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 a mixed pituitary tumor secreting TSH and GH was treated, starting 3 months after partial adenomectomy, with the somatostatin analog SMS 201-995 for 8 months. Somatostatin itself inhibited TSH, GH, and alpha-subunit release by the tumor both in vivo and in vitro. Long term treatment with twice daily sc injections of SMS 201-995 resulted in decreased TSH secretion and lower serum thyroid hormone levels. However, euthyroidism was achieved only when the patient was treated with three daily 200-micrograms injections of SMS 201-995. After 30 weeks of SMS 201-995 therapy, TSH secretion increased, while GH secretion remained suppressed. After withdrawal for 6 months, SMS 201-995 (100 micrograms, sc, twice daily) again completely inhibited TSH secretion. SMS 201-995 did not alter the volume of the residual adenomatous tissue. We conclude that SMS 201-995 may be a valuable therapeutic agent for the management of patients with a thyrotroph adenoma. However, desensitization may occur during long term treatment.
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PMID:Long term treatment with the somatostatin analog SMS 201-995 in a patient with a thyrotropin- and growth hormone-secreting pituitary adenoma. 289 19

Two patients with neurofibromatosis and somatostatinoma are described, one patient in addition having a parathyroid adenoma diagnosed post mortem. The other patient had a partial somatostatinoma syndrome with diabetes, abdominal pain and cholelithiasis. The tumour was diagnosed preoperatively and metabolic studies demonstrated mild diabetes mellitus apparently due to suppression of insulin secretion by somatostatin, since oral glucose tolerance returned to normal post-operatively despite hemipancreatectomy. The tumour also secreted gastrin. There are now 18 reported cases of neurofibromatosis and duodenal carcinoid tumours which makes a genuine association between these two conditions very likely. With the present two cases, seven of the carcinoid tumours in this group have been positively identified as somatostatinomas. The histological finding of psammoma bodies is important in the diagnosis of duodenal somatostatinomas.
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PMID:Neurofibromatosis associated with somatostatinoma: a report of two patients. 290 5

The biological activity of the natural somatostatin can be quantitatively and qualitatively altered by the substitution and/or the exclusion of some of its amino-acids. The most used synthetic analog, SMS 201-995, has a potent inhibiting effect on GH secretion, but is less effective on insulin and glucagon secretions. It is mainly used in Endocrinology for the treatment of acromegaly. It is also useful for inhibiting the inappropriate TSH secretion from a thyrotroph adenoma. The LH-RH agonists ast essentially by desensitizing the gonadotroph from the endogenous LH-RH. By sub-cutaneous, intra-muscular or nasal route, they allow to inhibit the gonadal functions in some hormone-dependent cancers and in true precocious puberty. More recently, they have been tested for the treatment of gonadotropic adenomas, where they may have sometimes a paradoxical effect. In combination with exogenous gonadotropins, they enhance the control of ovulation and are new valuable tools for IVF programs. Clinical studies with the LH-RH antagonists are just beginning. The long-acting bromocriptine affords a new alternative to the oral treatment of hyperprolactinaemia. Its suppressive effects lasts at least 35 days in normal subjects and 21 days in patients with macroprolactinomas.
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PMID:[Selective control of different hypophysial secretions by long-lasting pharmacodynamic agents. Analogs of somatostatin and LHRH and long-lasting bromocriptine]. 290 89

A case of multiple nonfunctional pancreatic islet cell tumor in multiple endocrine neoplasia type I (MEN I) is reported. The patient was a 41-year-old woman who had a past history of thyroid cancer (papillary carcinoma) and hyperparathyroidism due to parathyroid adenoma. Later, a nonfunctional pituitary tumor and five nonfunctional pancreatic tumors were found simultaneously and the patient was finally diagnosed as having MEN I. Following surgical enucleation, the pancreatic tumors were histopathologically diagnosed as benign islet cell tumors. One of them (tumor 3) exhibited a solid nodular pattern while the others showed gyriform patterns. They were divided histochemically and immunohistochemically into three types: two (tumors 1 and 2) produced a single hormone (glucagon), one (tumor 3) produced five (insulin, glucagon, somatostatin, gastrin and pancreatic polypeptide) and the remaining two (tumors 4 and 5) produced two (glucagon and pancreatic polypeptide). Electron microscopically, three types of endosecretory granules were found in the tumor cells of tumor 3 but only one type was found in tumor 4. However, in the tumor 4 extract, glucagon, pancreatic polypeptide, C-peptide, somatostatin, vasoactive intestinal peptide and growth hormone releasing factor were detected by radioimmunoassay. These findings suggest that these pancreatic tumors were both multicellular and multihormonal.
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PMID:Multiple nonfunctional pancreatic islet cell tumor in multiple endocrine neoplasia type I. A case report. 290 67

