Infections increase the risk of developing Sjogren's syndrome

被引:26
作者
Mofors, J. [1 ]
Arkema, E. V. [2 ]
Bjork, A. [1 ]
Westermark, L. [3 ]
Kvarnstrom, M. [1 ]
Forsblad-d'Elia, H. [4 ]
Bucher, S. Magnusson [5 ]
Eriksson, P. [6 ]
Mandl, T. [7 ]
Nordmark, G. [3 ]
Wahren-Herlenius, M. [1 ]
机构
[1] Karolinska Univ Hosp, Karolinska Inst, Dept Med Solna, Div Rheumatol, Stockholm, Sweden
[2] Karolinska Univ Hosp, Karolinska Inst, Dept Med Solna, Div Clin Epidemiol, Stockholm, Sweden
[3] Uppsala Univ, Rheumatol & Sci Life Lab, Dept Med Sci, Uppsala, Sweden
[4] Umea Univ, Rheumatol, Dept Publ Hlth & Clin Med, Umea, Sweden
[5] Orebro Univ, Fac Med & Hlth, Dept Rheumatol, Orebro, Sweden
[6] Linkoping Univ, Dept Clin Expt Med, Div Rheumatol, Linkoping, Sweden
[7] Lund Univ, Dept Clin Sci, Rheumatol, Malmo, Sweden
基金
瑞典研究理事会;
关键词
autoantibodies; infection; La; SSB; Ro; SSA; Sjogren's syndrome; RHEUMATOID-ARTHRITIS; DISEASE; ASSOCIATION; PREVALENCE; NATIONWIDE; IMMUNITY; SMOKING; ONSET; HLA;
D O I
10.1111/joim.12888
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective Environmental factors have been suggested in the pathogenesis of rheumatic diseases. We here investigated whether infections increase the risk of developing primary Sjogren'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.
引用
收藏
页码:670 / 680
页数:11
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