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 young Japanese female demonstrated unusual features of Cushing's syndrome, cardiac myxomas and mucocutaneous lentigines. At the age of 12 years she presented with growth failure and obesity. The dexamethasone suppression test, the metyrapone test and low corticotropin concentrations indicated a primary adrenal disorder. At surgery, the adrenal glands were not enlarged (the right, 4.0 g; the left; 4.5 g) but had numerous small dark brown nodules. The pathological findings showed multiple small black cortical nodules containing large cells with eosinophilic cytoplasm and lipofuscin, and internodular cortical atrophy. These abnormalities were consistent with primary pigmented nodular adrenocortical disease. At age 22 years she complained of fatigue and palpitations associated with mid-chest pain. Four cardiac myxomas, suspected from the echocardiogram, were surgically removed. Because Cushing's syndrome and cardiac myxomas are life-threatening conditions, an awareness of the complex is important.
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PMID:Cushing's syndrome due to primary pigmented nodular adrenocortical disease with cardiac myxomas and mucocutaneous lentigines. 160 Mar 14

In a 10-year-old boy with Cushing's syndrome, the dexamethasone suppression test, the metyrapone test, and both basal and corticotropin-releasing factor-stimulated corticotropin levels all indicated a primary adrenal disorder. However, a computed tomographic scan failed to detect an adrenal tumor. At surgery, the adrenal glands were not enlarged but were studded with small pigmented nodules composed of enlarged nonmalignant adrenocortical cells. This unusual abnormality, referred to as primary pigmented nodular adrenocortical disease, is associated with autonomous hypersecretion of cortisol primarily in children and young adults. Our patient was cured by total bilateral adrenalectomy and corticosteroid replacement therapy, the treatment of choice for this condition.
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PMID:Cushing's syndrome resulting from primary pigmented nodular adrenocortical disease. 375 18

Micronodular adrenal hyperplasia is an uncommon adrenal disorder characterized by failure of urinary corticosteroid excretion to be suppressed by high-dose dexamethasone therapy. Thus, micronodular adrenal hyperplasia demonstrates dexamethasone suppressibility that resembles primary adrenal neoplasia. However, since some cases have been reported to have measurable plasma adrenocorticotropic hormone (ACTH) levels, it is unclear whether this disorder arises primarily in the pituitary-hypothalamic region or in the adrenal gland. Our patient had clinical features of Cushing's syndrome and elevated urinary corticosteroid excretion that did not suppress with even high doses of dexamethasone; however, ACTH levels were elevated and were suppressible with high-dose dexamethasone therapy. At operation, enlarged adrenal glands with multiple micronodules were found. This case is compatible with the hypothesis that hypothalamic-pituitary hyperfunction precedes the development of micronodular adrenal disease in some cases.
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PMID:Nodular adrenal hyperplasia with elevated adrenocorticotropic hormone levels. 629 97

Adrenal disease is an uncommon manifestation of hepatitis C infection and its related treatment regimen. This is a case of subclinical hypoadrenalism, probably induced by hepatitis C infection and further exacerbated by interferon-alpha2beta and Ribavirin therapy. The adrenal deterioration during the treatment course was observed closely with 24-hour salivary profiles and 250 mug adrenocorticotropin stimulation tests using parallel serum and salivary cortisol concentrations. A number of possible pathogenic mechanisms are discussed, and the controversy over its management is emphasized.
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PMID:Exacerbation of hepatitis C induced subclinical hypoadrenalism by Interferon-alpha2beta: A case report. 1880 Nov 74