The aim of the present study was to evaluate various functional tests for the differentiation of hyperinsulinaemic hypoglycaemia. The pathophysiological and histological findings in six infants, aged 2-7 months, with persistent hyperinsulinaemic hypoglycaemia are described. Islet cell adenoma was found in four infants and pancreatic nesidioblastosis in two others. Circulating levels of blood glucose (BG), immunoreactive insulin and C-peptide immunoreactivity were measured under basal conditions and during both stimulation and suppression. The diagnosis of hyperinsulinaemia was made by estimation of the BG/serum insulin ratio, which was the most important diagnostic criterion of hyperinsulinism. Control subjects of comparable age showed a ratio of 8.3 +/- 4.4 (range 4.1-13.3), whereas the six patients had values between 0.3 and 5.1. At least four determinations with ratios lower than 2.6 were necessary for confirming the diagnosis. Preoperatively we performed oral glucose tolerance, diazoxide infusion, somatostatin infusion and C-peptide suppression tests. It is suggested that the various function tests, especially the suppression tests, do not differentiate hyperinsulinism caused by an adenoma from that caused by diffuse pancreatic nesidioblastosis.
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PMID:The hyperinsulinaemic hypoglycaemias in infancy: a study of six cases. 290 71

We have examined the effects of human GH-releasing factor (1-44) (GRF), cortisol and somatostatin-(1-14) on GH gene expression in solid tissue and dispersed cells from human pituitary adenomas using quantitative in-situ hybridization histochemistry. Sections cut from tissue obtained at hypophysectomy from three acromegalic patients were hybridized to probes directed against mature alpha-subunit, GH, prolactin, pro-opiomelanocortin, TSH beta-subunit and LH beta-subunit mRNA. Only one biopsy contained GH mRNA in isolation. A second was found to coexhibit GH, prolactin and alpha-subunit mRNA, and a third was found to contain prolactin, TSH beta-subunit, alpha-subunit and LH beta-subunit mRNA, with GH mRNA below the limit of specific detection, indicating that the sample was composed of normal rather than adenomatous pituitary tissue. GH mRNA in individual dispersed cells derived from the latter declined to barely detectable levels over 287 h, both in cultures containing GRF (10 ng/ml) or GRF (10 ng/ml) plus somatostatin (10 ng/ml) and in controls, but increased fourfold in cultures containing GRF (10 ng/ml) plus cortisol (0.5 mumol/l). GH mRNA remained unchanged in both adenoma samples over 138 and 450 h, irrespective of the addition of GRF or GRF plus hydrocortisone. In these samples, somatostatin plus GRF had no consistent effect. These studies confirm that quantitative in-situ hybridization histochemistry can be used to investigate hormone gene regulation in small samples of human tissue and should enable us to define more clearly the level at which abnormal gene regulation occurs.
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PMID:Quantitative in-situ hybridization histochemistry studies on growth hormone (GH) gene expression in acromegalic somatotrophs: effects of somatostatin, GH-releasing factor and cortisol. 290 68

