scholarly journals Cigarette smoking and the pathogenesis of systemic lupus erythematosus

2018 ◽  
Vol 14 (6) ◽  
pp. 481-487 ◽  
Author(s):  
Cameron B. Speyer ◽  
Karen H. Costenbader
2013 ◽  
Vol 72 (Suppl 3) ◽  
pp. A911.1-A911
Author(s):  
J. Amaya-Amaya ◽  
J. L. Pérez-Fernández ◽  
N. Molano-González ◽  
R. D. Mantilla ◽  
A. Rojas-Villarraga ◽  
...  

2012 ◽  
Vol 39 (7) ◽  
pp. 1363-1370 ◽  
Author(s):  
CHIKAKO KIYOHARA ◽  
MASAKAZU WASHIO ◽  
TAKAHIKO HORIUCHI ◽  
TOYOKO ASAMI ◽  
SABURO IDE ◽  
...  

Objective.Cigarette smoking may be associated with increased risk of systemic lupus erythematosus (SLE), whereas the role of alcohol consumption is unknown. We examined the association between SLE risk and smoking or drinking.Methods.We investigated the relationship of smoking and drinking compared to SLE risk among 171 SLE cases and 492 healthy controls in female Japanese subjects. Unconditional logistic regression was used to compute OR and 95% CI, with adjustments for several covariates.Results.Compared with nonsmoking, current smoking was significantly associated with increased risk of SLE (OR 3.06, 95% CI 1.86–5.03). The higher the level of exposure to cigarette smoke, the higher the risk of SLE. Inhalation was also associated with increased SLE risk (OR 3.73, 95% CI 1.46–9.94 for moderate inhalation; OR 3.06, 95% CI 1.81–5.15 for deep inhalation). In contrast, light/moderate alcohol consumption had a protective effect on SLE risk (OR 0.38, 95% CI 0.19–0.76). As for beer, the risks for non-beer drinkers and beer drinkers were similar. This also applies to alcoholic beverages other than beer.Conclusion.Our results suggest that smoking was positively associated with increased SLE risk whereas light/moderate alcohol consumption was inversely associated with SLE risk, irrespective of the type of alcoholic beverage. Additional studies are warranted to confirm these findings.


2004 ◽  
Vol 50 (3) ◽  
pp. 849-857 ◽  
Author(s):  
Karen H. Costenbader ◽  
Daniel J. Kim ◽  
Jehanna Peerzada ◽  
Shahin Lockman ◽  
Dolores Nobles-Knight ◽  
...  

2009 ◽  
Vol 36 (12) ◽  
pp. 2691-2693 ◽  
Author(s):  
IRINA TURCHIN ◽  
SASHA BERNATSKY ◽  
ANN E. CLARKE ◽  
YVAN ST-PIERRE ◽  
CHRISTIAN A. PINEAU

Objective.To evaluate the association between cigarette smoking and cutaneous damage in systemic lupus erythematosus (SLE).Methods.Our study was performed in SLE clinic registry cohort patients, all of whom fulfilled revised American College of Rheumatology criteria for SLE; patients are followed prospectively with annual assessments that include collection of demographic variables, smoking history, disease activity (SLE Disease Activity Index version 2000, SLEDAI-2K), medications, and damage scores (Systemic Lupus International Collaborating Clinics/ACR Damage Index). Cumulative cutaneous damage scores were used for the primary analyses. Logistic and logit regression models were performed to examine potential associations between current smoking and cutaneous damage, controlling for age, sex, race, lupus disease duration, antimalarial or immunosuppressant use, and anti-DNA and anti-SSA antibody status.Results.Of our sample (N = 276), 92% were women and 73.7% were Caucasian; the mean age was 45.1 years, mean disease duration 13.5 years, and 17.5% were current smokers. In the regression analyses, current cigarette smoking was associated with total cutaneous damage (OR 2.73, 95% CI 1.10, 6.81) and with scarring (OR 4.70, 95 CI 1.04, 21.2). In additional analyses, current smoking was also associated with active lupus rash (OR 6.18, 95% CI 1.63, 23.3).Conclusions.Current cigarette smoking may be associated with cutaneous damage and active lupus rash in SLE, suggesting another reason to emphasize smoking cessation in patients with SLE.


2009 ◽  
Vol 36 (10) ◽  
pp. 2195-2203 ◽  
Author(s):  
CHIKAKO KIYOHARA ◽  
MASAKAZU WASHIO ◽  
TAKAHIKO HORIUCHI ◽  
YOSHIFUMI TADA ◽  
TOYOKO ASAMI ◽  
...  

Objective.Recent studies have identified signal transducer and activator of transcription 4 (STAT4) as a susceptibility gene for systemic lupus erythematosus (SLE) in different populations. Similarly, tumor necrosis factor receptor superfamily, member 1B (TNFRSF1B) has been reported to be associated with SLE risk in Japanese populations. Along with environmental factors such as smoking, both polymorphisms may modulate an individual’s susceptibility to SLE. We investigated these relationships in a case-control study to evaluate risk factors for SLE among Japanese women.Methods.We investigated the relationship of theSTAT4rs7574865 andTNFRSF1Brs1061622 polymorphisms to SLE risk with special reference to their combination and interaction with cigarette smoking among 152 SLE cases and 427 controls.Results.The TT genotype ofSTAT4rs7574865 was significantly associated with increased risk of SLE (OR 2.21, 95% CI 1.10–4.68). Subjects with at least one G allele ofTNFRSF1Brs1061622 had an increased risk of SLE (OR 1.56, 95% CI 0.99–2.47). The attributable proportion due to the interaction between theTNFRSF1Brs1061622 genotypes and smoking was estimated to be 0.49 (95% CI 0.07–0.92), indicating that 49% of the excess risk for SLE in smokers with at least one G allele was due to an additive interaction. A lack of significant associations ofSTAT4with smoking was observed. No significant gene-gene interactions were found among polymorphisms ofSTAT4andTNFRSF1B.Conclusion.Our findings suggest that the association between cigarette smoking and SLE could be differentiated by theTNFRSF1Brs1061622 T allele among female Japanese subjects. This preliminary exploratory result should be confirmed in a larger study.


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