Researchers in Ankara, Turkey, found no connection between cigarette smoking — either active or passive — and disease activity in people with rheumatoid arthritis (RA), according to the study “Effect of Exposure to Tobacco Smoke on Response to Anti-Tumor Necrosis Factor-Alpha Treatment in Patients with Rheumatoid Arthritis“ published in the Iranian Journal of Public Health.
RA is a chronic inflammatory immune-system disorder that affects the joints, typically the hands and feet. Tumor necrosis factor (TNF) is what is known as a cytokine, an immune system molecule that can cause damage in people with diseases characterized by a heightened immune response, such as RA. High TNF levels have been found in rheumatoid arthritis patients who are active smokers.
First author Ozgur Zeliha Karaahmet, from Diskapi Yildirim Beyazit Education and Research Hospital, led the study. Investigators retrospectively evaluated RA patients under treatment with infliximab, etanercept, and adalimubab, as well as the anti-TNF medication methotrexate (MTX). The analysis included 39 people. Patients were questioned about their smoking habits and close exposure to passive smoking. The researchers measured RA disease activity at 12 months, using a standard measurement called the Disease Activity Score-28 (DAS28).
Overall, the study revealed that cigarette smoking or cigarette smoke exposure did not affect RA disease activity. “The distribution of DAS-28 levels were statistically similar in patients with and without cigarette smoking,” the team wrote. “Similar results were observed between the groups with and without exposure to smoking.”
Smoking or smoke exposure also did not seem to affect how participants responded to the anti-TNF therapy MTX. This finding is in contrast to other studies, which reported an association between poor MTX response and smoking in RA.
“In summary, findings show that no difference was detected between active smokers, exposed to tobacco smoke, and non-smokers in terms of response to anti-TNF treatment in RA. Prospective controlled studies that include exposed to tobacco smoke are required to better define the response to anti-TNF-α agents,” the researchers concluded.
