Introduction Up to a third of patients with coeliac disease fail to have a symptomatic response to a gluten-free diet (GFD), or relapse after initial response. Causes include inadvertent gluten exposure and complications of coeliac disease such as lymphoma. There are limited published data assessing the role of capsule endoscopy (CE) in patients with coeliac disease and persisting symptoms. For this reason we evaluated our experience of CE in this group of coeliac patients.
Methods Data from all patients with established, biopsy-proven coeliac disease and persisting symptoms despite 12 months GFD, who underwent CE between 2004 and 2011 in a tertiary gastroenterology department were analysed. Concurrently we performed serology (endomysial antibody [EMA] and tissue transglutaminase [tTG]), and a duodenal biopsy (Marsh grading, and where appropriate T cell clonality). At CE changes of coeliac disease such as scalloping, mosaic pattern and loss of folds were assessed including extent of disease (proximal or diffuse). Concordance between serology, histology and CE was assessed using Spearman's coefficient.
Results 69 patients (47 female, median age 56 years, range 22–83 y) were identified. 8/69 (13.0%) had significantly abnormal CE findings with either mass lesions, extensive disease or ulceration. In these eight cases: two had enteropathy associated lymphoma (EATL), four Type 1 refractory disease, one fibroepithelial polyp, one had ulcerative jejunitis. Of the 4 (4/69, 5.8%) refractory Type 1 cases, two were started on immunosuppressants, one died of unrelated causes and another was a tertiary referral case in whom outcome data are unknown. There was no correlation between the likelihood of having complicated coeliac disease and the serological titres (either a positive EMA or significantly raised tTG). However, there was a positive correlation between more extensive changes at CE (diffuse) and the level of tTG (r=0.448, p=0.001). A similar observation was made for the relationship between diffuse involvement at CE and EMA positivity (r=0.351, p=0.003). There was also a correlation between the extent of disease observed at CE and histology (r=0.455, p<0.0001).
Conclusion This is the largest internationally reported series demonstrating a role for CE in coeliac disease patients with persisting symptoms. A significant proportion are found to have complicated or refractory coeliac disease. Extensive changes of coeliac disease seen on CE should prompt clinicians to investigate for refractory disease, request PCR on duodenal biopsy (for monoclonality) and consider immunosuppressive therapy.
Competing interests None declared.