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)

Treatment with Sandostatin is established in acromegaly, thyroid-stimulating hormone (TSH)-producing pituitary, and endocrine-active gastroenteropancreatic tumors. Potential indications include ectopic hormone syndromes, medullary thyroid carcinomas, pituitary resistance to thyroid hormones, tall stature children, diabetes mellitus and diabetic complications, polycystic ovary syndrome, and Graves' ophthalmopathy. Particularly in the ectopic growth hormone-releasing hormone (GHRH) syndrome, Sandostatin is unequivocally effective and, in the ectopic corticotropin syndrome selected cases can be treated successfully with Sandostatin, leading to marked clinical improvement. In many of the above situations, only subgroups show a response to Sandostatin, which may be identified by scintigraphy with labeled Sandostatin. This pertains also to Graves' ophthalmopathy, for which Sandostatin may be particularly promising and where positive and negative Sandostatin scans have been demonstrated. However, for all these potential indications, larger, well-studied series are needed, before definitive conclusions can be drawn.
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PMID:Potential indications for octreotide in endocrinology. 151 41

The influence exerted by somatostatin on the secretion of ACTH and opioid peptides has still to be clarified. To gain further information on this issue, we performed in 10 normal volunteers two CRF tests (100 micrograms i.v.) one of which was preceded by s.c. injection of 100 micrograms of the long-acting somatostatin analogue SMS 201-995 (Sandostatin, Sandoz) (SMS), given 30 minutes before CRF. Premedication with SMS markedly inhibited the response of beta-EP to CRF, leaving unchanged the response of beta-LPH, ACTH and cortisol; mean incremental areas of beta-EP were 199.8 +/- 49.31 (SEM) vs 532.9 +/- 95.91 pmol 120 min (P less than 0.01) in the CRF test with and without SMS, respectively. To interpret the selective inhibitory effect of SMS on CRF-stimulated beta-EP secretion, it can be hypothesized that: a) the action of SMS was confined to a population of pituicytes preferentially secreting beta-EP; b) SMS interfered with the processing of POMC inhibiting the formation of beta-EP; c) SMS acted on extrapituitary, possibly peripheral, sources of beta-EP. In conclusion, this study indicates that, in man, somatostatin selectively inhibits the CRF-induced secretion of beta-EP, but not that of ACTH and beta-LPH, by an action that may be exerted at pituitary or extrapituitary level. This is a further example of dissociated secretion of POMC-derived peptides.
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PMID:Effect of sandostatin on CRF-stimulated secretion of ACTH, beta-lipotropin and beta-endorphin. 165 95

Somatostatin analogue (Sandostatin; SMS 201-995) is utilized as a therapy in acromegaly because of its efficiency in inhibiting GH secretion; it induces some clinical improvements, such as headache remission in acromegalic patient, which seem to be unrelated to Gh normalization. We have examined 8 acromegalic patients, suffering from headache, after injection of saline solution and subsequently of SMS 201-995 (100 y), in order to study the mechanism of analgesic effect induced by Sandostatin administration. Headache, by autovaluation test, heart rate frequency, PAO, sistolic and diastolic blood velocity in medial cerebral artery, by utilizing Transcranial Doppler Sonography (SDSV), have been measured before and after saline and after SMS 201-995. GH and beta-endorphin have been also assayed in plasma samples. All patients have shown a rapid and complete improvement in headache after Sandostatin administration. At the same time we have observed an increase in SDSV and a parallel slight increase in PAO values, more evident in the diastolic phase. Plasma beta-endorphin assay has shown rather conflicting results after SMS 201-995 administration. Our results confirm an important and rapid analgesis effect of Sandostatin on acromegaly headache unrelated to GH normalization. The cerebral emodinamic changes suggest their involvement in Sandostatin induced analgesia.
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PMID:[Analgesic effect of Sandostatin (SMS 201-995) in acromegaly headache]. 227 13

The present work was aimed at studying the combined effects of somatostatin and corticotropin releasing hormone on the activities of the pituitary-adrenocortical axis and neurohypophysis. Patients with active acromegaly were intravenously injected with a 100 micrograms human corticotropin releasing hormone bolus before and after a 3-month subcutaneous treatment with somatostatin-octreotide (SMS 201 995; Sandostatin; 200 micrograms t. i. d.). When the Sandostatin effect was investigated, corticotropin releasing hormone test was started 2 hrs after its first daily dose. Peripheral venous blood samples were taken before and 20, 60, 90 and 120 min after the corticotropin releasing hormone load. Plasma corticotropin, arginine-8-vasopressin and oxytocin were measured by radioimmunoassay, and serum cortisol by fluorimetry. In healthy subjects, corticotropin releasing hormone stimulus elicited increases of plasma corticotropin, serum cortisol, plasma arginine-8-vasopressin and oxytocin levels by 186, 41, 178 and 58 per cent, respectively. Untreated acromegalics exhibited missing arginine-8-vasopressin, blunted corticotropin, and normal oxytocin and cortisol responses. Sandostatin therapy improved the arginine-8-vasopressin reaction, suppressed the basal levels of corticotropin and cortisol with the maintenance of cortisol stimulability; the peak-reaction of corticotropin became normal in two patients, however, with a shortened duration of response. Diuresis of the patients increased under the treatment. Sandostatin markedly alleviated the clinical symptoms and suppressed the growth hormone secretion, but did not influence the size of the pituitary adenomas. Among other factors, the alterations of growth hormone and cortisol may be hypothesized to take part in the changes of the corticotroph and neurohypophysial functions.
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PMID:[Effect of somatostatin-octreotide on secretion of adrenocorticotropin, cortisol and neuro-hypophyseal hormones in acromegaly]. 991 27