoma, n = 1) were catheterized. Two of the patients with Cushing's disease received 4.0 mg naloxone iv 15 min before stimulation with CRH. Patients with Cushing's disease demonstrated a central/peripheral gradient and an intersinus gradient not only for ACTH, but also for PRL, alpha-subunit, GH, and TSH, provided that the latter two hormones were not completely suppressed by the glucocorticoid excess. Moreover, all hormones increased in response to CRH on the side with the highest ACTH concentration; PRL rose from 31.2 +/- 6.4 to 61.6 +/- 12.4 micrograms/L (P less than 0.01), and alpha-subunit from 2.6 +/- 0.6 to 6.4 +/- 1.7 micrograms/L, (P less than 0.01). Naloxone was unable to abolish the PRL or alpha-subunit increase in response to CRH. A multihormonal response to CRH in inferior petrosal sinus blood was also observed in the patient with glucocorticoid resistance and in the patient with the hormonally inactive tumor, but not in the patients with ectopic ACTH secretion. The multihormonal response to CRH could be explained by cosecretion of other hormones together with ACTH from corticotroph adenoma, by an effect of CRH on pituitary blood flow, or by a paracrine action of pituitary corticotrophs on adjacent normal pituitary cells. Our results do not support the concept that such a paracrine action is mediated by beta-endorphin. However, a higher dose of naloxone may be required to antagonize the action of pituitary beta-endorphin.
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PMID:A multihormonal response to corticotropin-releasing hormone in inferior petrosal sinus blood of patients with Cushing's disease. 169 62

Bilateral simultaneous blood samples were taken from the inferior petrosal sinuses of nine patients with Cushing's disease for measurement of adrenocorticotropin (ACTH), vasopressin (AVP), prolactin, growth hormone, luteinising hormone (LH), and follicle stimulating hormone (FSH). Inter-sinus gradients for ACTH (range 3.3-18.2) and AVP (2.0-375) correctly lateralised the microadenoma in seven of these patients. One additional patient showed an increased gradient for AVP but not ACTH on the side of the tumour. The correlation between the AVP and ACTH concentrations in the petrosal sinus draining the microadenoma was significant. Petrosal sinus plasma concentrations of prolactin and growth hormone were also significantly higher on the side of the tumour than on the non-tumour side. Evidence against a non-specific tumour effect on the secretion of all pituitary hormones was the fact that in most cases the gradients for LH and FSH were not significant. It is proposed that increased delivery of AVP to part of the pituitary may result from an aberrant blood supply, and that AVP may interact with corticotropin releasing factor to promote tumour growth and ACTH release.
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PMID:Arginine vasopressin in Cushing's disease. 197 Jan 7

Although somatostatin inhibits a variety of pituitary and non-pituitary hormones, not univocal data on its effects on ACTH release have been reported so far. In this study we investigated the effects of somatostatin or octreotide on ACTH levels of patients with corticotropin hypersecretion: 7 patients with Addison's disease, 2 patients previously adrenalectomized for Cushing's disease, 4 patients with Cushing's disease and 3 patients with ectopic ACTH syndrome. Plasma ACTH and cortisol levels were determined after somatostatin (500 micrograms over 60 min) infusion or octreotide (100 micrograms sc) injection. In 5 other patients with Cushing's disease ACTH and cortisol responses to CRH (1 microgram/kg iv) were evaluated in basal conditions and after octreotide acute administration. In no patients with Addison's disease any inhibitory influence of somatostatin (delta % = -21, -25) or octreotide (delta % = -38 +/- 12 vs -39 +/- 12 after saline) on plasma ACTH was found. Somatostatin did not significantly inhibit plasma ACTH in the two patients previously adrenalectomized for Cushing's disease and in 3 patients with Cushing's syndrome; in other 4 patients with Cushing's syndrome octreotide did not affect plasma ACTH levels. In 5 patients with Cushing's disease the plasma ACTH and cortisol responses to CRH were similar both before (ACTH from 9.9 +/- 1.7 pmol/L to 19.4 +/- 6.1 pmol/L; cortisol from 496 +/- 43.9 nmol/L to 923 +/- 355 nmol/L) and after octreotide injection (ACTH from 8.8 +/- 2.4 pmol/L to 19.1 +/- 8.2 pmol/L; cortisol from 510 +/- 54.6 nmol/L to 735 +/- 220 nmol/L). In conclusion, the acute administration of somatostatin or octreotide is not able to modify ACTH levels in patients with corticotropin hypersecretion either due to hypocortisolemic state or consequent to ACTH-secreting pituitary or ectopic tumors; moreover, octreotide does not affect the pituitary-adrenal responsiveness to CRH in patients with Cushing's disease.
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PMID:Failure of somatostatin and octreotide to acutely affect the hypothalamic-pituitary-adrenal function in patients with corticotropin hypersecretion. 197 78

