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 consecutive series of 38 lung carcinoid tumours (36 surgical and two necropsy specimens) was studied. Histopathological features and amine and peptide hormone immunoreactivity were correlated with gross characteristics (size, location) and clinical data. Peripheral carcinoids were detected a decade later than central carcinoids and tended to be bigger. In general, the histological characteristics of peripheral and central carcinoids were similar; atypical features, however, were more common in peripheral carcinoids. Most carcinoids contained many argyrophilic cells (58%). Although argentaffinic cells were not found, serotonin immunoreactive cells were present in 32% of the tumours. Peptide hormone immunoreactivity (adrenocorticotrophic hormone (ACTH), calcitonin, somatostatin, gastrin) was rare. In one case massive ACTH production had caused clinically manifest Cushing's syndrome. In two other cases few ACTH immunoreactive cells were found and in one case calcitonin immunoreactive cells were present. The relative rarity of hormone production in lung carcinoids and the predominantly benign course of the tumour preclude the use of peptide hormone production as a prognostic indicator.
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PMID:Amine and peptide hormone production by lung carcinoid: a clinicopathological and immunocytochemical study. 614 59

Clinical and laboratory data, histologic, electron microscopic and immunocytochemical findings of the tumors of eight patients suffering from Cushing's syndrome and of one patient with hypercalcemia are described. The unlabeled antibody enzyme method was used for the detection of insulin, glucagon, somatostatin, pancreatic polypeptide, corticotropin, beta-lipotropin, calcitonin, parathyroid hormone, and gastrin. Ectopic Cushing's syndrome was caused by pancreatic endocrine tumors, medullary thyroid carcinoma, a bronchial, a gastric and a thymic carcinoid, and a carcinoid of the mediastinum. Hypercalcemia in one patient was related to a pancreatic endocrine tumor. After surgery the clinical symptoms disappeared in two patients, but persisted or relapsed in five patients. ACTH-immunoreactivity could be demonstrated in six of eight tumors; calcitonin-immunoreactivity was found in the tumor of the patient suffering from hypercalcemia. ACTH-immunoreactivity could be localized to secretory granules by immunoelectron microscopy, and the presence of ACTH and beta-LPH in the same tumor cells could be shown in one pancreatic tumor. A combination of production of orthotopic and ectopic hormones was found in one, and secretion of two ectopic hormones was detected in another pancreatic endocrine tumor.
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PMID:Ectopic hormone production by endocrine tumors: localization of hormones at the cellular level by immunocytochemistry. 627 90

The prognosis of patients with metastatic adrenal cortical carcinoma is poor, and their disabling symptoms are usually unresponsive to conventional therapy. A patient with Cushing's syndrome secondary to a secretory adrenal cortical carcinoma was treated with octreotide, endocrine therapy and chemotherapy having failed. Treatment led to a dramatic relief of her symptoms with a fall in corticosteroid secretion. Somatostatin analogue therapy for this tumour should be encouraged in view of the lack of alternative palliative treatment.
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PMID:Secretory symptoms from metastatic adrenal cortical carcinoma responding to octreotide. 754 Mar

High numbers of high-affinity somatostatin binding sites have been found on carcinoid tumors, gastrinomas, small cell lung cancers and the majority of medullary thyroid cancers, enabling in vivo visualization of these tumors with octreotide scintigraphy. A comparison of the results obtained at our institution and another 15 centers in Europe show a few remarkable similarities and differences. The overall sensitivity of octreotide receptor scintigraphy to detect the primary GEP tumor and its metastases is high, e.g. 80-90%. The main difference was found in gastrinomas and to a lesser extent in insulinomas. These differences might be attributed to different scanning protocols. Furthermore, octreotide scintigraphy also has a high sensitivity to localize the primary tumor and its metastases causing Cushing's syndrome by ectopic production of ACTH or CRH. Octreotide scintigraphy is a new, sensitive and noninvasive technique to localize somatostatin receptor expressing endocrine tumors and their metastases.
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PMID:Somatostatin receptor scintigraphy in carcinoids, gastrinomas and Cushing's syndrome. 769 38

