Irritable bowel syndrome (IBS) is one of the most prevalent functional gastrointestinal disorders. It is a multifactorial disorder with its pathogenesis attributed to abnormal gastrointestinal motility, low-grade inflammation, visceral hypersensitivity, communication in the gut-brain axis, and so on. Traditionally, IBS has been treated with diet and lifestyle modification, fiber supplementation, psychological therapy, and pharmacological treatment. Carbohydrates are intermingled with a wide range of regularly consumed food including grains such as rye and wheat, vegetables, fruits, and legumes. Short-chain carbohydrates that are poorly absorbed exert osmotic effects in the intestinal lumen increasing its water volume, and are rapidly fermented by bacteria with consequent gas production. These effects may be the basis for the induction of most of the gastrointestinal symptoms. This has led to the use of lactose-free diets in those with lactose intolerance and of fructose-reduced diets for fructose malabsorption. As all poorly absorbed short-chain carbohydrates have similar and additive effects in the intestine, a concept has been developed to regard them collectively as FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides and polyols) and to evaluate a dietary approach that restricts them all. Based on the observational and comparative studies, and randomized-controlled trials, FODMAPs have been shown to trigger gastrointestinal symptoms in patients with IBS. Food choice via the low FODMAPs and potentially other dietary strategies is now a realistic and efficacious therapeutic approach for managing symptoms of IBS.
*Diet, Carbohydrate-Restricted ; Dietary Supplements ; Humans ; Hypersensitivity/complications ; Inflammation/complications ; Intestines/pathology ; Irritable Bowel Syndrome/complications/*diagnosis/diet therapy ; Malabsorption Syndromes/complications ; Monosaccharides/metabolism ; Oligosaccharides/metabolism

Previous reviews have highlighted complementary and alternative medicine therapies that are used to treat irritable bowel syndrome (IBS) based on published clinical trial data. Here the author describes and comments on a number of potentially relevant factors that have been commonly emphasized by practitioners who treat IBS and patients who have the disease. They include gluten and other food allergies, the candida syndrome and biofilm, interference fields and post-infectious IBS, as well as mind-body factors.
Food Hypersensitivity ; complications ; immunology ; Glutens ; immunology ; Humans ; Integrative Medicine ; Irritable Bowel Syndrome ; complications ; microbiology ; pathology ; therapy ; Mind-Body Therapies ; Wound Healing

Bile acid diarrhea (BAD) is usually seen in patients with ileal Crohn's disease or ileal resection. However, 25% to 50% of patients with functional diarrhea or diarrhea-predominant irritable bowel syndrome (IBS-D) also have evidence of BAD. It is estimated that 1% of the population may have BAD. The causes of BAD include a deficiency in fibroblast growth factor 19 (FGF-19), a hormone produced in enterocytes that regulates hepatic bile acid (BA) synthesis. Other potential causes include genetic variations that affect the proteins involved in BA enterohepatic circulation and synthesis or in the TGR5 receptor that mediates the actions of BA in colonic secretion and motility. BAs enhance mucosal permeability, induce water and electrolyte secretion, and accelerate colonic transit partly by stimulating propulsive high-amplitude colonic contractions. There is an increased proportion of primary BAs in the stool of patients with IBS-D, and some changes in the fecal microbiome have been described. There are several methods of diagnosing BAD, such as 75selenium homotaurocholic acid test retention, serum C4, FGF-19, and fecal BA measurement; presently, therapeutic trials with BA sequestrants are most commonly used for diagnosis. Management involves the use of BA sequestrants including cholestyramine, colestipol, and colesevelam. FXR agonists such as obeticholic acid constitute a promising new approach to treating BAD.
Anticholesteremic Agents/therapeutic use ; Bile Acids and Salts/*physiology ; Crohn Disease/complications ; Diarrhea/*etiology/pathology/therapy ; Feces/chemistry ; Fibroblast Growth Factors/deficiency ; Gastrointestinal Microbiome ; Humans ; Irritable Bowel Syndrome/complications

