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

A patient with ectopic Cushing's syndrome secondary to a malignant thymic carcinoid tumour was treated with the somatostatin analogue SMS 201-995. The administration of the drug subcutaneously in increasing doses over a 34 day period failed to control the ACTH or glucocorticoid excess.
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PMID:Failure of somatostatin analogue SMS 201-995 to control Cushing's syndrome due to ectopic release of ACTH from a bronchial carcinoid. 255 18

Two patients with Cushing's syndrome due to lung carcinoid tumours were given the long-acting somatostatin analogue SMS 201-995 (Sandostatin). One received a single 50 micrograms dose which produced a 50% reduction in circulating ACTH levels within 4 h. The other has been maintained in clinical and biochemical remission for 10 weeks on 100 micrograms tid. This is the first report of the successful use of SMS 201-995 in carcinoid-induced Cushing's syndrome, and suggests that this hormone analogue could be valuable in the long term medical management of such patients.
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PMID:Lung carcinoid with Cushing's syndrome: control of serum ACTH and cortisol levels using SMS 201-995 (sandostatin). 284 45

Signs and symptoms of Cushing's syndrome developed rapidly after total gastrectomy in a 37-yr-old man with a metastatic gastrin-secreting islet cell carcinoma. Argyrophilic tumor cells in a lymph node removed during operation immunostained for gastrin and ACTH. Treatment for more than 6 months with the somatostatin analog SMS 201-995 (300 micrograms/day) greatly reduced serum gastrin levels and normalized plasma ACTH and cortisol levels and urinary cortisol excretion, and the signs and symptoms of Cushing's syndrome disappeared. The size of the primary tumor in the head of the pancreas, which had grown rapidly before SMS 201-995 therapy, stabilized after 6 months of treatment with the analog. We conclude that SMS 201-995 can reduce ACTH as well as gastrin secretion from islet cell carcinomas as well as control tumor growth.
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PMID:Successful treatment with SMS 201-995 of Cushing's syndrome caused by ectopic adrenocorticotropin secretion from a metastatic gastrin-secreting pancreatic islet cell carcinoma. 284 25

Cushing's syndrome, caused by ectopic ACTH production during Zollinger-Ellison syndrome, raises difficult therapeutic problems. We report a case of clinical and biological efficacy of long acting somatostatin (SMS) in this condition. In a short term study with 200 micrograms SMS bid, symptoms of hypercorticism disappeared while cortisol and ACTH serum concentrations fell below the normal values. Longterm treatment was instituted with 50 micrograms SMS bid. Excellent clinical efficacy as well as normal cortisol and ACTH serum concentrations were maintained during the nine month follow up. Lipotrophic hormone (LPH) serum concentration remained raised. No decrease in size of hepatic metastases was observed. Long acting somatostatin analogues may be useful in endocrine paraneoplastic syndromes.
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PMID:Long acting somatostatin treatment of paraneoplastic Cushing's syndrome in a case of Zollinger-Ellison syndrome. 289 23

A case is described of a patient with a small-cell prostatic carcinoma containing immunoreactive CRH, in conjunction with ACTH-dependent Cushing's syndrome. The serum concentrations of CRH, ACTH, beta-endorphin and calcitonin were all found to be above normal. Post-mortem examination revealed a prostatic tumour with multiple metastases, and a diffuse hyperplasia of pituitary corticotropic cells and adrenal cortical cells. In sections of the primary prostatic tumour, immunoreactive cells were demonstrable with antisera raised against human CRH, TSH, calcitonin and somatostatin, but not with antisera against ACTH or beta-endorphin. By radioimmunoassay the CRH-like material could also be demonstrated in extract of the prostatic tumour and the material from both plasma and tumour extract eluted at the position of human CRH on gel chromatography (Sephadex G-75). These findings provide support for the interpretation that the patient's Cushing's syndrome was due to a CRH-producing prostatic tumour. Finally, the origin and the clinical significance of the neuroendocrine cells in the prostatic carcinoma is discussed.
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PMID:Carcinoma of the prostate with Cushing's syndrome. A case report with histochemical and chemical demonstration of immunoreactive corticotropin-releasing hormone in plasma and tumoral tissue. 326 36

