Irritable bowel syndrome (IBS)

Enck et al. found that irritable bowel syndrome manifests with a relative decrease in populations of bifidobacteria and significant differences in a variety of other microbes, including those that cause the production of gas.(Enck et al. 2009)

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Intern Med J. 2006 Nov;36(11):724-8. Irritable bowel syndrome. Talley NJ. Mayo Clinic College of Medicine, Dyspepsia Center, Clinical Enteric Neuroscience Translational and Epidemiological Research Program, Rochester, Minnesota 55905, USA. talley.nicholas@mayo.edu Abstract Conceptually, the irritable bowel syndrome (IBS) has been considered a brain-gut functional disorder, but this paradigm is under serious challenge. There is increasing evidence that organic disease of the gastrointestinal tract can be identified in subsets of patients who fulfil the Rome criteria for IBS. Evidence for subtle inflammatory bowel disease, serotonin dysregulation, bacterial overgrowth and central dysregulation continue to accumulate. The underlying causes of IBS remain to be adequately identified, but postinfectious IBS is a clear-cut entity. Furthermore, a genetic contribution to IBS also seems likely. Diagnosis continues to be based on the symptom profile and the absence of alarm features. A heightened awareness of coeliac disease masquerading as IBS is becoming accepted. Management remains largely based on symptomatic rather than on disease-modifying therapy, but this is likely to change in the near future. Here, recent advances in the pathophysiology and management of IBS are considered. PMID: 17040359

Psychosomatics. 2010 May;51(3):225-9. Motivation for psychotherapy in patients with functional gastrointestinal disorders. Martens U, Enck P, Matheis A, Herzog W, Klosterhalfen S, Rühl A, Zipfel S, Sammet I. University Hospitals, Tübingen, Department of Internal Medicine VI, Psychosomatic Medicine and Psychotherapy, Frondsbergstr. 23, 72076 Tübingen, Germany. Abstract BACKGROUND: The motivation of patients with functional gastrointestinal disorders to accept psychotherapy (PT) as a treatment option is not known. OBJECTIVE: The authors investigated motivation for patients' refusal to participate and dropout from PT/medical management programs. METHOD: Consecutive patients with symptoms suggestive of functional bowel disorders, seen at the outpatient clinic of a tertiary gastrointestinal (GI) center were evaluated for their motivation to undergo PT. Data from 85 patients were evaluated in two phases: In Phase 1, patients were asked about willingness to participate in PT if it were offered; in Phase 2, patients were offered PT. In both samples, PT motivation was also measured by standardized psychometric scales. RESULTS: Age, gender, social status, and clinical symptom severity did not predict willingness to participate in or accept PT. Motivation was higher when patients were directly recruited in a GI setting than a psychosomatic outpatient unit. Quantitative assessment of PT motivation also did not correlate with declared PT motivation or participation. Assessment of interpersonal problems were among the few variables that were related to participation in PT. CONCLUSION: Motivation for PT in patients with functional gastrointestinal disorders is low and is not determined by clinical, but, rather, by interpersonal problems that may exist beyond and independent of GI symptoms. PMID: 20484720

Am J Gastroenterol. 2006 Jun;101(6):1295-8. Mucosal barrier defects in irritable bowel syndrome. Who left the door open? Barbara G. Comment on: Am J Gastroenterol. 2006 Jun;101(6):1288-94. Abstract There has been recent interest into the potential role of cellular and molecular mechanisms in the pathophysiology of irritable bowel syndrome (IBS). Although the intestinal mucosa of IBS patients is endoscopically and histologically “normal,” it contains an increased number of activated T lymphocytes and mast cells, along with evidence of an increased release of mediators known to signal to epithelial, neuronal, and muscle cells leading to intestinal dysfunction. In this issue, Dunlop et al. provide evidence of increased intestinal permeability in patients with diarrhea predominant IBS. There is now consistent evidence indicating that mucosal barrier defects allow the passage of an increased load of luminal antigens of dietary and bacterial origin which, in turn, elicit the activation of mucosal immune responses involved in the generation of diarrhea. Further work has now to be done to better understand the interplay among luminal factors, epithelial cells, and mucosal immunocytes in the pathogenesis of IBS. PMID: 16771952

