Introduction Functional dyspepsia (FD), defined by unexplained pain or discomfort centred in the upper abdomen, affects 15% of the population. Diagnosis and treatment of FD based on the symptom-based Rome III criteria remains challenging. Recently, subtle eosinophilic inflammation in the duodenum has been implicated in the pathophysiology of FD in adults based on a Swedish case-control study.1 Specifically, increased eosinophils in early satiety and postprandial distress have been replicated in the UK,2 in paediatric dyspepsia in the USA3 and in post-infectious FD in Japan,4 but the association remains controversial. The aim of this study was to characterise upper gastrointestinal tract pathology in an Australian cohort and correlate this with available clinical data in FD cases and controls.
Methods Patients prospectively referred for an upper gastrointestinal endoscopy (n=55; mean age, 49.6 years; 61.8% female) were entered to the study (with informed consent), stratified to FD cases (n=33) and controls (n=22) by Rome II criteria and completed a validated Bowel Symptom Questionnaire. Two blinded independent observers assessed the eosinophil count in five high power fields, in the duodenal bulb (D1) and second part (D2). H pylori status was assessed by gastric histology. Associations with clinical symptoms were assessed by Mann–Whitney U test.
Results Cases and controls were demographically similar. There was a significant increase in eosinophils in D1 vs D2 for both cases (p=0.0003) and controls (p=0.008). Abdominal pain was associated with eosinophilia in both D1 (p=0.03) and D2 (p=0.007). Duodenal eosinophilia was significantly increased in subjects experiencing early satiety, (p=0.015). This association remained after exclusion of coeliac disease (n=2) and H pylori (n=9, 16%) (p=0.04) in D2 but not in D1. Subjects who “felt food staying in their stomach” similarly had increased D2 eosinophilia (p=0.002); this remained significant on exclusion of coeliac disease and H pylori (p=0.004). Smoking was also associated with eosinophilia in D2 (p=0.008).
Conclusion Data supporting subtle duodenal eosinophilia in subsets of FD has become credible. The potential role of duodenal eosinophils as biomarkers has implications for diagnosis and therapeutic trials.
Competing interests None declared.
References 1. Talley NJ, Walker MM, Aro P, et al. Non-ulcer dyspepsia and duodenal eosinophilia: an adult endoscopic population-based case-control study. Clin Gastroenterol Hepatol 2007;5:1175–83.
2. Walker MM, Salehian SS, Murray CE, et al. Implications of eosinophilia in the normal duodenal biopsy - an association with allergy and functional dyspepsia. Aliment Pharmacol Ther 2010;31:1229–36.
3. Friesen CA, Sandridge L, Andre L, et al. Mucosal eosinophilia and response to H1/H2 antagonist and cromolyn therapy in pediatric dyspepsia. Clin Pediatr (Phila) 2006;45:143–7.
4. Futagami S, Shindo T, Kawagoe T, et al. Migration of eosinophils and CCR2-/CD68-double positive cells into the duodenal mucosa of patients with postinfectious functional dyspepsia. Am J Gastroenterol 2010;105:1835–42.
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