The Effects of Smoking in Rheumatoid Arthritis Patients

Article

A review of current literature by researchers from Korea examines the effects of cigarette smoking in patients with rheumatoid arthritis.

Response to rheumatoid arthritis (RA) treatment with anti tumor necrosis factor (anti TNF) is poorer in heavy smokers, according to research published in the International Journal of Molecular Sciences.

Researchers from various hospitals in Korea reviewed prior epidemiological studies which identified smoking as a risk factor of RA in order to determine the impact of smoking on the treatment with anti TNF therapy. The researchers noted that in other meta analyses, the risk for developing RA was nearly twice as likely in smokers than in non smokers, and the risk for female smokers was approximately 1.3 times higher than for female non smokers. However, the authors also mentioned many studies did not find an association between smoking and RA development in women.

The investigators broke down their findings by first presenting the effects of smoking on the immune system. They noted that the effect on nicotine on RA had not been widely studied. However, they importantly noted that smoking can increase the oxidative stress in the body which can increase rheumatoid inflammation due to impaired antioxidant systems caused by free radicals. Nicotine contributes to immunosuppression in general cases, but animal models of RA displayed suppressed adjuvant induced arthritis post treatment. Depending on the cell types, smoking can both increase and decrease apoptosis, and the authors advocated further research to determine the effect of smoking on apoptosis in RA. Smoking cigarettes was believed by the researchers to trigger various morphological, physiological, biochemical, and enzymatic changes that could lead to impaired antibacterial defenses, cellular regulatory activity, and inflammatory responses. Autoantibodies are also affected by cigarette smoking, in that when they are against citrullinated proteins, autoimmune diseases can be triggered in cases of RA. Epigenetic changes, like DNA methylation, are sometimes present in smokers.

RA patients’ response to anti rheumatic drugs could be effected by cigarette smoking, too, the researchers determined in their paper. Prior findings displayed a reduced clinical response to infliximab in smokers with RA, but no studies have examined smoking and its effects on tocilizumab or rituximab. One reason for poor pharmacological response is that smokers have higher basal metabolic rates than non smokers, according to one study. Another study proposed a higher dose of disease modifying anti rheumatic drugs (DMARDs) in smoker RA patients because of the diminished potency of the drug.

Extra articular manifestations (EAM) of RA included the presence of various diseases. The incidence of EAM is anywhere between 20 and 45% in RA, the researchers noted. EAM included rheumatoid nodules, rheumatoid vasculitis, polyneuropathy, pleuritis, and interstitial lung disease with fibrosis, pericarditis, hematological abnormalities, certain ocular inflammations, and secondary Sjogren’s syndrome. One study proved a main indicator of severe EAM was smoking at RA diagnosis and early disability. Some EAM were associated with longer disease duration and smoking habit in another study. A third study demonstrated those with RA and EAM were more often current smokers.

“The immunological changes that cause RA in smokers have been traced back to several mechanisms, which especially affect genetically predisposed individuals,” the authors concluded, while promoting further research in the area. “Persistent inflammation due to oxidative stress, proinflammatory state, autoantibody production and epigenetic effects might be implicated in the autoimmunity of RA.”

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