Thyrotropic pituitary adenoma is a rare disease fortunately diagnosed with increasing frequency. Its originality lies in the fact that it occurs in two very different pathological contexts. The first form raises few problems: the occurrence of a pituitary tumoral syndrome in a patient with hypothyroidism, even of relatively short duration, should suggest the diagnosis. In such cases of reactive thyrotropic adenoma, simple correction of the hypothyroidism by replacement therapy seems to be capable not only of curing the thyroid disorder and lowering TSH values, but also of promoting regression of the pituitary tumour. Primary autonomous adenoma responsible for TSH hypersecretion followed by thyrotoxicosis belongs to the realm of inappropriate TSH secretion, and it should be diagnosed whenever high, or even normal (at least non-suppressed). TSH levels coexist with peripheral hyperthyroidism. As a rule, the presence of a pituitary tumour differentiates this adenoma from non-tumoral inappropriate TSH secretion due to resistance to thyroid hormones. Primary thyrotropic pituitary adenoma is treated by surgery. In case of failure or relapse, radiotherapy or medical treatment with a dopaminergic agonist or a long-acting somatostatin analogue may be considered.
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PMID:[Thyrotropic pituitary adenoma. Clinical aspects, course and treatment]. 295 27

Although the benign counterpart of medullary carcinoma of the thyroid has never been indicated in textbooks, we propose that C cell adenoma is a rare but distinct clinical entity. Two patients, a 43-year-old man and a 53-year-old woman, had similar thyroid tumors, both about 4 cm in diameter. The cut surfaces of the resected tumors were indistinguishable from a common microfollicular adenoma of the thyroid. Microscopically, the tumors were uniformly composed of fusiform cells without any follicle formation. Neither amyloid deposition nor calcification was found. Although some kind of C cell tumors were suggested, the exact nature was debatable. However, extremely high levels of calcitonin (1330 and 2065 pg/ml, respectively; normal level, less than 170 pg/ml) were found in the stored sera taken preoperatively. Serum levels of carcinoembryonic antigen (CEA) were normal in both patients. Immunohistochemically, the tumor tissues were positive for calcitonin and neuron-specific enolase but negative for CEA with a monoclonal anti-CEA antibody. No somatostatin, glucagon, or adrenocorticotropic hormone activity was found. It is highly probable that such tumors have not been closely studied and have been regarded as eccentric adenomas of the thyroid or simply as the so-called medullary carcinomas of the thyroid.
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PMID:C cell adenoma of the thyroid: a rare but distinct clinical entity. 319 51

Postoperative persistence of elevated growth hormone (GH) levels in patients with acromegaly usually suggests residual adenoma tissue secreting GH and is an indication for further treatment. In rare cases, spontaneous normalization of serum GH levels in patients with acromegaly has been reported to occur as a consequence of intratumoral hemorrhage (pituitary apoplexy). We report two patients in whom persisting acromegaly was documented 1 and 2 weeks, respectively, after transsphenoidal operation and who experienced spontaneous normalization of GH levels. In one patient, this favorable outcome was found 1.5 years after the operation and followed a pregnancy. The other patient, whose GH values normalized 3 months after operation, had received preoperative treatment with a new, long-acting somatostatin analog.
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PMID:Spontaneous postoperative normalization of growth hormone levels in two patients with acromegaly not cured by transsphenoidal surgery. 320 Mar 94

Acromegaly is caused by GH-secreting pituitary adenomas and, in rare cases, by ectopic production of GRH with resultant hypersecretion of GH. Important systemic manifestations include acral enlargement, swelling, disfigurement, glucose intolerance and diabetes, hypertension, nerve entrapment, arthropathy, and cardiac disease. Tumor-related major manifestations are visual impairment, oculomotor paralysis, and hypopituitarism. Morbidity is substantial, and mortality is increased. Diagnosis should be made as early as possible by measuring plasma GH after an oral glucose load and plasma somatomedin C levels. Assessment of a pituitary lesion is best made by CT scanning in the coronal plane. Therapy is mandatory and consists of surgical removal of the pituitary adenoma (usually by the transsphenoidal route) or of the ectopic source of GRH (carcinoids or islet cell tumors). Adjunctive radiation and/or drug therapy is often necessary if complete surgical ablation of the adenoma is not possible. Radiation therapy can be administered as conventional supervoltage x-ray treatment or in the form of heavy particle beams. Drugs effective in partially lowering GH levels are bromocriptine and (not yet released) somatostatin analogues. Long-term follow-up of treated patients is important to guard against recurrence, progression, or development of hypopituitarism.
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PMID:Acromegaly. 331 99


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