Smoking and rheumatoid arthritis.

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.