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Smoking Raises Risk for Seropositive SLE

Discussion in 'Immunology and Rheumatology' started by Dr.Scorpiowoman, Oct 13, 2017.

  1. Dr.Scorpiowoman

    Dr.Scorpiowoman Golden Member

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    Risk with current smoking increased twofold



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    Current smoking was strongly associated with the development of the subtype of systemic lupus erythematosus (SLE) characterized by seropositivity for double stranded DNA (dsDNA) antibodies, analysis of data from two prospective cohort studies showed.

    In a multivariate analysis that included more than 230,000 women, the risk for dsDNA-positive SLE was increased almost twofold for those currently smoking (HR 1.86, 95% CI 1.14-3.04), according to Medha Barbhaiya, MD, and colleagues from Harvard Medical School in Boston.

    In addition, seropositive women whose smoking exceeded 10 pack-years had a 60% increased risk (HR 1.60, 95% CI 1.04-2.45, P=0.04), the researchers reported online in Annals of the Rheumatic Diseases.

    Smoking has previously been shown to be associated with other autoimmune diseases, most notably rheumatoid arthritis, in which these researchers have demonstrated an increased risk for seropositive disease among both current (RR 1.58, 95% CI 1.21-2.06) and former (RR 1.60, 95% CI 1.27-2.02) smokers.

    However, previous studies in SLE have had conflicting results, with some, though not all, reports showing higher risks for smokers.

    To further examine this in a large population with long-term follow-up, and to assess the potential association of dsDNA positivity -- which confers a more severe disease phenotype -- the researchers analyzed data from the Nurses' Health Study and the Nurses' Health Study II, which consist of 230,672 women with 5.6 million years of follow-up.

    Participants in these studies completed biennial questionnaires on lifestyle, risk factors, and medical diagnoses.

    At baseline, 45% of the women were ever smokers, with 51% of those reporting current smoking. In both cohorts, factors such as age, race, body mass index, menopausal status, and postmenopausal hormone use were similar regardless of smoking. Alcohol use was greater among smokers, and most current smokers had a history of more than 10 pack-years.

    In the two studies, the researchers identified 286 incident cases of SLE, with 42% being dsDNA-positive at the time of diagnosis.

    Mean age at the time of diagnosis was 49, and more nonwhites were dsDNA-positive (12.6%) than dsDNA-negative (6.1%).

    Among the dsDNA-positive subgroup, there were higher rates of hematologic involvement (65.3% versus 53.3%) but lower rates of arthritis (65.3% versus 79.4%). Rates of kidney disease were similar, at 16% for both positive and negative subgroups.

    Most past or current smokers reported smoking 15 to 24 cigarettes per day, but duration of smoking was longer for current smokers (26.4 years versus 16.1 years). Mean time since smoking cessation for past smokers was 16.8 years.


    There was no increased risk of SLE overall (without considering autoantibody status) or for dsDNA-negative SLE. There also was no association among past smokers between time since quitting and risk of SLE overall or dsDNA-negative disease.

    However, for dsDNA-positive past smokers, the risk was no longer significant 5 years after quitting (HR 1.11, 95% CI 0.69-1.79), "suggesting that dsDNA-positive SLE risk is modifiable," the authors observed. This differs from what has been reported for rheumatoid arthritis, where the risk remained high until 20 years after quitting

    "In these large prospective cohorts of women followed for many years prior to SLE onset, we found a strong and specific association between smoking and dsDNA-positive SLE," they stated.

    The potential mechanisms by which smoking influences the risk for seropositive SLE are not yet known, but may involve gene mutations and activation following exposure to free radicals, carbon monoxide, and polycyclic aromatic hydrocarbons in tobacco smoke.

    "Toxic smoke components also induce epigenetic changes, resulting in altered gene expression affecting immunity and production of proinflammatory cytokines including tumor necrosis factor-α and interleukin-6," Barbhaiya and colleagues wrote.

    Genetic factors also are likely to be in play, and future research should investigate potential gene-environment interactions in SLE risk, as well as risks associated with autoantibodies other than dsDNA, they concluded.

    Limitations of the study included the possibility that some SLE cases may have been overlooked or misclassified according to autoantibody status, while strengths included its large population, long follow-up, and frequent data updates.

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