Eosinophilic esophagitis (EoE) is a chronic, non-IgE immune-mediated reaction characterized by eosinophilic infiltration leading to esophageal dysfunction, inflammation, and potential for fibrotic remodeling. Although food allergens are generally considered the leading trigger for EoE, emerging evidence suggests that modifiable environmental factors may also play a role in the pathogenesis of EoE. This article discusses the latest data regarding the role of the exposome, microbiome, and environmental allergens on the development and ongoing inflammation of EoE, focusing on the last 10 years of relevant studies.
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Synopsis of European Society of Pediatric astroenterology, Hepatology and Nutrition (ESPGHAN) Guidelines (2024) on the Diagnosis and Treatment of Eosinophilic Esophagitis.
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Department of Pediatric Gastroenterology, Sanjay Gandhi Postgraduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India. Correspondence to: Dr Arghya Samanta, Assistant Professor, Department of Pediatric Gastroenterology, SGPGIMS, Raebareli Road, Lucknow-226014, Uttar Pradesh, India.
The European Society of Pediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) 2024 guidelines on eosinophilic esophagitis in children provide a systematic approach to the diagnosis and management of this rising disease entity in children. We present a concise update of the guideline to simplify management protocols, thus improving patient outcome.
View Article and Find Full Text PDFType 2 inflammation: a Portuguese consensus using Web-Delphi and decision conferencing (INFLAT2-PT).
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CEGIST-Centro de Estudos de Gestão, Instituto Superior Técnico, Universidade de Lisboa, Lisbon, Portugal.
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Kennth C. Griffin Esophageal Center, Division of Gastroenterology and Hepatology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
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Similarly to acute intestinal helminth infection, several conditions of chronic eosinophilic type 2 inflammation of mucosal surfaces, including asthma and eosinophilic esophagitis, feature robust expansions of intraepithelial mast cells (MCs). Also the hyperplastic mucosa of nasal polyposis in the context of chronic rhinosinusitis, with or without COX1 inhibitor intolerance, contains impressive numbers of intraepithelial MCs. In this issue of the JCI, Derakhshan et al.
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