A 58-year-old woman was admitted to our hospital with complaints of general fatigue, thirst and lumbago. A diagnosis of Cushing's syndrome was made on the basis of elevated serum levels of cortisol and adrenocorticotropic hormone (ACTH). Although Cushing's disease was most suspected, no evident image of pituitary adenoma could be found on brain CT scan and MRI. Therefore, treatment with oral Trilostane was started. Three months after admission, left hemiplegia was noticed and cerebral abscess in the right frontal lobe was demonstrated by brain CT scan. In spite of surgical removal of the abscess by total resection, she had a relapse in the same site and also developed a new lesion in the left lateral lobe. Surgical drainage was performed and Nocardia asteroides was isolated from the drained pus. An intensive chemotherapy with aminobenzylpenicillin (ABPC) and latamoxef (LMOX) in combination resulted in marked decrease in size of the lesion in the brain and subsequent improvement of left hemiplegia was achieved. Since approximately one month before when a diagnosis of cerebral abscess was made, there had been demonstrated a coin lesion in the right middle field on chest X-ray films. This lesion in the right lung disappeared concomitantly with the improvement of the lesions in the brain. This fact strongly suggests that the lesion in both brain and lung were of the same nature. Nocardia is known to make a primary lesion in the lung after being inhaled and then through hematogenous dissemination to make distant lesions in various sites, especially in the brain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of Cushing's syndrome associated with Nocardia cerebral abscess]. 206 9

The silent corticotroph-cell adenoma (SCCA) is characterized by the presence of immunoreactive adrenocorticotropic hormone (ACTH) in the tumor tissue in patients without symptoms of Cushing's disease. To elucidate the pathophysiology of SCCA, the expression of pro-opiomelanocortin (a ACTH precursor) genes was studied in a patient with SCCA and in three patients with Cushing's disease. Pro-opiomelanocortin messenger ribonucleic acid (mRNA) was found in the SCCA tissue to a greater degree than in the adenomas of the patients with Cushing's disease. Northern blot analysis revealed that the size of pro-opiomelanocortin mRNA present in the SCCA tissue was indistinguishable from that in the adenomas associated with Cushing's disease. A ribonuclease mapping study indicated that there were no point mutations in the coding sequence of pro-opiomelanocortin mRNA present in the SCCA tissue. Because of the presence of pro-opiomelanocortin mRNA and immunoreactive ACTH in the adenoma tissue, it is proposed that translation of the mRNA and subsequent accumulation of ACTH precursor occurred in the SCCA. Thus, the absence of Cushing's disease symptoms in this SCCA could not be caused by abnormality in the coding sequence of the pro-opiomelanocortin gene or in ribonucleic acid processing. The occurrence of abnormality at or after the translational steps was strongly suggested.
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PMID:Pro-opiomelanocortin gene expression in silent corticotroph-cell adenoma and Cushing's disease. 215 97

