Background & Aims: Our aim was to evaluate the outcomes of maintenance treatments for eosinophilic esophagitis (EoE) among observational studies (OSs) and randomized controlled trials (RCTs).
Materials And Methods: Studies reporting histologic success of maintenance therapy ≥48 weeks were included. The primary outcome was histologic success rate (defined as <15/<6 eosinophils/high-power field).
Inflammatory bowel diseases (IBD) are classified into two entities, namely Crohn's disease (CD) and ulcerative colitis (UC), which differ in disease trajectories, genetics, epidemiological, clinical, endoscopic, and histopathological aspects. As no single golden standard modality for diagnosing IBD exists, the differential diagnosis among UC, CD, and non-IBD involves a multidisciplinary approach, considering professional groups that include gastroenterologists, endoscopists, radiologists, and pathologists. In this context, histological examination of endoscopic or surgical specimens plays a fundamental role.
View Article and Find Full Text PDFEosinophilic esophagitis (EoE) is a chronic inflammatory disorder of the esophagus. EoE shares a common pathogenetic mechanism with other chronic disorders pertaining to the type 2 inflammatory spectrum, such as atopic dermatitis (AD), allergic rhinitis (AR), asthma, and chronic rhinosinusitis with nasal polyps (CRSwNP). The recent advancements in EoE pathogenesis understanding have unveiled new molecular targets implied within the "atopic march" picture as well as specific to EoE.
View Article and Find Full Text PDFIntroduction: The pathogenesis of inflammatory bowel disease (IBD) involves the dysregulation of multiple inflammatory pathways. The understanding of these mechanisms allows their selective targeting for therapeutic purposes. The discovery of Tumor Necrosis Factor-alpha's (TNF-α) role in mucosal inflammation ushered an exciting new era of drug development which now comprises agents targeting multiple pro-inflammatory signaling pathways, integrins, and leukocyte trafficking regulators.
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