Small ACTH-secreting carcinoid tumors responsible for Cushing's syndrome are often difficult to localize using available radiological investigations. Somatostatin receptors have been found in about 90% of carcinoid tumors studied, leading to a new approach for the localization of tumors or metastasis by using radiolabeled somatostatin analogs. We report a case of Cushing's syndrome due to an ACTH-secreting bronchial carcinoid tumor, completely suppressible with octreotide treatment and evidenced by body scintigraphy with 111In-labeled pentreotide. After removal, which led to patient recovery, the tumor was studied in vitro. In situ hybridization, using a complementary DNA probe, revealed POMC messenger ribonucleic acid in a subpopulation of tumor cells. These cells were labeled by immunochemistry using an antiserum directed against ACTH. Confocal laser scanning microscopy analysis showed that the ACTH-immunoreactive peptide was sequestered in secretory granules. Autoradiographic labeling using [125I-Tyrzero,D-Trp8]somatostatin-14 demonstrated the presence of somatostatin-binding sites in the whole tumor tissue. The relative affinities of various selective somatostatin analogs and the ability of GTP to inhibit radioligand binding suggested that the receptor expressed in the tumor cells belonged to the SSTR-2 subtype.
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PMID:Characterization of the somatostatin receptor subtype in a bronchial carcinoid tumor responsible for Cushing's syndrome. 771 18

The effects of clonidine, a growth hormone (GH) secretagogue, acting at the hypothalamic level and synthetic GH-releasing hormone (GHRH), a physiological stimulus of somatotrophs, on GH secretion were measured in 11 dogs with Cushing's syndrome. Eight healthy dogs served as controls. After the administration of GHRH the dogs with hyperadrenocorticism had a mean (SEM) GH peak of 11.2 (2.5) ng ml-1 which was significantly lower than the peak of 48.6 (13.4) ng ml-1 observed in the healthy dogs. Similarly, the GH response to clonidine was inhibited in the dogs with hyperadrenocorticism, the mean GH peak being 9.3 (3.3) ng ml-1 compared with 135.6 (43.3) ng ml-1 in the control dogs. No significant difference between the GH responses to GHRH and clonidine was observed in the dogs with Cushing's syndrome, the areas under the response curves being 567.9 (78.2) and 478.0 (102.6) ng.min ml-1, respectively. These results demonstrate that the function of somatotrophs is abnormal in dogs with Cushing's syndrome. There is evidence that the likely action of clonidine in dogs is to inhibit the release of somatostatin and the results therefore suggest that the effect of an excess of glucocorticoid in the dog is probably not mediated through an increase in somatostatin tone.
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PMID:Growth hormone responses to growth hormone-releasing hormone and clonidine in dogs with Cushing's syndrome. 776 97

Medical management of Nelson's syndrome by drugs such as bromocriptine, sodium and magnesium valproate has provided disappointing or, at least, controversial results. We report here on the results of long-term (2 yr) treatment with the somatostatin analogue octreotide (300 micrograms daily sc) in one patient affected by Nelson's syndrome occurring after bilateral adrenalectomy for Cushing's syndrome. During treatment, skin hyperpigmentation and serum ACTH levels decreased dramatically and a slight (about 10%) reduction in tumor size, as assessed by computerized tomography, was also observed. These results suggest that octreotide may be useful for the medical management of Nelson's syndrome.
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PMID:Long-term treatment of Nelson's syndrome by octreotide: a case report. 800 35

