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Central Clinical School, Faculty of Medicine, Nursing and Health Sciences, Monash University, Melbourne 3800, Australia


Department of Pediatrics, Severance Childrens Hospital, Yonsei University College of Medicine, Seoul 120-752, Korea


Department of Pediatrics, Pusan National University Childrens Hospital, Yangsan 626-770, Korea


Department of Pediatrics, Jeju National University School of Medicine, Jeju 690-767, Korea


Department of Pediatrics, Ajou University School of Medicine, Daewoo General Hospital, Geoje 656-711, Korea


Author to whom correspondence should be addressed.

Abstract Rheumatoid arthritis RA is a chronic inflammatory disease caused by both genetic and environmental factors. Smoking has been implicated as one of the most important extrinsic risk factors for its development and severity. Recent developments have shed light on the pathophysiology of RA in smokers, including oxidative stress, inflammation, autoantibody formation and epigenetic changes. The association of smoking and the development of RA have been demonstrated through epidemiologic studies, as well as through in vivo and animal models of RA. With increased use of biological agents in addition to standard disease-modifying antirheumatic drugs DMARDs, there has been interest in how smoking affects drug response in RA treatment. Recent evidence suggests the response and drug survival in people treated with anti-tumour necrosis factor anti-TNF therapy is poorer in heavy smokers, and possible immunological mechanisms for this effect are presented in the current paper. View Full-Text

Keywords: rheumatoid arthritis; smoking; cyclic citrullinated peptide; synovial fibroblasts; drug response rheumatoid arthritis; smoking; cyclic citrullinated peptide; synovial fibroblasts; drug response

Autor: Kathleen Chang 1, So Min Yang 2, Seong Heon Kim 3, Kyoung Hee Han 4, Se Jin Park 5 and Jae Il Shin 2,*



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