A 42-year-old female with clinical and endocrine indications of Cushing's syndrome, as well as periodic hypertension and increased urinary catecholamines and their metabolites, benefitted from removal of a pheochromocytoma. Adrenocortical hyperplasia was present. Electron microscopy showed catecholamine-type granules in the tumor cells; in addition, immunoreactive ACTH, leu-enkephalin, somatostatin, and serotonin were identified. Such studies were performed for the first time in this unusual condition.
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PMID:Pheochromocytoma producing immunoreactive ACTH with Cushing's syndrome. 609 99

Two patients with somatostatin-secreting pancreatic tumours are described, one presenting with hypoglycaemia due to hyperinsulinism, and the other with Cushing's syndrome due to ectopic ACTH production. When plasma from these patients was subjected to gel chromatography under conditions designed to prevent somatostatin binding to larger proteins, a peak of monomeric immunoreactive somatostatin was observed as well as several large molecular weight forms. These larger forms of somatostatin could be dissociated into monomeric somatostatin by dithiothreitol. Similar studies on plasma obtained from normal subjects also showed heterogeneity of circulating somatostatin. Extracts of tumour tissue from both patients contained predominantly monomeric somatostatin, but only small amounts of high molecular weight somatostatin which differed from the profile seen in plasma. The site(s) of origin of the large molecualr weight forms of somatostatin seen in plasma and their relative biological activities remain to be established.
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PMID:Molecular forms of somatostatin in normal subjects and in patients with pancreatic somatostatinoma. 610 27

An islet cell carcinoma of the pancreas is described in a 68-year old woman which clinically produced Zollinger-Ellison syndrome and, later in its course, Cushing syndrome. The tumor was found to contain gastrin, ACTH, alpha-endorphin, somatostatin and calcitonin, by the immunoperoxidase technic. Electron microscopy revealed a single tumor cell type containing secretory granules of variable size, morphology and electron density. It appears that a single tumor cell population produced all five hormones and caused a transition in clinical symptomatology, while undergoing no change in morphology.
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PMID:Pancreatic islet cell carcinoma producing gastrin, ACTH, alpha-endorphin, somatostatin and calcitonin. 610 42

In a case study of medullary thyroid carcinoma (MTC) associated with Cushing's syndrome, elevated levels of urinary 17-hydroxycorticosteroids, plasma ACTH, cortisol, calcitonin (CT) and somatostatin (GHRIH) were documented. Lysine vasopressin administration further increased the levels of plasma ACTH, cortisol and CT, whereas the administration of calcium and pentagastrin increased only the level of plasma CT. Immunoreactive ACTH, CT and GHRIH were highly concentrated in the tumour tissues. Basal plasma ACTH levels were more progressively increased than plasma CT during the postoperative course when the patient was treated with o,p'-DDD, since the tumour was not completely resected. These findings suggest that the secretion of ACTH and CT from MTC were regulated in a different manner.
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PMID:Plasma calcitonin and ACTH responses to lysine vasopressin, calcium and pentagastrin in a patient with medullary thyroid carcinoma associated with Cushing's syndrome. 613 58

Twelve cases of thymic carcinoid were studied by electron microscopy and immunohistochemistry. Clinically, all of them presented either as asymptomatic, radiographically detected mediastinal masses or as neoplasms producing symptoms of thoracic structural displacement or Cushing's syndrome. By light microscopic examination, the carcinoids manifested an organoid growth pattern, being composed of uniform polygonal cells with central, oval nuclei and finely dispersed chromatin. Immunohistochemical analysis disclosed the presence of cytoplasmic adrenocorticotropic hormone in four cases (three associated with Cushing's syndrome), of somatostatin in seven cases, and of serotonin in one case. Ultrastructurally, these tumors generally showed short, blunt, interdigitating cell processes; focal, scanty basement membrane material; infrequent but well-formed junctional complexes; moderate to large numbers of dense-core granules; and lipoautophagosomes. Six tumors contained small numbers of type I microfilaments, and three demonstrated perinuclear whorls of type II microfilaments. Rough and smooth endoplasmic reticulum was well developed in each tumor, the smooth form being prominent in cases with clinical Cushing's syndrome.
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PMID:Thymic carcinoid. A histologic, immunohistochemical, and ultrastructural study of 12 cases. 614 Oct


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