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)

To study the possible alteration of mucosal-submucosal somatostatin-containing cells in inflammatory bowel diseases (IBD), the total numbers of somatostatin-containing endocrine cells (SCEC) and submucosal ganglion cells (SGC) were counted in Crohn's disease (CD) and ulcerative colitis (UC). Tissue specimens from 25 CD and 25 UC patients were fixed in Hollande's fixative immediately after resection and were investigated by immunohistochemical staining. A single specimen was collected from 25 colorectal cancer patients, the control group. There was a significant difference in the number of SCEC between the tissues taken from the proximal colon (ascending and transverse colon) and the distal colon (descending and sigmoid colon). The distal colon tended to contain more somatostatin-immunoreactive cells than did the proximal colon. In IBD, SCEC were decreased in number compared with the controls. This decrease was related to the degree of inflammation in CD; the higher the grade of inflammation, the lower the number of SCEC. The number of SGC was decreased in IBD: however, a significant decrease was noticed only in CD. The anatomic origin and the degree of inflammation did not affect the number of SGC. In the present study, the decrease of somatostatin-containing cells was noticed in both CD and UC, but there was no significant difference between CD and UC. Therefore, it was assumed that this decrease was secondary to inflammation. However, the decrease of somatostatin, which works as an inhibitory peptide for inflammation, might have some role in the pathogenesis of IBD.
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PMID:Distribution and quantification of somatostatin in inflammatory disease. 134 80

Filiform polyposis (FP) is a rare condition of uncertain pathogenesis, 28 cases of which have been published since it was first described in 1965. It is usually found in association with chronic inflammatory bowel disease, especially Crohn's disease and ulcerative colitis. The condition is characterized by the presence of numerous, densely packed, filiform polyps in the colon, which may resemble villous adenomas on endoscopy. We describe a case of FP occurring in a 33-year-old man with a 5-year history of Crohn's disease, in whom subtotal colectomy was performed because of perforation of the sigmoid colon. Microscopy revealed inflammatory pseudopolyps covered by largely normal and non-dysplastic colonic epithelium. The neuroendocrine system of the intestine in FP was investigated for the first time in this case: marked hyperplasia of endocrine cells immunoreactive for serotonin, somatostatin and enteroglucagon and of neural structures immunoreactive for substance P and vasoactive intestinal peptide was noted in the polyps and the adjacent intestinal mucosa. The patient has experienced no further complications in the 12 months since the operation. Medication administered in FP depends mainly on the nature of the underlying disease, and the amount of information published about this condition is as yet insufficient to allow any one specific type of treatment to be recommended. FP alone is not an indication for bowel resection but complications, such as massive haemorrhage or intestinal obstruction, may necessitate surgical intervention.
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PMID:Filiform polyposis: a case report describing clinical, morphological, and immunohistochemical findings. 139 19

Glutamate and several neuropeptides are synthesized and released by subpopulations of primary afferent neurons. These sensory neurons play a role in regulating the inflammatory and immune responses in peripheral tissues. We have explored what changes occur in the location and concentration of receptor binding sites for sensory neurotransmitters in two human inflammatory diseases, ulcerative colitis and Crohn's disease, using quantitative receptor autoradiography. The sensory neurotransmitter receptors included bombesin, calcitonin gene-related peptide-alpha, cholecystokinin, galanin, glutamate, somatostatin, neurokinin A (substance K), substance P, and vasoactive intestinal polypeptide. Of the nine receptor binding sites examined only binding sites for substance P and vasoactive intestinal peptide were significantly altered in the inflamed tissue. These data suggest that substance P is involved in regulating the inflammatory and immune responses in human inflammatory diseases and indicate a specificity of efferent action for each sensory neurotransmitter in peripheral tissues.
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PMID:Alterations in receptors for sensory neuropeptides in human inflammatory bowel disease. 165 49

