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Proton pump inhibitors and dysbiosis: Current knowledge and aspects to be clarified.
Bruno, G, Zaccari, P, Rocco, G, Scalese, G, Panetta, C, Porowska, B, Pontone, S, Severi, C
World journal of gastroenterology. 2019;(22):2706-2719
Abstract
Proton pump inhibitors (PPIs) are common medications within the practice of gastroenterology. These drugs, which act through the irreversible inhibition of the hydrogen/potassium pump (H+/K+-ATPase pump) in the gastric parietal cells, are used in the treatment of several acid-related disorders. PPIs are generally well tolerated but, through the long-term reduction of gastric acid secretion, can increase the risk of an imbalance in gut microbiota composition (i.e., dysbiosis). The gut microbiota is a complex ecosystem in which microbes coexist and interact with the human host. Indeed, the resident gut bacteria are needed for multiple vital functions, such as nutrient and drug metabolism, the production of energy, defense against pathogens, the modulation of the immune system and support of the integrity of the gut mucosal barrier. The bacteria are collected in communities that vary in density and composition within each segment of the gastrointestinal (GI) tract. Therefore, every change in the gut ecosystem has been connected to an increased susceptibility or exacerbation of various GI disorders. The aim of this review is to summarize the recently available data on PPI-related microbiota alterations in each segment of the GI tract and to analyze the possible involvement of PPIs in the pathogenesis of several specific GI diseases.
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Does Helicobacter pylori eradication therapy trigger or protect against Crohn's disease?
Murad, HA
Acta gastro-enterologica Belgica. 2016;(3):349-354
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).
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Advances in clinical management of eosinophilic esophagitis.
Dellon, ES, Liacouras, CA
Gastroenterology. 2014;(6):1238-54
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Abstract
Eosinophilic esophagitis (EoE) is a chronic immune/antigen-mediated clinicopathologic condition that has become an increasingly important cause of upper gastrointestinal morbidity in adults and children over the past 2 decades. It is diagnosed based on symptoms of esophageal dysfunction, the presence of at least 15 eosinophils/high-power field in esophageal biopsy specimens, and exclusion of competing causes of esophageal eosinophilia, including proton pump inhibitor-responsive esophageal eosinophilia. We review what we have recently learned about the clinical aspects of EoE, discussing the clinical, endoscopic, and histological features of EoE in adults and children. We explain the current diagnostic criteria and challenges to diagnosis, including the role of gastroesophageal reflux disease and proton pump inhibitor-responsive esophageal eosinophilia. It is also important to consider the epidemiology of EoE (with a current incidence of 1 new case per 10,000 per year and prevalence of 0.5 to 1 case per 1000 per year) and disease progression. We review the main treatment approaches and new treatment options; EoE can be treated with topical corticosteroids, such as fluticasone and budesonide, or dietary strategies, such as amino acid-based formulas, allergy test-directed elimination diets, and nondirected empiric elimination diets. Endoscopic dilation has also become an important tool for treatment of fibrostenotic complications of EoE. There are a number of unresolved issues in EoE, including phenotypes, optimal treatment end points, the role of maintenance therapy, and treatment of refractory EoE. The care of patients with EoE and the study of the disease span many disciplines; EoE is ideally managed by a multidisciplinary team of gastroenterologists, allergists, pathologists, and dieticians.
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Eosinophilic esophagitis.
Bordea, MA, Moşteanu, O, Pop, TA, Gheban, D, Samaşca, G, Miu, N
Acta gastro-enterologica Belgica. 2013;(4):407-12
Abstract
Eosinophilic esophagitis is a chronic, immune-mediated disorder, isolated to the esophagus. Current theory suggests that the former may be caused by cell-mediated food hypersensitivity or may be a subset of eosinophilic gastrointestinal disease, an autoimmune disorder. During the last decade, the increasing prevalence of EoE has been recognized in pediatric populations. Reports support the efficacy of dietary restriction or corticosteroid therapy. Aditional research is needed to determine etiology, allow earlier clinical recognition and improve treatment. Because no single symptom, endoscopic finding or histopathologic feature is pathognomonic, the diagnosis can frequently be challenging. The current article reviews the possible etiology, clinical presentation, diagnosis, and treatment of this disorder, which has been called not only allergic esophagitis (which may be the most important cause), but also eosinophilic esophagitis, primary eosinophilic esophagitis, and idiopathic eosinophilic esophagitis.