Abstract
ObjectiveWe investigated the correlation between nontyphoidal Salmonella (NTS) infection and systemic lupus erythematosus (SLE) risk.MethodsThis case-control study comprised 6,517 patients with newly diagnosed SLE between 2006 and 2013. Patients without SLE were randomly selected as the control group and were matched at a case-control ratio of 1:20 by age, sex, and index year. All study individuals were traced from the index date back to their NTS exposure, other relevant covariates, or to the beginning of year 2000. Conditional logistic regression analysis was used to analyze the risk of SLE with adjusted odds ratios (aORs) and 95% confidence intervals (CIs) between the NTS and control groups.ResultsThe mean age was 37.8 years in the case and control groups. Females accounted for 85.5%. The aOR of having NTS infection were significantly increased in SLE relative to controls (aOR, 9.20; 95% CI, 4.51-18.78) in 1:20 sex-age matching analysis and (aOR, 7.47; 95% CI=2.08-26.82) in propensity score matching analysis. Subgroup analysis indicated that the SLE risk was high among those who dwelled in rural areas; had rheumatoid arthritis, multiple sclerosis, or Sjogren’s syndrome; and developed intensive and severe NTS infection during admission.ConclusionsExposure to NTS infection is associated with the development of subsequent SLE in Taiwanese individuals. Severe NTS infection and other autoimmune diseases such as rheumatoid arthritis, multiple sclerosis, or Sjogren’s syndrome also contributed to the risk of developing SLE.
Highlights
Systemic lupus erythematosus (SLE), whose global prevalence and incidence respectively range from 9–241 and 0.3–23.2 per 1,00,000 person-years [1], is among the top 20 leading causes of death in women aged 5–64 years [2]
We investigated the correlation between nontyphoidal Salmonella (NTS) infection and systemic lupus erythematosus (SLE) risk
The adjusted odds ratios (aORs) of having NTS infection were significantly increased in SLE relative to controls in 1:20 sex-age matching analysis and in propensity score matching analysis
Summary
Systemic lupus erythematosus (SLE), whose global prevalence and incidence respectively range from 9–241 and 0.3–23.2 per 1,00,000 person-years [1], is among the top 20 leading causes of death in women aged 5–64 years [2]. Genetic susceptibility alone is insufficient to trigger the onset of SLE, with the evidence of only 24% concordance rates among monozygotic twins with SLE manifestation [4]. This indicates that besides genetic factors, the environment plays a crucial role in the pathophysiology of SLE [5]. Heritability, shared (familial) environmental-, and nonshared environmental factors were reported to account for SLE susceptibility in 43.9%, 25.8%, and 30.3% Taiwanese patients, respectively [6]. The major environmental factors influencing SLE development include exposure to ultraviolet radiation, particulate air pollution, trace elements, alcohol use, and infections [7]. A common anti-DNA idiotype (16/6Id) carried by antibodies against Mycobacterium tuberculosis accounts for the antinuclear autoantibody positivity in tuberculosis patients [11], which may lead to autoimmune phenomena [12]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