Glutamate and several neuropeptides are synthesized and released by subpopulations of primary afferent neurons. These sensory neurons play a role in regulating the inflammatory and immune responses in peripheral tissues. Using quantitative receptor autoradiography we have explored what changes occur in the location and concentration of receptor binding sites for sensory neurotransmitters in the colon in two human inflammatory diseases, ulcerative colitis and Crohn's disease. The sensory neurotransmitter receptors examined included bombesin, calcitonin gene related peptide-alpha, cholecystokinin, galanin, glutamate, somatostatin, neurokinin A (substance K), substance P, and vasoactive intestinal polypeptide. Of the nine receptor binding sites examined only substance P binding sites associated with arterioles, venules and lymph nodules were dramatically up-regulated in the inflamed tissue. These data suggest that substance P is involved in regulating the inflammatory and immune responses in human inflammatory diseases and indicate a specificity of efferent action for each sensory neurotransmitter in peripheral tissues.
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PMID:Receptors for sensory neuropeptides in human inflammatory diseases: implications for the effector role of sensory neurons. 255 Sep 12

The effect of a long acting somatostatin analogue SMS 201-995 on stomal effluents in patients with severe short bowel syndrome was investigated in a double blind placebo controlled balance study. Six patients, five with Crohn's disease and one with radiation enteropathy were studied. Five patients had a jejunostomy and one an ileostomy. The patients had a normal food intake, but because of severe malabsorption had received home parenteral nutrition for several years. Faecal mass was reduced (p less than 0.005) and intestinal net sodium absorption was increased (p less than 0.005) by intravenous infusion of SMS 25 micrograms/h. Net absorption of potassium, calcium, magnesium phosphate, zinc, nitrogen and fat was not influenced. Subcutaneous injections of 50 micrograms SMS every 12 hours had a similar effect on net intestinal absorption of sodium and water. Four patients continued with a five to six months open follow up study when subcutaneous SMS in the same dose was administered by the patients at home. The effect on faecal sodium loss persisted, but in one patient faecal mass gradually increased and finally exceeded pretreatment values. SMS may decrease net absorption of water and sodium following reduced secretion of digestive juices rather than by increasing absorptive capacity. SMS may be useful as an antidiarrhoeal drug in patients with high output jejuno- or ileostomies, but in patients who need permanent parenteral nutrition the effect is too small to significantly alter management.
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PMID:Effect of a long acting somatostatin analogue SMS 201-995 on jejunostomy effluents in patients with severe short bowel syndrome. 231 26

The author gives an account of clinical syndromes which develop as a result of overproduction of gastrointestinal hormones. From the various diagnostic approaches, which are not always available or are expensive, the author summarizes the importance of thin-needle biopsy under sonographic control, the argentaffine technique (Grimelius) and histoenzymatic examination for neuron specific enolase. In addition to surgical treatment treatment with streptozotocine, 5-FU, dimethyl triazenoimidazole carboxamide and somatostatin is possible. The author draws attention to the possibility of using somatostatin not only in the treatment of apudomas but also of haemorrhage into the gastrointestinal tract and in the treatment of fistulae. Neuroendocrine factors probably play a significant role in the pathophysiology of irritable colon, Crohn's disease, achalasia and Hirschsprung's disease.
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PMID:[Gastrointestinal hormones--clinical significance]. 273 95

To study the effect of mucosal inflammation on tissue concentrations of somatostatin, the distribution and concentration of somatostatin in specimens of normal and abnormal (ulcerative colitis and Crohn's disease) ileum and colon were determined by a specific radioimmunoassay. Each tissue specimen obtained at surgery was separated by microdissection into the mucosa-submucosa and the muscularis externa. Immunoreactive somatostatin was acid-extracted from each layer before measurement. Gel chromatography was used to characterize immunoreactive somatostatin measured by radioimmunoassay; somatostatin-28 was the major immunoreactive species measured in human intestine. In normal colon, concentrations of somatostatin were not related to patient age. Concentrations of immunoreactive somatostatin in the mucosa-submucosa of the descending colon were significantly decreased in ulcerative colitis and in Crohn's colitis, compared with normal colon. There was no apparent relationship between concentrations of somatostatin and the duration of inflammatory bowel disease. However, somatostatin concentrations appeared to be lower in patients with severe colitis than in patients with minimal colitis. The decrease in mucosal-submucosal concentrations of somatostatin is in agreement with previous morphologic studies, which have suggested diminished populations of endocrine cells in ulcerative colitis. The possible role of somatostatin in the colon suggests that further studies of the alteration of this gut peptide may be useful in understanding a component of the pathophysiology of idiopathic inflammatory bowel disease.
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PMID:Somatostatin in the idiopathic inflammatory bowel diseases. 289 35

