Influenza and risk of later celiac disease: a cohort study of 2.6 million people. (2nd January 2018)

• Record Type: Journal Article
• Authors: Kårhus, Line Lund; Gunnes, Nina; Størdal, Ketil; Bakken, Inger Johanne; Tapia, German; Stene, Lars C.; Håberg, Siri E.; Mårild, Karl
• Is Part Of: Scandinavian journal of gastroenterology. Volume 53:Number 1(2018)
• Page Start: 15
• Page End: 23
• Publication Date: 2018-01-02
• Subjects: Celiac disease -- cohort studies -- influenza a virus (H1N1 subtype) -- mass vaccination; Gastroenterology -- Periodicals; Digestive organs -- Diseases -- Periodicals; 616.33
• DOI: 10.1080/00365521.2017.1362464
• Languages: English
• ISSNs: 0036-5521

Abstract

Abstract: Objectives: Influenza has been linked to autoimmune conditions, but its relationship to subsequent celiac disease (CD) is unknown. Our primary aim was to determine the risk of CD after influenza. A secondary analysis examined the risk of CD following pandemic influenza vaccination. Methods: This nationwide register-based cohort study included 2, 637, 746 Norwegians (born between 1967–2013) followed during 2006–2014 with information on influenza diagnosed in primary or non-primary care, pandemic vaccination (Pandemrix), and subsequent CD. Cox regression yielded hazard ratios adjusted (HR) for socio-demographic characteristics and earlier healthcare use. Results: During 13, 011, 323 person-years of follow-up 7321 individuals were diagnosed with CD (56/100, 000 person-years). There were 351, 666 individuals diagnosed with influenza, including 82, 980 during the 2009–2010 pandemic, and 969, 968 individuals were vaccinated. Compared with participants without influenza, who had a CD incidence of 55/100, 000 person-years, those diagnosed with seasonal and pandemic influenza had a rate of 68 and 78, per 100, 000 person-years, respectively. The HR for CD was 1.29 (95%CI, 1.21–1.38) after seasonal influenza and 1.29 (95%CI, 1.15–1.44) after pandemic influenza; HRs remained significantly increased one year after exposure, when restricted to laboratory-confirmed influenza, and after multivariate adjustments. The reverse association, i.e., risk of influenza after CD, was not significant (HR 1.05; 95%CI, 0.98–1.12). The HR for CD after pandemic vaccination was 1.08 (95%CI, 1.03–1.14). Conclusion: A positive association with influenza diagnosis is consistent with the hypothesis that infections may play a role in CD development. We could neither confirm a causal association with pandemic vaccination, nor refute entirely a small excess risk.