N-Terminal (1-76) portion of proopiomelanocortin (hNT) was measured in normals, Addison's, Nelson's, Cushing's disease, and in dexamethasone suppressible hyperaldosteronism (DSH) by using a specific homologous RIA. Mean basal immunoreactive hNT level was 94.2 +/- 6 pg/ml (mean +/- SE) in normal subjects. In Cushing's disease hNT values were slightly but not significantly (121 +/- 26.5 pg/ml) higher. In patients with DSH the levels were within normal range while they were much higher in Addison's and Nelson's syndromes. A strong correlation was found between IR-hNT and ACTH in plasma of normal subjects and patients with different disorders of the pituitary-adrenal axis (r = 0.83, p less than 0.01). Corticotropin-Releasing-Hormone (CRH) test in Cushing's disease stimulated the release of both ACTH and IR-hNT, showing a slightly different pattern of secretion. Similar patterns of secretion were found for hNT and ACTH in various pituitary-adrenal abnormalities. Normal levels of hNT in DSH do not support a role of this peptide in the pathogenesis of the disorder. Measurement of hNT in plasma can provide an additional tool for the diagnosis of patients with various disorders of the hypothalamic-pituitary-adrenal axis.
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PMID:Pro-gamma-MSH levels in various disorders of pituitary-adrenal axis. 215 20

The paper is concerned with the results of investigation of the blood concentration of alpha-melanocyte-stimulating hormone (alpha-MSH), hypophyseal reactivity to stress caused by insulin hypoglycemia in 26 patients with diseases of the hypothalamo-hypophyseal-adrenocortical system (Itsenko-Cushing disease and syndrome, hypothalamic syndrome of the pubertal period). A radioimmunoassay was used for the determination of the blood levels of alpha-MSH, ACTH and cortisol. In healthy persons the blood level of alpha-MSH rose 2-fold as compared to the basal one under the influence of insulin hypoglycemia-induced stress. In patients with Itsenko-Cushing disease at the active stage, alpha-MSH blood concentration was significantly elevated and a hypophyseal reaction to stress was disturbed. In Itsenko-Cushing syndrome, a decrease in the blood basal level of alpha-MSH and a hormone reaction to insulin hypoglycemia was noted. In patients with the hypothalamic syndrome of the pubertal period the blood level of alpha-MSH was raised and hypophyseal reactivity to insulin hypoglycemia was changed. Correlation analysis of the levels of alpha-MSH, ACTH and cortisol showed direct noticeable close relationships between the level of alpha-MSH and ACTH concentration in healthy persons and direct high close relationships between these indices in patients with Itsenko-Cushing disease. Correlation between the blood levels of alpha-MSH and cortisol was undetectable.
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PMID:[The secretion of alpha-melanotropin in diseases of the hypothalamus-hypophysis-adrenal cortex system]. 216 27

Petrosal sinus sampling was performed 171 times in 157 patients with known or suspected Cushing disease. In all cases, samples for measuring adrenocorticotropic hormone (ACTH) levels were obtained from both inferior petrosal sinuses and a peripheral vein, both before and after intravenous corticotropin-releasing hormone (CRH) administration. In seven examinations in seven patients, a ratio, or gradient, between the ACTH levels in the inferior petrosal sinuses existed in the samples obtained prior to CRH stimulation; however, poststimulation samples demonstrated reversal of the gradient, suggesting lateralization to the contralateral side of the pituitary gland. Data from surgical exploration of the pituitary gland were available for six of these patients, all of whom had adenomas. Prestimulation samples provided correct lateralization in three patients, and in two patients the poststimulation samples provided correct lateralization. One patient had a midline adenoma. When the results of pre- and poststimulation petrosal sinus sampling conflict, neither can be relied on uniformly to provide correct lateralization of ACTH-secreting pituitary adenomas.
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PMID:Petrosal sinus sampling: discordant lateralization of ACTH-secreting pituitary microadenomas before and after stimulation with corticotropin-releasing hormone. 216 35


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