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Query: UMLS:C0024523 (malabsorption)
 7,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Postinfective irritable bowel syndrome with diarrhoea and idiopathic bile acid malabsorption remains an enigma. We examined the records of 84 patients whose 75SeHCAT scans were indicative of bile acid malabsorption (< 15% one week retention). Identifiable causes of bile acid malabsorption were: previous ileal surgery (7), Crohn's disease (22), radiation enteritis (13), vagotomy, gastrectomy or cholecystectomy (10) and miscellaneous (3). Sixteen of 29 patients with apparently idiopathic bile acid malabsorption gave a clear history of acute gastroenteritis before the onset of chronic diarrhoea lasting from 0.25-18 years until their positive 75SeHCAT scan. Only four cases of campylobacter, and one each of shigella and salmonella were documented. Extensive investigation failed to detect other possible pathologies. In response to bile acid sequestrants, mean stool frequency fell from 7.2 per day to 2.1 per day (p < 0.001). We have observed that postinfective chronic diarrhoea is associated with chronic bile acid malabsorption, which can be successfully treated with bile acid sequestrants such as cholestyramine.
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PMID:Postinfective diarrhoea and bile acid malabsorption. 1133 65

Short bowel syndrome (SBS) refers to the malabsorption of nutrients, water, and essential vitamins as a result of disease or surgical removal of parts of the small intestine. The most common reasons for removing part of the small intestine are due to surgical intervention for the treatment of either Crohn's disease or necrotizing enterocolitis. Intestinal adaptation following resection may take weeks to months to be achieved, thus nutritional support requires a variety of therapeutic measures, which include parenteral nutrition. Improper nutrition management can leave the SBS patient malnourished and/or dehydrated, which can be life threatening. The development of therapeutic strategies that reduce both the complications and medical costs associated with SBS/long-term parenteral nutrition while enhancing the intestinal adaptive response would be valuable. Currently, therapeutic options available for the treatment of SBS are limited. There are many potential stimulators of intestinal adaptation including peptide hormones, growth factors, and neuronally-derived components. Glucagon-like peptide-2 (GLP-2) is one potential treatment for gastrointestinal disorders associated with insufficient mucosal function. A significant body of evidence demonstrates that GLP-2 is a trophic hormone that plays an important role in controlling intestinal adaptation. Recent data from clinical trials demonstrate that GLP-2 is safe, well-tolerated, and promotes intestinal growth in SBS patients. However, the mechanism of action and the localization of the glucagon-like peptide-2 receptor (GLP-2R) remains an enigma. This review summarizes the role of a number of mucosal-derived factors that might be involved with intestinal adaptation processes; however, this discussion primarily examines the physiology, mechanism of action, and utility of GLP-2 in the regulation of intestinal mucosal growth.
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PMID:Gut hormones, and short bowel syndrome: the enigmatic role of glucagon-like peptide-2 in the regulation of intestinal adaptation. 1683 Mar 59

The global epidemic of obesity and its related disease in combination with robust physiological defence of intentional weight loss generates a pressing need for effective weight loss therapies. Bariatric surgery, which works very effectively at delivering substantial sustained weight loss, has been an enigma with respect to mechanism of action. Naive concepts of restriction and malabsorption do not explain the efficacy of the most commonly used bariatric procedures. This century has seen increased interest in unravelling the mystery of the mechanisms underlying surgery associated weight loss with a focus on integrative gastrointestinal (GI) physiology, gut-brain signalling, and beyond weight loss effects on metabolism. GI interventions, some very minor, can alter GI wall stretch and pressure receptors; a range of GI hormones affecting hunger and satiety; bile acid metabolism and signalling; the characteristics of GI microbiome; portal vein nutrient sensing; and circulating concentrations of amino acids. Understanding the mechanisms involved should present targets for less invasive effective therapies.
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PMID:Neuroendocrine adaptations to bariatric surgery. 2604 66