Article Text

FRI0073 Recent, Common Infections Are Associated with Decreased Risk of Rheumatoid Arthritis
  1. M.E. Sandberg1,
  2. L. Klareskog2,
  3. L. Alfredsson1,
  4. S. Saevarsdottir2
  1. 1Inst. of Environmental Medicine
  2. 2Dept of Medicine, Unit of Rheumatology, Karolinska Institutet, Stockholm, Sweden


Background A hypothesis has been put forward that infections may trigger the clinical onset of rheumatoid arthritis (RA), although the underlying evidence is sparse.

Objectives We asked whether recent, common infections affect the risk of RA.

Methods We used the population-based case-control study EIRA on incident RA, matched for sex, age and county of residence. In total, 6401 participants completed a questionnaire regarding infections during the 2 years before diagnosis. Conditional logistic regression was used to calculate odds ratios (OR), adjusting for smoking and socioeconomic status.

Results Infections in the gastrointestinal and urogenital tract before clinical onset were associated with a lowered risk of RA: gastroenteritis (OR=0.71 [95%CI: 0.63-0.80]) urinary tract infections (OR=0.78 [95%CI: 0.68-0.90]) and genital infections (OR=0.80 [95%CI: 0.64-1.00]), while a non-significant association of similar magnitude was observed for the less common prostatitis (OR=0.64 [95%CI: 0.38-1.08]). An even lower risk was observed for those who had experienced both gastrointestinal and urogenital infections (OR=0.50 (95%CI:0.32-0.79). In striking contrast, no association was observed for upper respiratory infections (sinusitis, tonsillitis) or infections in the teeth/gum (OR=0.96 [95%CI: 0.82-1.13], 0.99 [95% CI: 0.86-1.14] and 1.10 [95%CI: 0.96-1.26], respectively). Gastroenteritis was significantly associated with a lowered risk of both ACPA-positive and ACPA-negative RA, while the lowered risk associated with urogenital infections, despite no statistically significant interactions, was more pronounced in the ACPA-positive subset.

Conclusions Gastrointestinal and urogenital infections, but not respiratory infections, are associated with a lowered risk of RA. Thus, our findings do not support the notion that common infections trigger RA onset. Perhaps, this reflects strong immune defenses in RA patients, that make them less vulnerable for infections but prone to develop autoimmune reactions. That fact that the infections are protective speaks against recall bias in the study.

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.4450

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