Clinical introduction of octreotide, a long-acting somatostatin analog, has opened a new era in the medical therapy of patients with growth hormone (GH)- and thyroid-stimulating hormone (TSH)-secreting pituitary tumors. Good control of hormonal hypersecretion occurred in most patients, and tumor shrinkage has been observed in more than half of them. Octreotide therapy is of no value in most patients with Prolactin (PRL)- and adrenocorticotrophic (ACTH)-secreting pituitary tumors. However patients with Cushing's syndrome caused by ectopic ACTH secretion from a variety of endocrine tumors benefit from octreotide administration. In patients with visual disturbances related to chiasmal compression by nonfunctioning pituitary tumors, somatostatin analog administration has been reported to result in rapid improvement in visual acuity. This beneficial effect might not be related to a direct action of octreotide, but may reflect an effect on the retina and/or optic nerve. The presence of somatostatin receptors on a wide variety of pituitary tumors as well as on a number of parasellar tumors allows their in vivo visualization with radionucleotide-labelled somatostatin analogs. A positive scan in patients with GH- and TSH-secreting pituitary tumors is predictive of a good suppressive effect of octreotide on hormone release by these tumors. PRL- and ACTH-secreting pituitary adenomas cannot be visualized, but clinically nonfunctioning pituitary adenomas are visualized in 75% of cases with 111In-DTPA-octreotide. At present it is unclear whether this has consequences with regard to the medical treatment of these last group of patients. Somatostatin receptor scintigraphy can be successfully used in the differential diagnosis between pituitary hypersecretion of GH and/or ACTH and the ectopic secretion of growth hormone-releasing hormone (GHRH) and ACTH by peripherally localized endocrine tumors. Again the visualization of such tumors also predicts successful control of hormonal hypersecretion by octreotide.
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PMID:Octreotide and related somatostatin analogs in the diagnosis and treatment of pituitary disease and somatostatin receptor scintigraphy. 809 80

We report on the efficacy of the long-acting somatostatin analog octreotide in a 43-yr old woman with ectopic ACTH syndrome. Plasma cortisol, ACTH, beta-endorphin (beta-END) and urinary free cortisol (UFC) were elevated (range 743-920 nmol/l, 29.2-49.7 pmol/l, 71.0-84.1 pmol/l, 2117-3119 nmol/day respectively). Ovine CRH (oCRH) and high dose dexamethasone did not affect cortisol and ACTH levels, while UFC significantly decreased after dexamethasone. Initially radiological investigation failed to localize the ACTH secreting tumor. Ketoconazole was not tolerated. Plasma cortisol significantly decreased both after single (100 micrograms sc) (baseline 531 nmol/l, nadir 218 nmol/l) and 3-day octreotide administration (from 810 to 448 nmol/l); plasma ACTH decreased slightly (from 30.4 to 21.3 pmol/l and from 32.4 to 22.5 pmol/l respectively); UFC decreased from 2616 to 711 nmol/day after the 3-day test. Long-term octreotide treatment (100 micrograms/8h per 54 weeks) led to clinical and biochemical improvement and recurrence followed drug withdrawal; no side effects were observed. Six months after octreotide administration a 2 cm lung mass was detected with CT and MR. Surgery was performed and a bronchial carcinoid was removed. Immunoreactive ACTH in the tumor has been demonstrated by histochemistry. Postoperatively a lasting remission of Cushing's syndrome was observed without further therapy.
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PMID:Successful treatment of ectopic Cushing's syndrome with the long-acting somatostatin analog octreotide. 829 10

We investigated 2 patients affected with Cushing's syndrome due to the ectopic production of adrenocorticotropic hormone (ACTH) by a small cell lung carcinoma. In the 2 patients, the long-acting somatostatin analogue octreotide (100 micrograms, subcutaneously) induced a paradoxical increase in plasma ACTH and cortisol levels. In 1 patient, lanreotide, a new somatostatin analogue in a slow-release formulation (30 mg, intramuscularly), induced a similar rise in ACTH and cortisol secretion. To our knowledge, such a response has not been previously reported. Further use of somatostatin analogues in ectopic ACTH-producing tumors, especially lung tumors, requires preliminary evaluation of their therapeutic efficacy by a short test with somatostatin analogue.
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PMID:Paradoxical effect of somatostatin analogues on the ectopic secretion of corticotropin in two cases of small cell lung carcinoma. 831 5


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