RESEARCH - The influence of cigarette smoking on autoantibodies in SLE

[Guest guest]

ACR/AHRP 2008 Scientific Meeting

Session: SLE: Clinical Aspects III

Tuesday, Oct 28, 2008, 9:00 AM - 6:00 PM

Presentation: 1736 - The Influence of Cigarette Smoking on

Autoantibodies in SLE

Author(s): F. Brandt, Schmitz, Melinda Drum, Tammy O.

Utset. University of Chicago, Chicago, IL

Abstract:

Purpose: How cigarette smoking in SLE patients influences SLE

associated autoantibodies is largely unknown. Sparse data suggests

that smoking is correlated with anti-dsDNA. We evaluated the impact of

current smoking, ever smoking, and never smoking on SLE serologies.

Methods: Ambulatory patients fulfilling ACR criteria for SLE were

enrolled in a clinical database during visits at the University of

Chicago Rheumatology Clinic. SLE medical history and demographic data

were obtained by standardized questionnaires. Smoking status was

defined as current, past, or never-smoker. Ever-smokers were defined

as either past or current smokers. Serologic data was obtained from

chart review. DsDNA, Sm, RNP, SSA and SSB assays (Inova Diagnostics)

were performed at the University of Chicago Laboratories in nearly all

cases. The enrollment anti-dsDNA titer was defined as the dsDNA titer

nearest to time of enrollment if performed within 6 months. Data was

entered into a Microsoft Access Database and analyzed using Stata

10.0. Associations between smoking status (current/past/never and

ever/never) and autoantibodies were determined by using Fisher's exact

test, ANOVAs, t tests, Kruskal-Wallis rank tests and Wilcoxon rank sum

tests where appropriate.

Results: 219 SLE subjects enrolled in the cross-sectional database.

207 subjects had data on both smoking status and enrollment anti-dsDNA

available. Ever-positive status for anti-RNP, anti-, anti-SSA and

anti-SSB and smoking status was available in 138 to 164 patients. Mean

enrollment anti-dsDNA titer in never-smokers was higher compared to

ever-smokers (p = 0.007). While ever-positive anti-dsDNA did not vary

in ever-smokers relative to never-smokers, current non-smokers were

significantly more likely than current smokers to have had

ever-positive anti-dsDNA (p=.02). Additionally, the highest observed

past anti-dsDNA titer was significantly higher in never-smokers

compared to ever-smokers (p=0.04). Compared to ever-smokers,

never-smokers had a higher frequency positivity of anti-RNP (p=0.05),

anti-SSA (p=0.03) and a trend towards anti- (p=0.07). The value

of the highest observed anti-RNP (p=0.03) and anti-SSA (p=0.03) was

also higher in never-smokers. Interestingly, never-smokers had an

earlier mean age of SLE onset compared to ever-smokers of almost 5

years (p=0.003).

Conclusion: In many diseases, including RA, smoking contributes to

disease and is not protective. However, a protective effect in

ulcerative colitis in terms of disease activity and age of onset has

been seen. Our data suggests that a history of smoking in SLE patients

is protective against the development as well as the titer of SLE

autoantibodies. In addition, current smokers appear protected against

the development of anti-dsDNA. As in ulcerative colitis, our data

suggests a history of smoking may also delay age of SLE onset.

Although smoking is harmful in many other respects in SLE, this data

suggests there may be a possible novel immunomodulatory effect on

disease that is worth further study.

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