Article Text


Small bowel II
PWE-114 Does gastrointestinal infection trigger coeliac disease?
  1. K Evans1,
  2. S M Barrett1,
  3. A Smythe1,2,
  4. D S Sanders1,
  5. A Arnout1
  1. 1Sheffield Teaching Hospitals NHS Trust, Sheffield, UK
  2. 2University of Sheffield, Sheffield, UK


Introduction It is thought that a “second hit” is required to trigger coeliac disease in genetically susceptible individuals. Various infective agents have been postulated as the second hit but there is little evidence to support this. We aimed to establish the recall rate of antecedent gastrointestinal infection in patients with coeliac disease, and the prevalence of undetected coeliac disease in those with stool culture proven gastroenteritis.

Methods Group A comprised histologically proven patients with coeliac disease (n=233, 61 male, median 60 years) who were asked to complete a validated questionnaire and then compared to healthy controls (n=219, 79 male, median 46 years), and controls with inflammatory bowel disease (IBD) (n=196, 124 males, median 56 years). Group B were patients with stool culture proven gastroenteritis (n=101, 48 males, median 57 years) who underwent serologic testing for coeliac disease (endomysial antibody [EMA], tissue transglutaminase [tTG], immunoglobulin A [IgA]). They were compared with healthy controls (n=1200, 447 male, median 46 years). Those with positive serology underwent endoscopy and duodenal biopsy.

Results In Group A 69/233 (29.6%) with coeliac disease, and 53/196 (27.1%) with IBD reported having a gastrointestinal infection within the 12 months prior to diagnosis. In both diseases this was significantly greater than in healthy controls 15/219 (6.8%) (p<0.0001). In Group B 94/101 (93%) were coeliac antibody negative. The demographics, serology and biopsy results of the seven stool-culture positive subjects with positive coeliac serology are shown in Abstract PWE-114 table 1. The prevalence of coeliac disease in patients with stool culture positive gastroenteritis was 2.97%. This was higher than in healthy controls (12/1200, 1%) (p=0.10). In Group B the gastroenteritis pathogen was identified as Campylobacter species in 96/101 (95.0%), Salmonella species in 4/101 (4.0%), and Shigella in 1/101 (1.0%). One participant had IgA deficiency. This individual had normal IgG titres, IgG EMA and IgG tTG.

Abstract PWE-114 Table 1

Conclusion Patients with coeliac disease have a recall rate of previous gastrointestinal infection similar to those with inflammatory bowel disease, and significantly greater than healthy controls. In coeliac disease gastrointestinal infection may well be the “second hit” required to trigger disease but further work is required.

Competing interests None declared.

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