The mucosal concentrations of seven regulatory peptides and the density properties and integrity of their storage granules have been studied in mucosal biopsies from the human jejunum in eight gastrointestinal disease states and compared with normal controls. In diseases with associated mucosal inflammation (coeliac disease, Crohn's disease with jejunal involvement, postinfective tropical malabsorption, and common variable immunodeficiency) there was a selective increase in fragility of the gastric inhibitory polypeptide (GIP) and somatostatin storage granules. The gastrin, motilin, enteroglucagon, secretin, and vasoactive intestinal polypeptide granules had normal properties in these conditions. In diseases in which diarrhoea occurred in the absence of changes in jejunal mucosal histology (irritable bowel syndrome, pancreatic insufficiency, jejuno-ileal bypass for morbid obesity, and purgative abuse) there were no abnormalities of the storage granules. Increased mucosal concentrations of all peptides except vasoactive intestinal polypeptide (VIP) were found in coeliac disease and selective increases of VIP found in Crohn's disease, motilin in the irritable bowel syndrome and gastrin and GIP in pancreatic insufficiency. It is suggested that the storage granule abnormalities in the diseases with abnormal mucosal histology are secondary to the inflammatory changes.
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PMID:Gastrointestinal regulatory peptide storage granule abnormalities in jejunal mucosal diseases. 614 62

Autoantibodies reacting with endocrine cells in the gastrointestinal mucosa were found by indirect immunofluorescence in 22 out of 268 sera (8.2%) obtained from patients with coeliac disease, Crohn's disease, ulcerative colitis, irritable bowel syndrome, and from subjects without bowel disease. A double immunofluorescence technique showed that the autoantibodies reacted with cells secreting gastric inhibitory polypeptide (glucose dependent insulinotropic polypeptide, GIP), secretin, somatostatin or enteroglucagon. Most sera contained antibodies against more than one cell type. Neither the presence of a particular antibody nor the pattern of antibody combinations appeared to be specific for any diagnostic category. The mean plasma GIP concentrations, however, both fasting and two hours after a test meal, were significantly lower in subjects with GIP cell autoantibodies. Thus gut hormone cell autoantibodies may be markers of impaired hormone secretion.
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PMID:Autoantibodies to gut hormone secreting cells as markers of peptide deficiency. 634 Nov 78

A 72-year-old man with Crohn's disease for about 6 years was urgently hospitalized in hypovolaemic shock. On admission, serum creatinine concentration was 4.2 mg/dl, serum sodium 124 mmol/l, as a result of massive fluid and electrolyte loss via a loop ileostomy which had been placed 4 weeks previously because of a complicated perianal fistula. The basic aetiology of the diarrhoea probably lay in the previous resection of 30 cm of terminal ileum, other possible causes having been excluded. The ileostomy diarrhoea persisted despite the administration of loperamide, ranitidine, glucocorticoids, opium and pancreatic enzymes. Metronidazole, given in case the diarrhoea was due to a change in bacterial flora, also failed to achieve improvement. But when the somatostatin analogue octreotide was administered, the fluid loss via the ileostomy was quickly reduced so that both fluid and electrolyte infusions could be stopped. In subsequent months the initially required daily octreotide dosage of three times 100 micrograms could be reduced to once 50 micrograms subcutaneously. But it was not possible to stop this drug completely: it has now been continued and well tolerated for 2 years.
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PMID:[Successful treatment of a life-threatening ileostomy diarrhea with the somatostatin analog octreotide]. 800 65


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