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• W2567686958 abstract "Helicobacter pylori (H. pylori) infection is involved in multiple gastrointestinal and extra-gastrointestinal disorders. This review focuses on possible link between H. pylori eradication and Crohn's disease (CD) which is a chronic inflammatory bowel disease (IBD). Fecal calprotectin and; to lesser extent; fecal lactoferrin are sensitive and specific markers for monitoring CD activity. Data about link between H. pylori eradication and CD are limited and inconclusive. The infection likely shifts equilibrium between T helper 1 (Th1) and Th2 immune responses to the Th2 pattern. In subjects genetically predisposed to CD (a Th1-related disease), H. pylori eradication increases Th1 proinflammatory cytokines causing development of CD. In contrast, clarithromycin and/or proton pump inhibitors that are used to eradicate H. pylori can suppress Th1 factors, and theoretically can protect against CD, but there are no data to support this supposition. This Th1/Th2 approach seems very simplistic. Another theory is that alterations in gut microbiota form continuous antigenic stimulation predisposing to IBD. H. pylori infection can inhibit such stimulation through activation of regulatory T cells, and thus eradication may predispose to CD. Probiotics weren't found useful in treatment of CD. The reported data about link between H. pylori eradication and CD are currently limited. Case reports, suggesting a positive association between both conditions, provide a very little evidence. On eradicating H. pylori in CD patients and/or patients with high risk for CD, patient counseling and follow-up in addition to measuring fecal calprotectin may help monitor CD activity. (Acta gastro-enterol. belg., 2016, 79, 349-354)." @default.
• W2567686958 created "2017-01-06" @default.
• W2567686958 creator A5056687510 @default.
• W2567686958 date "2016-11-09" @default.
• W2567686958 modified "2023-09-23" @default.
• W2567686958 title "Does Helicobacter pylori eradication therapy trigger or protect against Crohn's disease?" @default.
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