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Infections increase...
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Mofors, J.Karolinska Institutet,Karolinska Univ Hosp, Sweden
(author)
Infections increase the risk of developing Sjögren's syndrome
- Article/chapterEnglish2019
Publisher, publication year, extent ...
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2019-04-17
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Wiley-Blackwell,2019
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printrdacarrier
Numbers
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LIBRIS-ID:oai:DiVA.org:umu-161599
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https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-161599URI
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https://doi.org/10.1111/joim.12888DOI
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-390586URI
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http://kipublications.ki.se/Default.aspx?queryparsed=id:141227534URI
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https://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-158981URI
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https://lup.lub.lu.se/record/145b39fb-fbee-48f3-bc46-1db03b7e1765URI
Supplementary language notes
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Language:English
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Summary in:English
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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Funding Agencies|Swedish Research Council; Swedish Rheumatism association; King Gustaf the V:th 80-year foundation; Heart-Lung Foundation; Stockholm County Council; Karolinska Institute
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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.
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Arkema, E. V.Karolinska Univ Hosp, Karolinska Inst, Dept Med Solna, Div Clin Epidemiol, Stockholm, Sweden,Karolinska University Hospital
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Björk, A.Karolinska Institutet,Karolinska Univ Hosp, Sweden
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Westermark, L.Uppsala University,Uppsala universitet,Reumatologi,Science for Life Laboratory, SciLifeLab,Uppsala Univ, Sweden
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Kvarnström, M.Karolinska Institutet
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Forsblad-d'Elia, HelenaUmeå University,Umeå universitet,Reumatologi,Umea Univ, Rheumatol, Dept Publ Hlth & Clin Med, Umea, Sweden(Swepub:umu)hefo0034
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Magnusson Bucher, S.Örebro University
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Eriksson, PerLinköping University,Linköpings universitet,Avdelningen för neuro- och inflammationsvetenskap,Medicinska fakulteten,Region Östergötland, Reumatologiska kliniken i Östergötland(Swepub:liu)perer22
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Mandl, ThomasLund University,Lunds universitet,Reumatologi och molekylär skelettbiologi,Sektion III,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Internmedicin - epidemiologi,Forskargrupper vid Lunds universitet,Rheumatology,Section III,Department of Clinical Sciences, Lund,Faculty of Medicine,Internal Medicine - Epidemiology,Lund University Research Groups(Swepub:lu)medf-tma
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Nordmark, GunnelUppsala University,Uppsala universitet,Reumatologi,Science for Life Laboratory, SciLifeLab,Uppsala Univ, Sweden(Swepub:uu)gunnnord
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Wahren-Herlenius, M.Karolinska Institutet
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Karolinska InstitutetKarolinska Univ Hosp, Sweden
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In:Journal of Internal Medicine: Wiley-Blackwell285:6, s. 670-6800954-68201365-2796
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