Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P61278 (somatostatin)
 22,083 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hirsutism, acne and androgenic alopecia represent, in females, some of the manifestations of the clinical spectrum of hyperandrogenism. These pictures represent not only cosmetic damage, but also a source of remarkable psychological distress. Often hirsutism is regarded as presumptive evidence of a lack of femininity. The major diagnostic concern is to exclude an ovarian or adrenal androgen-secreting tumor, a congenital hyperplasia or polycystic ovary disease. Ethnic background should be taken into account together with the progression of the symptoms. Following the etiology, surgery and exogenous glucocorticoids or inhibition of gonadotropin secretion have to be carefully chosen in the management of different kinds of hyperandrogenism. Several pharmacologic agents have recently shown the ability to block the androgen receptors at target organ sites, thus allowing a specific antiandrogenic treatment. In some cases cosmetic measures could be of great value. Obesity accompanied by hyperinsulinemia can represent the main cause of ovary androgen hypersecretion; therefore a reduced body weight and muscle activity represent the basis of any treatment. Some other drugs, such as long-acting analogs of somatostatin, could be considered among possible drugs for the future. The aim of this article is to provide an appraisal of what is presently known about the regulation of hair growth, the various causes of excessive androgen secretion and the current methods to solve, safely, this important feminine clinical problem.
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PMID:Treatment of androgen excess in females: yesterday, today and tomorrow. 947 91

A 31-year-old woman presented with progressive weight gain, facial acne, round facies, hirsutism, and secondary amenorrhea. Her plasma cortisol, urinary free cortisol, and plasma ACTH were elevated. CT scan of abdomen revealed bilateral diffuse adrenal enlargement. MRI of pituitary failed to identify a lesion. CT scan of chest revealed an 8 mm nodule in the lower lobe of the left lung. The diagnosis of ectopic Cushing's syndrome was made. The lung tumor was surgically removed. The tumor measured up to 1.5 cm in diameter. By light microscopy, a tumor with characteristic features of bronchial carcinoid was noted. Immunostains were positive for neuron-specific enolase, synaptophysin, chromogranin, low-molecular-weight keratin, ACTH, beta endorphin, corticotropin-releasing hormone, bombesin, alpha subunit, and somatostatin. Electron microscopy revealed an endocrine neoplasm. The secretory granules displayed great variation subdividing the endocrine neoplasm. The secretory granules displayed great variation subdividing the cell population into an undetermined number of phenotypes. In situ hybridization demonstrated positivity for pro-opiomelanocortin mRNA in the tumor cells. Postoperatively, plasma cortisol had fallen. The patient remained symptom-free one year later. The case presented here was regarded as a plurihormonal bronchial carcinoid associated with ectopic Cushing's syndrome. This unique plurihormonal bronchial carcinoid tumor produced three hormones, ACTH, CRH, and bombesin, that may have contributed to the patient's ectopic Cushing's syndrome.
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PMID:Plurihormonal Bronchial Carcinoid Associated with Ectopic Cushing's Syndrome. 1211 73