BACKGROUND: Genetic predisposition and gliadin exposure are known to be crucial factors in the development of coeliac disease. Circumstantial evidence suggests that other unidentified environmental factors may also be of pathogenetic importance. AIM: To define the relation between cigarette smoking and the risk of development of symptomatic adult onset coeliac disease. SUBJECTS: Eighty six recently diagnosed adult coeliac disease patients and 172 controls matched for age and sex. METHOD: Matched case control study, using a simple questionnaire to determine smoking history, and in particular smoking status at the time of diagnosis of coeliac disease. RESULTS: At the time of diagnosis, the proportion of current smokers was 7% in the coeliac group, and 32.6% in the control group, giving a matched odds ratio of 0.15 (95% confidence intervals 0.06, 0.38). The difference could not be accounted for by social class, nor by coeliac patients giving up smoking after the onset of symptoms as most non-smokers in the coeliac group had never smoked. CONCLUSION: Cigarette smoking, or a factor closely linked to it, seems to exert a major protective effect against the development of symptomatic adult onset coeliac disease. The implication is that gliadin exposure is not the only important environmental factor involved in the pathogenesis of this condition.
BACKGROUND: Genetic predisposition and gliadin exposure are known to be crucial factors in the development of coeliac disease. Circumstantial evidence suggests that other unidentified environmental factors may also be of pathogenetic importance. AIM: To define the relation between cigarette smoking and the risk of development of symptomatic adult onset coeliac disease. SUBJECTS: Eighty six recently diagnosed adult coeliac diseasepatients and 172 controls matched for age and sex. METHOD: Matched case control study, using a simple questionnaire to determine smoking history, and in particular smoking status at the time of diagnosis of coeliac disease. RESULTS: At the time of diagnosis, the proportion of current smokers was 7% in the coeliac group, and 32.6% in the control group, giving a matched odds ratio of 0.15 (95% confidence intervals 0.06, 0.38). The difference could not be accounted for by social class, nor by coeliac patients giving up smoking after the onset of symptoms as most non-smokers in the coeliac group had never smoked. CONCLUSION: Cigarette smoking, or a factor closely linked to it, seems to exert a major protective effect against the development of symptomatic adult onset coeliac disease. The implication is that gliadin exposure is not the only important environmental factor involved in the pathogenesis of this condition.
Authors: Jonas F Ludvigsson; Pertti Aro; Marjorie M Walker; Michael Vieth; Lars Agréus; Nicholas J Talley; Joseph A Murray; Jukka Ronkainen Journal: Scand J Gastroenterol Date: 2013-05-14 Impact factor: 2.423