Key result
Combined tobacco exposure and shared epitope significantly increased the odds of positive anti-CCP antibodies in rheumatoid arthritis compared to unexposed patients (OR 4.233; 95% CI 2.458-7.291).
Why the study?
Does the combination of smoking and shared epitope increase the risk of developing anti-CCP antibodies in patients with rheumatoid arthritis?
Meta-Analysis (n=5,317)
Does the combination of smoking and shared epitope increase the risk of developing anti-CCP antibodies in patients with rheumatoid arthritis?
This meta-analysis demonstrates a significant gene-environment interaction between smoking and shared epitope in increasing the risk of anti-CCP antibody development in rheumatoid arthritis.
Answers are grounded in this paper and cite their sources.
Supports risk stratification and smoking cessation in shared epitope carriers with RA; confirms gene-environment interaction for anti-CCP development.
OBJECTIVE: The aim of this study was to determine the gene-environment interactions of smoking and shared epitope (SE) both separately and combined on anti-cyclic citrullinated peptide (CCP) antibodies in patients with rheumatoid arthritis (RA). METHODS: The literature was searched using the MEDLINE, EMBASE and Cochrane databases. A meta-analysis on the associations between tobacco exposure (TE) and/or SE and the development of anti-CCP antibodies in patients with RA was performed. RESULTS: Eight comparison studies with 5317 RA patients were considered in this meta-analysis. The odds ratio (OR) for positive anti-CCP antibodies in TE+/SE- patients with RA was increased compared with TE-/SE- patients (OR = 1.373, 95% CI = 1.111-1.698, P = 0.003). The ORs for positive anti-CCP antibodies in TE-/SE+ patients and TE+/SE+ patients with RA were also increased compared with TE-/SE- patients (OR = 2.678, 95% CI = 2.031-3.532, P < 1.0 × 1(0-9) in TE-/SE+; OR = 4.233, 95% CI = 2.458-7.291, P = 1.9 × 10(-8) in TE+/SE+). Stratification by ethnicity indicated the same pattern as that shown in the overall group. The OR for positive anti-CCP antibodies in TE+/SE+ patients with RA was much higher than in TE-/SE- patients in Europeans and Asians (OR = 3.879, 95% CI = 2.203-6.830, P = 2.6 × 10(-7); OR = 10.504, 95% CI = 3.182-34.67, P = 1.1 × 10(-4)). CONCLUSIONS: This meta-analysis suggests a gene-environmental interaction between smoking and SE for the development of anti-CCP antibodies.
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Lee et al. (2014) conducted a meta-analysis in Rheumatoid arthritis (n=5,317). Tobacco exposure and shared epitope (TE+/SE+) vs. No tobacco exposure and no shared epitope (TE-/SE-) was evaluated on Positive anti-cyclic citrullinated peptide (CCP) antibodies (OR 4.233, 95% CI 2.458-7.291, p=1.9 × 10(-8)). Combined tobacco exposure and shared epitope significantly increased the odds of positive anti-CCP antibodies in rheumatoid arthritis compared to unexposed patients (OR 4.233; 95% CI 2.458-7.291).
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