Guest guest Posted April 26, 2006 Report Share Posted April 26, 2006 Smoking linked to autoantibodies associated with lupus nephritis  April 24, 2006  Janis  San Francisco, California - Current smoking raises the level of autoantibodies to double-stranded DNA (dsDNA) in patients with systemic lupus erythematosus (SLE), which suggests that lupus patients who continue to smoke might be setting themselves up for more severe disease manifestations such as lupus nephritis, according to a report in the May 2006 issue of ls of the Rheumatic Diseases [1]. " There is an association between smoking and dsDNA antibodies, which are usually seen in SLE patients with more severe disease (eg, renal disease). The effect of smoking, if it is a causal association, is short-lived. Therefore, it is in SLE patients' best interest to quit smoking as soon as possible. Their smoking may worsen their disease (in addition to the multitude of other health risks of smoking), " lead author Dr Freemer (University of California, San Francisco) told rheumawire. Current but not former smoking associated with dsDNA autoantibodies  " There is an association between smoking and dsDNA antibodies, which are usually seen in SLE patients with more severe disease. "  Freemer and colleagues reviewed medical records of 410 SLE patients from the University of California, San Francisco Lupus Genetics Project to evaluate dsDNA-antibody status and smoking status to determine whether dsDNA seropositivity (dsDNA+) is more common in lupus patients who smoke than in lupus patients who do not smoke. " Possibly, " they write, " DNA damage in smokers leads to dsDNA- autoantibody formation and may have a role in the development of SLE. " They found: An association of dsDNA seropositivity with current smoking but not with never or former smoking. In tests of 92 of the 410 patients, no relationship between dsDNA- autoantibody titer level and smoking status in SLE patients. No significant interaction between smoking and age at SLE diagnosis. No significant effect of cumulative amount smoked on dsDNA status. No significant effect of age of smoking onset on dsDNA status. The message is that current smoking is likely to create additional risk for SLE patients, but that it appears to be a relatively short- term risk that abates within months after smoking cessation. The authors note that smoking-related DNA adducts have a half-life of only nine to 13 weeks. The investigators' hypothesis was that smoking might increase DNA- adduct formation and dsDNA-autoantibody production in patients with SLE, which might increase susceptibility to or worsen SLE. In regard to the clinical significance of the association between current smoking and dsDNA seropositivity, Freemer said, " The statistical analysis limits the 'chance' association (between smoking and dsDNA positivity) to less than 2.5% that there is not at least a 1.6-fold increase in the risk of dsDNA+ in current (vs never smokers). " With respect to whether this association is clinically significant, the association between dsDNA seropositivity and disease severity has been established previously. In this study, one might pursue an assessment of SLE severity ([systemic Lupus International Collaborating Clinics] SLICC or [systemic Lupus Erythematosus Disease Activity Index] SLEADAI depending on when you want to or are able to assess severity) and compare the dsDNA-positive vs -negative individuals and smoking status. " Freemer MM, King TE, Criswell LA. Association of smoking with dsDNA autoantibody production in systemic lupus erythematosus. Ann Rheum Dis 2006; 65:581-584. 16150789 http://www.jointandbone.org/viewArticle.do?primaryKey=690743 Quote Link to comment Share on other sites More sharing options...
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