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Int. J. Mol. Sci. 2014, 15(12), 22279-22295; doi:10.3390/ijms151222279

Smoking and Rheumatoid Arthritis

1
Central Clinical School, Faculty of Medicine, Nursing and Health Sciences, Monash University, Melbourne 3800, Australia
2
Department of Pediatrics, Severance Children's Hospital, Yonsei University College of Medicine, Seoul 120-752, Korea
3
Department of Pediatrics, Pusan National University Children's Hospital, Yangsan 626-770, Korea
4
Department of Pediatrics, Jeju National University School of Medicine, Jeju 690-767, Korea
5
Department of Pediatrics, Ajou University School of Medicine, Daewoo General Hospital, Geoje 656-711, Korea
*
Author to whom correspondence should be addressed.
Received: 27 August 2014 / Revised: 11 October 2014 / Accepted: 17 October 2014 / Published: 3 December 2014
(This article belongs to the Special Issue Environmental Toxicants and Autoimmune Disease)
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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
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Chang, K.; Yang, S.M.; Kim, S.H.; Han, K.H.; Park, S.J.; Shin, J.I. Smoking and Rheumatoid Arthritis. Int. J. Mol. Sci. 2014, 15, 22279-22295.

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