BACKGROUND/AIMS: The endoscopic findings and clinical relevance of portal hypertensive colopathy are not well described in Korea. We aimed to do a retrospective study of mucosal changes in the colon of patients with liver cirrhosis and to find their association with clinical characteristics. METHODS: We reviewed the clinical data and endoscopic findings of 48 patients with liver cirrhosis and 48 patients, matched for age and sex, with irritable bowel disease (IBS) who underwent colonoscopy over a 5 year span. RESULTS: Patients with liver cirrhosis were more likely to have colitis-like lesions and vascular abnormalities than IBS patients. Low platelet count (p=0.005) and severe esophageal varices (p=0.011) were associated with portal hypertensive colopathy, whereas the etiologies and severity of cirrhosis were not associated with these findings. CONCLUSIONS: Portal hypertensive colopathy can be defined with colitis-like lesions or vascular lesions. These lesions are more frequently present in patients with more severe esophageal varices and thrombocytopenia.
Adult ; Aged ; Colonoscopy ; Esophageal and Gastric Varices/etiology ; Female ; Humans ; Hypertension, Portal/complications/*pathology ; Intestinal Mucosa/pathology ; Irritable Bowel Syndrome/complications/*pathology ; Liver Cirrhosis/complications/*pathology ; Male ; Middle Aged ; Platelet Count ; Retrospective Studies ; Severity of Illness Index ; Thrombocytopenia/etiology

PURPOSE: Postinfectiously irritable bowel syndrome (PI-IBS) develops in 3-30% of individuals with bacterial gastroenteritis. Recent studies demonstrated increases in inflammatory components in gut mucosa of PI-IBS patients even after complete resolution of infection. We aimed to investigate histological changes in colon and rectum of PI-IBS subjects after long term period of infection. MATERIALS AND METHODS: We recruited PI-IBS subjects who had been diagnosed IBS after complete resolution of enteritis caused by shigellosis outbreak 3 years earlier. We compared unmatched four groups, PI-IBS (n = 4), non PI-IBS (n = 7), D-IBS (n = 7, diarrhea predominant type) and healthy controls (n = 10). All of them underwent colonoscopic biopsy at three areas, including descending colon (DC), sigmoid colon (SC) and rectum, which were assessed for 5-hydroxytryptamine (5-HT)/peptide YY (PYY)-containing enterochromaffin (EC) cell, intraepithelial (IEL) and lamina propria T lymphocyte (CD3), CD8 lymphocytes, mast cells and CD68/calprotectin+ macrophages. RESULTS: All subjects had no structural or gross abnormalities at colonoscopy. In PI-IBS, 5-HT containing EC cells, PYY containing EC cells, IELs, CD3 lymphocytes, CD8 lymphocytes, mast cells, and CD68 + macrophages were increased compared to control (p < 0.05). In D-IBS, PYY containing EC cells, IELs, and CD3 lymphocytes were increased compared to control (p < 0.05). In PI-IBS, 5-HT containing EC cells tended to increase and PYY containing EC cells, CD8 lymphocytes, mast cells, and CD68+ macrophages were increased compared to non PI-IBS (p < 0.05). Calprotectin + marcrophages were decreased in PI-IBS, non PI-IBS and IBS compared to control. CONCLUSION: The immunoendocrine cells were sporadically increased in PI-IBS, non PI-IBS and D-IBS compared with control. Our findings in a very small number of patients suggest that mucosal inflammation may play a role in long-term PI-IBS, and that other sub-groups of IBS and larger scale studies are needed to confirm this observation.
Adult ; Antigens, CD/metabolism ; Antigens, Differentiation, Myelomonocytic/metabolism ; CD8-Positive T-Lymphocytes/cytology ; Case-Control Studies ; Colon, Descending/pathology ; Colon, Sigmoid/pathology ; Colonoscopy ; Dysentery, Bacillary/*complications ; Enterochromaffin Cells/cytology ; Female ; Humans ; Immunohistochemistry ; Intestinal Mucosa/*pathology ; Irritable Bowel Syndrome/metabolism/*pathology ; Macrophages/cytology ; Male ; Mast Cells/cytology ; Peptide YY/metabolism ; Rectum/pathology ; Serotonin/metabolism