Increased Prevalence of Esophageal Eosinophilia in Patients with Inflammatory Bowel Disease

Fan, Yali; Steele, David; Kochar, Bharati; Arsene, Diana; Long, Millie D.; Dellon, Evan S.

doi:10.1159/000497236

Cited by 27 publications

(22 citation statements)

References 34 publications

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“…However, 6% of the total patients had biopsies consistent with eosinophilic esophagitis. A previous population study demonstrated an increased prevalence of eosinophilic esophagitis in patients with IBD [22]. Gastritis was the most common upper gastrointestinal tract pathology finding, being present in nearly three-fourths of patients.…”

Section: Discussionmentioning

confidence: 86%

Disaccharidase Deficiency in Pediatric Patients with Inflammatory Bowel Disease

Friesen

Pablo

Bass

et al. 2022

Gastrointestinal Disorders

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Background: Disaccharidase (DS) deficiencies have been reported in pediatric patients with inflammatory bowel disease (IBD), but the relationship between duodenal inflammation and DS deficiency has not been evaluated outside of lactase deficiency. Methods: This study assessed DS levels and DS deficiencies in pediatric IBD patients who underwent endoscopy with assessment of DS activity. Records were reviewed for IBD subtype, pathology findings, and the results of DS analysis. Results: A total of 136 patients were identified. Overall, 89 (65.4%) patients had a diagnosis of Crohn’s disease (CD), 31 (22.8%) patients had a diagnosis of ulcerative colitis (UC), and 16 (11.8%) patients had a diagnosis of indeterminant colitis. Lactase deficiency was identified in 55.9% of patients, followed by maltase deficiency (19.9%), sucrase and palatinase deficiency (14%), and pan-deficiency (12.5%). When analyzing only patients with CD, patients with duodenitis were more likely to exhibit sucrase deficiency, palatinase deficiency, and pan-deficiency with a trend towards maltase deficiency. Conclusions: The most common DS deficiency was lactase deficiency; however, this was not related to duodenal inflammation. Pediatric patients with CD and duodenal inflammation exhibit DS deficiencies, namely, sucrase, palatinase, and pan-deficiency. Dietary adjustments may be warranted temporarily until duodenal inflammation is healed in patients with CD and duodenitis.

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Section: Discussionmentioning

confidence: 86%

Disaccharidase Deficiency in Pediatric Patients with Inflammatory Bowel Disease

Friesen

Pablo

Bass

et al. 2022

Gastrointestinal Disorders

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“…In the present study, there were no significant differences in the endoscopic or histological findings based on the presence or absence of autoimmune disease. Fan et al reported no substantial clinical, endoscopic, or histologic differences between EoE patients with and without inflammatory bowel disease (IBD) ( 33 ). In several case reports of coexisting Crohn's disease and EoE ( 34 - 36 ), EoE developed after the induction of remission of Crohn's disease, suggesting that these diseases might be reciprocal.…”

Section: Discussionmentioning

confidence: 99%

Prevalence of Autoimmune Disease in Patients with Eosinophilic Esophagitis: A Cross-sectional Study of Three Hospitals in Japan

et al. 2021

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Objective Recent studies have found higher rates of autoimmune diseases, such as celiac disease, Crohn's disease, and ulcerative colitis, in patients with eosinophilic esophagitis (EoE) than in the general population. This study investigated the concomitant rate of autoimmune disease among Japanese patients with EoE and evaluated the clinicopathological characteristics of EoE patients with autoimmune disease. Methods The medical records of patients diagnosed with EoE between April 1, 2016, and June 30, 2020, were reviewed. We analyzed the concomitant rate of autoimmune diseases in patients with EoE and compared the clinical and histological differences between patients with and without autoimmune disease. Results Sixty-four patients with EoE were enrolled. Of them, 1 had ulcerative colitis (1.6%), 1 had autoimmune polyendocrine syndrome type 2 (1.6%), and 6 had endometriosis (28.5% of women, 44.4% of reproductive-aged women). No significant differences in the clinical course or histological findings were found between EoE patients with and without autoimmune diseases. No complications, including stenosis, were seen in EoE with autoimmune disease, and most patients with EoE and autoimmune diseases were responsive to proton pump inhibitors (PPIs). Conclusion In this study, 8 out of 64 patients with EoE had an autoimmune-related disease, including ulcerative colitis (n=1, 1.6%), autoimmune polyendocrine syndrome type 2 (n=1, 1.6%), or endometriosis (n=6, 44.4% of women of reproductive age), which is higher than that previously reported in the general population. Further investigations are required to clarify the relationship between EoE and autoimmune diseases.

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“…Moreover, the inflammation in the esophagus is unspecific [ 123 , 124 ] and rather has a lymphocytic than an eosinophilic pattern [ 125 , 126 ]. Although a recent publication showed a fivefold increased risk of EE in IBD [ 127 ], it is possible that most of these patients had rather an EoE than an isolated EE. Large epidemiologic data support a positive association between IBD and EoE with a up to fivefold increased risk of EoE in IBD patients and inversely an up to sixfold increased risk of IBD among EoE patients [ 128 ].…”

Section: Differential Diagnosis Of Esophageal Eosinophiliamentioning

confidence: 99%

Eosinophilic esophagitis—established facts and new horizons

2021

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Despite dramatic advances in our understanding of the pathogenesis and course of disease in the relatively short timeframe since the discovery and first description of eosinophilic esophagitis (EoE) less than three decades ago, many open questions remain to be elucidated. For instance, we will need to better characterize atypical clinical presentations of EoE and other forms of esophageal inflammatory conditions with often similar clinical presentations, nut fulfilling current diagnostic criteria for EoE and to determine their significance and interrelationship with genuine EoE. In addition, the interrelationship of EoE with other immune-mediated diseases remains to be clarified. Hopefully, a closer look at the role of environmental factors and their interaction with genetic susceptibility often in context of atopic predisposition may enable identifying the candidate substances/agents/allergens and potentially earlier (childhood) events to trigger the condition. It appears plausible to assume that in the end—comparable to current concepts in other immune-mediated chronic diseases, such as for instance inflammatory bowel disease or asthma bronchiale—we will not be rewarded with the identification of a “one-and-only” underlying pathogenetic trigger factor, with causal responsibility for the disease in each and every EoE patient. Rather, the relative contribution and importance of intrinsic susceptibility, i.e., patient-driven factors (genetics, aberrant immune response) and external trigger factors, such as food (or aero-) allergens as well as early childhood events (e.g., infection and exposure to antibiotics and other drugs) may substantially differ among given individuals with EoE. Accordingly, selection and treatment duration of medical therapy, success rates and extent of required restriction in dietary treatment, and the need for mechanical treatment to address strictures and stenosis require an individualized approach, tailored to each patient. With the advances of emerging treatment options, the importance of such an individualized and patient-centered assessment will increase even further.

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Increased Prevalence of Esophageal Eosinophilia in Patients with Inflammatory Bowel Disease

Cited by 27 publications

References 34 publications

Disaccharidase Deficiency in Pediatric Patients with Inflammatory Bowel Disease

Disaccharidase Deficiency in Pediatric Patients with Inflammatory Bowel Disease

Prevalence of Autoimmune Disease in Patients with Eosinophilic Esophagitis: A Cross-sectional Study of Three Hospitals in Japan

Eosinophilic esophagitis—established facts and new horizons

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