Arthritis & Rheumatism, Volume 60,
October 2009 Abstract Supplement

The 2009 ACR/ARHP Annual Scientific Meeting
Philadelphia October 16-21, 2009.


Smoking Is Not Associated with Autoantibodies in Unaffected First-Degree Relatives of SLE Patients

James1,  J.A., Stewart2,  S.A., Terrell3,  D., Guthridge4,  J.M., Bruner4,  G.R., Kamen5,  D.L., Gilkeson5,  G.S.

OMRF, OU, Oklahoma City, OK,
OMRF,
OUHSC,
Oklahoma Medical Res Fnd,
Medical Univ South Carolina,
Univ Texas Southwestern,
Cedars Sinai,
Univ Colorado,
Oklahoma Medical Research Foundation, Oklahoma City, OK

Purpose:

SLE is a complex human autoimmune disease with interacting genetic and environmental risks. Epidemiologic studies have identified an association between smoking and the presence of SLE; however, the mechanism by which smoking is associated with SLE in select individuals is not understood. One working model is that smoking modifies select autoantigens leading to a loss of tolerance and autoimmunity. This model suggests that autoantibody-positive family members should be smokers. This study tests whether smoking is associated with autoantibody production in SLE or unaffected first-degree blood relatives (FDRs).

Method:

Detailed clinical, serologic, demographic and treatment information was extracted from a coded database from a diverse collection of 1,242 SLE patients and 981 FDRs [55% EA, 23% AA, 16% HI]. Serum samples from each were tested for standard lupus autoantibodies by immunofluorescence and luminex bead-based assays. ANA positivity and the 13 select autoantibody test results were then analyzed on the basis of smoking status at the time of sample. Categorical values included never-smoker, ever smoker, and current smoker. Statistical analysis was conducted using chi-square and ANOVA methods.

Results:

SLE cases were less likely to have ever smoked (49% vs 53%) compared to their blood relatives (p=0.031), but not significantly less likely to be current smokers (18% vs 20%). No association was identified between smoking and having a positive ANA when SLE patients who were current smokers were compared with those who never smoked. Among FDRs, 19.1% of current smokers tested positive for at least one of 10 autoantibodies commonly associated with SLE, while 25.8% of never smokers (p=0.053) and 25.6% of former smokers tested positive for one or more autoantibody (p=0.086). Interestingly, the group of SLE patients who had ever smoked had a lower prevalence of autoantibodies against nRNP 70K (p<0.0012), ribosomal P (p=0.003), and dsDNA (p=0.01) than the group of SLE patients who had never smoked. Similarly, the prevalence of dsDNA positivity is lower in unaffected relatives who are current smokers than in unaffected relatives who are non-smokers (p = 0.045).

Conclusion:

SLE patients have no significant association between ANA positivity and smoking; moreover, SLE patients with antibodies against nRNP 70K, ribosomal P and dsDNA, as well as FDRs with antibodies against dsDNA, are more likely not to smoke in this cross-sectional cohort. No other strong correlation between smoking and the production of autoantibodies exists in FDRs. Therefore, the epidemiologic association of smoking with SLE may manifest its risk through mechanisms outside of autoantibody production.

To cite this abstract, please use the following information:
James, J.A., Stewart, S.A., Terrell, D., Guthridge, J.M., Bruner, G.R., Kamen, D.L., et al; Smoking Is Not Associated with Autoantibodies in Unaffected First-Degree Relatives of SLE Patients [abstract]. Arthritis Rheum 2009;60 Suppl 10 :904
DOI: 10.1002/art.25983

Abstract Supplement

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