Abstract

Abstract INTRODUCTION Inflammatory bowel disease (IBD) is well known for concurrent immune-mediated disorders such as eosinophilic esophagitis, psoriasis, and rheumatoid arthritis.(1) For the past two decades, we are seeing an increased occurrence of eosinophilic esophagitis (EoE) in long standing IBD patients (2) (3) (4), but the question has arisen as to new onset IBD in chronic EoE patients. One study that involved 4814 patients demonstrated that the prevalence of eosinophilic esophagitis in IBD was 5 times higher compared to general population and EoE in IBD is 2 times higher than expected.(5) Multiple factors have been identified that may trigger the exact inflammatory response in IBD and EoE patients. Both diseases are associated with an exaggerated response to interleukins, especially IL-13 sharing cytokines and helper T cell mediated pathophysiology that is linked to disruption of the gastrointestinal tract barrier. (6) (7) CASE DESCRIPTION A 25-year-old healthy male presented back in 2012 with a history of three months of worsening dysphagia that resulted in 15-lb weight loss. Upper endoscopy showed esophagus with small caliber lumen, linear furrows, and thin concentric rings with microscopic evidence of eosinophilic esophagitis. Over the years he developed multiple episodes of persistent dysphagia, several endoscopies demonstrated pangastritis and duodenitis with a new pyloric and duodenal bulb stricture. Due to his remitting-relapsing course despite long-term medical treatment, patient underwent additional workup including an abdominal CT and upper endoscopy that showed worsening of the pyloric stricture that improved after balloon dilation. In 2020, the patient developed diarrhea, rectal bleeding, generalized abdominal pain and 21 lb weight loss despite medical treatment. Colonoscopy showed multiple erosions in the ileum and rectum not seen on previous studies. The biopsy indicated ulcerated mucosa with necrosis in the ileum and rectal area with mixed inflammatory infiltration with the presence of a non-caseating granuloma consistent with Chron’s disease. DISCUSSION It is unclear which disease manifest first or if it is a clustering and co-occurrence of diseases. The fact that both diseases share the same pathogenetic mechanism with overexpression of mucosal interleukin-13 (IL-13) causing loss of functionality of the gastrointestinal barrier could explain symptoms observed on both. Many studies demonstrated that IBD was diagnosed before EoE in almost 2/3 of the cases. The association of EoE-IBD is found significantly more in males and occurs at a younger age compared to IBD alone. Further studies will be needed in order to confirm the co-occurrence of diseases because of the increased risk of IBD-related complications and higher chance of requiring systemic corticosteroids and anti-TNF therapy in patients who have coexisting EoE-IBD.

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