Multicenter Study on Season of Birth and Celiac Disease: Evidence for a New Theoretical Model of Pathogenesis
ABSTRACT OBJECTIVE: To investigate whether season of birth is associated with celiac disease (CD). STUDY DESIGN: We performed a medical record review of 1964 patients with biopsy-proven CD at 3 teaching hospitals (2 pediatric centers and 1 adult center) between 2000 and 2010. The first positive small intestinal biopsy result defined age of diagnosis. The observed proportions of births in each season (spring [March-May], summer [June-August], fall [September-November], and winter [December-February]) were compared with the expected proportions using binomial probability tests. RESULTS: The mean age at diagnosis was 9.8 ± 5.0 years in the 2 pediatric centers and 43.6 ± 15.8 years in the adult center. The cohort was predominately female (69%). Overall, more patients were born in spring (27%) than in any other season: summer (25%), fall (25%), and winter (23%). In patients diagnosed before age 15 years, the spring birth excess was present in boys (33%; P = .0005), but not in girls (26%; P = .43). The sex difference in season of birth was less striking in patients with CD diagnosed at age ≥15 years. CONCLUSION: Season of birth is an environmental risk factor for CD, particularly in boys diagnosed before age 15 years. The results are consistent with a new theoretical model that integrates potential environmental factors (eg, gluten introduction, ultraviolet-B exposure, vitamin D status) and acute viral gastrointestinal infections in early childhood.
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ABSTRACT: The prevalence of celiac disease and the use of medications that inhibit acid secretion have both increased in recent decades. To explore the association between antisecretory medication exposure and subsequent development of celiac disease. In this population-based case control study, we identified patients with celiac disease diagnosed at all pathology departments in Sweden from July 2005 through February 2008. Patients were matched by age and gender with up to 5 controls. We identified prior prescriptions for proton pump inhibitors and histamine-2 receptor antagonists in all subjects. We used conditional logistic regression to measure the association between these prescriptions and the subsequent diagnosis of celiac disease. Prior proton pump inhibitor prescription was strongly associated with celiac disease (OR 4.79; 95% CI 4.17-5.51). Patients prescribed both proton pump inhibitors and histamine-2 receptor antagonists had a higher risk of celiac disease (OR 5.96; 95% CI 3.58-9.91) than those prescribed proton pump inhibitors alone (OR 4.91; 95% CI 4.26-5.66) or histamine-2 receptor antagonists alone (OR 4.16; 95% CI 2.89-5.99). Exposure to antisecretory medications is associated with a subsequent diagnosis of celiac disease. The persistence of this association after excluding prescriptions in the year preceding the celiac disease diagnosis suggests a causal relationship.Digestive and Liver Disease 09/2013; 46(1). DOI:10.1016/j.dld.2013.08.128 · 2.89 Impact Factor
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ABSTRACT: Many studies have investigated the aetiological roles of genetic and environmental factors in coeliac disease (CD) with the long-term goal of developing an effective primary prevention strategy. CD is a condition with dysregulated systemic and intestinal mucosal immune responses to dietary gluten proteins among genetically predisposed individuals. We recently described spring birth as a novel risk factor for CD in children. We believe that the association between season of birth and CD is due to seasonal differences in sunlight exposure and subsequent vitamin D status. Concomitant with global increases in CD prevalence, vitamin D deficiency also is increasingly recognized in children worldwide. Recent studies have shown that vitamin D deficiency can cause improper immune responses, abnormal intestinal mucosal integrity and impaired local defence to pathogenic microbial agents. In conjunction with other potential aetiological factors, we propose a hypothesis model of early-life vitamin D deficiency in the pathogenesis of childhood-onset CD.Public Health Nutrition 04/2014; 17(4):823-6. DOI:10.1017/S1368980013003510 · 2.25 Impact Factor