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Infections increase the risk of developing Sjögren's syndrome
Author(s) -
Mofors J.,
Arkema E. V.,
Björk A.,
Westermark L.,
Kvarnström M.,
Forsbladd'Elia H.,
Magnusson Bucher S.,
Eriksson P.,
Mandl T.,
Nordmark G.,
WahrenHerlenius M.
Publication year - 2019
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/joim.12888
Subject(s) - medicine , dermatology
Abstract Objective Environmental factors have been suggested in the pathogenesis of rheumatic diseases. We here investigated whether infections increase the risk of developing primary Sjögren's syndrome ( pSS ). Methods Patients with pSS in Sweden ( n = 945) and matched controls from the general population ( n = 9048) were included, and data extracted from the National Patient Register to identify infections occurring before pSS diagnosis during a mean observational time of 16.0 years. Data were analysed using conditional logistic regression models. Sensitivity analyses were performed by varying exposure definition and adjusting for previous health care consumption. Results A history of infection associated with an increased risk of pSS ( OR 1.9, 95% CI 1.6–2.3). Infections were more prominently associated with the development of SSA / SSB autoantibody‐positive pSS ( OR 2.7, 95% CI 2.0–3.5). When stratifying the analysis by organ system infected, respiratory infections increased the risk of developing pSS , both in patients with ( OR 2.9, 95% CI 1.8–4.7) and without autoantibodies ( OR 2.1, 95% CI 1.1–3.8), whilst skin and urogenital infections only significantly associated with the development of autoantibody‐positive pSS ( OR 3.2, 95% CI 1.8–5.5 and OR 2.7, 95% CI 1.7–4.2). Furthermore, a dose–response relationship was observed for infections and a risk to develop pSS with Ro/ SSA and La/ SSB antibodies. Gastrointestinal infections were not significantly associated with a risk of pSS . Conclusions Infections increase the risk of developing pSS , most prominently SSA / SSB autoantibody‐positive disease, suggesting that microbial triggers of immunity may partake in the pathogenetic process of pSS .