ArticleArthritis and rheumatism2012
Impact of interactions of cigarette smoking with NAT2 polymorphisms on rheumatoid arthritis risk in African Americans.
Article in Arthritis and rheumatism, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- The glutathione S-transferase M1 and P1 polymorphisms and rheumatoid arthritis: a meta-analysis.Molecular biology reports · 2012Pooled it
- Article
- Etiology and Risk Factors for Rheumatoid Arthritis: A State-of-the-Art Review.Frontiers in medicine · 2021Review
- Is the prevention of rheumatoid arthritis possible?Clinical rheumatology · 2020Review
- Measurement of absolute copy number variation of Glutathione S-Transferase M1 gene by digital droplet PCR and association analysis in Tunisian Rheumatoid Arthritis population.Journal of clinical laboratory analysis · 2018Article
- Efficacy research of salazosulfamide in ankylosing spondylitis and NAT1 gene polymorphism.Experimental and therapeutic medicine · 2017Article
- Environmental factors and hormones in the development of rheumatoid arthritis.Seminars in immunopathology · 2017Review
- Porphyromonas gingivalis Stimulates Bone Resorption by Enhancing RANKL (Receptor Activator of NF-κB Ligand) through Activation of Toll-like Receptor 2 in Osteoblasts.The Journal of biological chemistry · 2015Article
- Smoking and rheumatoid arthritis.International journal of molecular sciences · 2014Review
- Arylamine N-acetyltransferase polymorphisms in Han Chinese patients with ankylosing spondylitis and their correlation to the adverse drug reactions to sulfasalazine.BMC pharmacology & toxicology · 2014Article
- Inter-ethnic differences in genetic polymorphisms of xenobiotic-metabolizing enzymes (CYP1A1, CYP2D6, NAT1 and NAT2) in healthy populations: correlation with the functional in silico prediction.Molecular biology reports · 2014Article
- Expert panel workshop consensus statement on the role of the environment in the development of autoimmune disease.International journal of molecular sciences · 2014Review
- Associations of alcohol use with radiographic disease progression in African Americans with recent-onset rheumatoid arthritis.The Journal of rheumatology · 2013Article
- Racial and ethnic disparities in rheumatoid arthritis.Current rheumatology reports · 2012Review
- Pre-rheumatoid arthritis: predisposition and transition to clinical synovitis.Nature reviews. Rheumatology · 2012Review
- Environmental and gene-environment interactions and risk of rheumatoid arthritis.Rheumatic diseases clinics of North America · 2012Review
Corrections and comments
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Authors and funding
15 authors at 11 institutions in 1 country.
Funding
Abstract
objectiveTo examine whether polymorphisms in genes coding for drug-metabolizing enzymes (DMEs) have an impact on rheumatoid arthritis (RA) risk due to cigarette smoking in African Americans.
methodsSmoking status was evaluated in African American patients with RA compared with non-RA controls, with smoking exposure categorized as heavy smoker (≥10 pack-years) versus never smoker/<10 pack-years. Individuals were genotyped for a homozygous deletion polymorphism in the M1 gene loci of glutathione S-transferase (GSTM1-null) in addition to tagging single-nucleotide polymorphisms (SNPs) in N-acetyltransferase 1 (NAT1), NAT2, and epoxide hydrolase 1 (EPXH1). Associations of these genotypes with RA risk were examined using logistic regression, and gene-smoking interactions were assessed.
resultsThere were no significant associations of any DME genotype with RA. After adjustment for multiple comparisons, there were significant additive interactions between heavy smoking and the NAT2 SNPs rs9987109 (P(additive) = 0.000003) and rs1208 (P(additive) = 0.00001); the attributable proportion due to interaction ranged from 0.61 to 0.67. None of the multiplicative gene-smoking interactions examined remained significant with regard to overall disease risk, after adjustment for multiple testing. There was no evidence of significant gene-smoking interactions in analyses of GSTM1-null, NAT1, or EPXH1. DME gene-smoking interactions were similar when cases were limited to those patients who were positive for anti-citrullinated protein antibodies.
conclusionAmong African Americans, RA risk imposed by heavy smoking appears to be mediated in part by genetic variation in NAT2. While further studies are needed to elucidate the mechanisms underpinning these interactions, these SNPs appear to identify African American smokers at a much higher risk for RA, in whom the relative risk is at least 2-fold higher when compared to nonsmokers lacking these risk alleles.
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