Format

Send to

Choose Destination
J Intern Med. 2019 Jun;285(6):670-680. doi: 10.1111/joim.12888. Epub 2019 Apr 17.

Infections increase the risk of developing Sjögren's syndrome.

Author information

1
Division of Rheumatology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
2
Division of Clinical Epidemiology, Department of Medicine Solna, Karolinska Institutet, Karolinska University Hospital, Stockholm, Sweden.
3
Department of Medical Sciences, Rheumatology and Science for Life Laboratory, Uppsala University, Uppsala, Sweden.
4
Department of Public Health and Clinical Medicine, Rheumatology, Umeå University, Umeå, Sweden.
5
Department of Rheumatology, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.
6
Division of Rheumatology, Department of Clinical Experimental Medicine, Linköping University, Linköping, Sweden.
7
Department of Clinical Sciences, Malmö, Rheumatology, Lund University, Malmö, Sweden.

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.

KEYWORDS:

La/SSB; Ro/SSA; Sjögren's syndrome; autoantibodies; infection

PMID:
30892751
DOI:
10.1111/joim.12888

Supplemental Content

Full text links

Icon for Wiley
Loading ...
Support Center