Volume 10, Issue 1 , Pages 30-36, January 2012
Low Risk of Gastrointestinal Cancer Among Patients With Celiac Disease, Inflammation, or Latent Celiac Disease
Background & Aims
Celiac disease has been associated with gastrointestinal (GI) cancers in small studies; risks have not been estimated from large populations or based on histopathology analyses.
Methods
We examined the risk of GI cancers by using data from cohorts of patients with celiac disease (villous atrophy, Marsh score of 3; n = 28,882) or inflammation (Marsh score of 1–2; n = 12,860); biopsy samples were evaluated at 28 pathology centers. A third cohort included 3705 individuals with latent celiac disease (normal mucosa, but positive serology results). Data were compared with those from an age- and sex-matched population.
Results
Of patients with celiac disease, 372 developed incident GI cancers; 347 patients with inflammation and 38 with latent celiac disease developed GI cancers. In the first year after diagnosis and initial biopsy, celiac disease was associated with 5.95-fold increase in risk of incident GI cancer (95% confidence interval [CI], 4.64–7.64); the hazard ratio [HR] for inflammation was 9.13 (95% CI, 7.19–11.6) and for latent celiac disease was 8.10 (95% CI, 4.69–14.0). After the first year, patients were at no significant increase in risk for GI cancers; the HR for celiac disease was 1.07 (95% CI, 0.93–1.23), for inflammation it was 1.16 (95% CI, 0.98–1.37), and for latent celiac disease it was 0.96 (95% CI, 0.56–1.66). The absolute risk for any GI cancer in patients with celiac disease was 101/100,000 person-years, with an excess risk of 2/100,000 person-years.
Conclusions
Although celiac disease, inflammation, and latent disease all increase risk for GI cancers in the first year after diagnosis, there is no increase in risk thereafter.
Keywords: Autoimmune Disorder , Malignancy , Cancer Incidence , Epidemiology
Abbreviations used in this paper: AGA, anti-gliadin antibodies, BMI, body mass index, CD, celiac disease, CI, confidence interval, EMA, endomysial antibody, GI, gastrointestinal, HR, hazard ratio, Ig, immunoglobulin, TTG, tissue transglutaminase, VA, villous atrophy
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Conflicts of interest The authors disclose no conflicts.
Funding This project was supported by grants from the Örebro University Hospital Research Foundation, Örebro University, Swedish Society of Medicine, the Swedish Research Council, the Sven Jerring Foundation, the Örebro Society of Medicine, the Karolinska Institutet, the Clas Groschinsky Foundation, the Juhlin Foundation, the Majblomman Foundation, the Uppsala-Örebro Regional Research Council, and the Swedish Celiac Society.
PII: S1542-3565(11)00670-7
doi:10.1016/j.cgh.2011.06.029
© 2012 AGA Institute. Published by Elsevier Inc. All rights reserved.
Volume 10, Issue 1 , Pages 30-36, January 2012

