Smoking and Rheumatoid Arthritis

DOI Web Site 2 Citations
  • Kathleen Chang
    Central Clinical School, Faculty of Medicine, Nursing and Health Sciences, Monash University, Melbourne 3800, Australia
  • So Yang
    Department of Pediatrics, Severance Children's Hospital, Yonsei University College of Medicine, Seoul 120-752, Korea
  • Seong Kim
    Department of Pediatrics, Pusan National University Children's Hospital, Yangsan 626-770, Korea
  • Kyoung Han
    Department of Pediatrics, Jeju National University School of Medicine, Jeju 690-767, Korea
  • Se Park
    Department of Pediatrics, Ajou University School of Medicine, Daewoo General Hospital, Geoje 656-711, Korea
  • Jae Shin
    Department of Pediatrics, Severance Children's Hospital, Yonsei University College of Medicine, Seoul 120-752, Korea

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<jats:p>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.</jats:p>

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