Diabetes. 2008 Oct;57(10):2555-62. The “perfect storm” for type 1 diabetes: the complex interplay between intestinal microbiota, gut permeability, and mucosal immunity. Vaarala O, Atkinson MA, Neu J. Laboratory for Immunobiology, Department of Viral Diseases and Immunology, National Public Health Institute, Helsinki, Finland. outi.vaarala@ktl.fi Abstract It is often stated that type 1 diabetes results from a complex interplay between varying degrees of genetic susceptibility and environmental factors. While agreeing with this principal, our desire is that this Perspectives article will highlight another complex interplay potentially associated with this disease involving facets related to the gut, one where individual factors that, upon their interaction with each another, form a “perfect storm” critical to the development of type 1 diabetes. This trio of factors includes an aberrant intestinal microbiota, a “leaky” intestinal mucosal barrier, and altered intestinal immune responsiveness. Studies examining the microecology of the gastrointestinal tract have identified specific microorganisms whose presence appears related (either quantitatively or qualitatively) to disease; in type 1 diabetes, a role for microflora in the pathogenesis of disease has recently been suggested. Increased intestinal permeability has also been observed in animal models of type 1 diabetes as well as in humans with or at increased-risk for the disease. Finally, an altered mucosal immune system has been associated with the disease and is likely a major contributor to the failure to form tolerance, resulting in the autoimmunity that underlies type 1 diabetes. Herein, we discuss the complex interplay between these factors and raise testable hypotheses that form a fertile area for future investigations as to the role of the gut in the pathogenesis and prevention of type 1 diabetes. PMID: 18820210

Gastroenterology. 2009 May;136(6):2015-31. Targeting the human microbiome with antibiotics, probiotics, and prebiotics: gastroenterology enters the metagenomics era. Preidis GA, Versalovic J. Interdepartmental Program in Translational Biology and Molecular Medicine, Baylor College of Medicine, Houston, Texas, USA. Abstract Studies of metagenomics and the human microbiome will tremendously expand our knowledge of the composition of microbial communities in the human body. As our understanding of microbial variation and corresponding genetic parameters is refined, this information can be applied to rational remodeling or “tailoring” of human-associated microbial communities and their associated functions. Physiologic features such as the development of innate and adaptive immunity, relative susceptibilities to infections, immune tolerance, bioavailability of nutrients, and intestinal barrier function may be modified by changing the composition and functions of the microbial communities. The specialty of gastroenterology will be affected profoundly by the ability to modify the gastrointestinal microbiota through the rational deployment of antibiotics, probiotics, and prebiotics. Antibiotics might be used to remove or suppress undesirable components of the human microbiome. Probiotics can introduce missing microbial components with known beneficial functions for the human host. Prebiotics can enhance the proliferation of beneficial microbes or probiotics, to maximize sustainable changes in the human microbiome. Combinations of these approaches might provide synergistic and effective therapies for specific disorders. The human microbiome could be manipulated by such “smart” strategies to prevent and treat acute gastroenteritis, antibiotic-associated diarrhea and colitis, inflammatory bowel disease, irritable bowel syndrome, necrotizing enterocolitis, and a variety of other disorders. PMID: 19462507

Curr Opin Gastroenterol. 2006 Nov;22(6):669-73. Bacterial overgrowth as a cause of irritable bowel syndrome. Riordan SM, Kim R. Source Gastrointestinal and Liver Unit and University of New South Wales, Sydney, NSW, Australia. sriordan@ozemail.com.au Abstract PURPOSE OF REVIEW: To review recently published studies investigating any association between gut flora and symptoms of irritable bowel syndrome.

RECENT FINDINGS: Experimental studies demonstrate associations between gut flora, gut motility, mucosal inflammation and visceral hypersensitivity. Scientific bases for possible benefits of selected probiotics on irritable bowel symptoms have been identified. Disturbances in viable counts of fecal flora have been demonstrated in patients with irritable bowel syndrome. Results of studies based on breath tests are conflicting as to whether the prevalence of small intestinal bacterial overgrowth is increased in this group. Nonetheless, a longitudinal analysis based on bacteriological assessments of serial small intestinal aspirates suggests that this entity should be considered in patients with irritable bowel symptoms, especially in the setting of predisposition to bacterial overgrowth. Clinical trials of probiotic treatment for irritable bowel syndrome have yielded conflicting results.

SUMMARY: Recent studies provide increasing support for the concept that disturbances in gut flora occur in patients with irritable bowel syndrome and that such abnormalities may contribute to irritable bowel syndrome-type symptoms. The relative importance of disturbed gut flora to symptom pathogenesis, along with the therapeutic potential of modulation of the gut flora for amelioration of irritable bowel syndrome symptoms, however, remains to be fully defined.

PMID: 17053447

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Melinda Stiles

Lyme disease, irritable bowel syndrome/ulcerative colitis, radiculitis

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Chris Eastlund

diabetes, sarcoidosis, irritable bowel syndrome

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Interviews of patients with other diseases are also available.

Infection of human enteroendocrine cells withChlamydia trachomatis: a possible model for pathogenesis in irritable bowel syndrome