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Nicotine may slow progression of rheumatoid arthritis
NEW YORK (Reuters Health) - In people with rheumatoid arthritis, heavy cigarette smoking appears to slow the rate of joint destruction, new research suggests.
"Potentially, this may be due to the anti-inflammatory properties of nicotine," Dr. Axel Finckh, University Hospital of Geneva, Switzerland told Reuters Health.
Cigarette smoking is a known risk factor for rheumatoid arthritis, a chronic inflammatory disease that causes progressive joint destruction, disability, and premature death, Finckh and colleagues reported in the Annals of the Rheumatic Diseases.
Yet, it remains unclear if smoking influences the progressive joint destruction and disability cause by rheumatoid arthritis. Finckh and colleagues therefore assessed joint X-rays and results from self-reported functional disability questionnaires for more than 2,000 rheumatoid arthritis patients in their early- to mid-fifties.
Most of the patients (1459) did not smoke; 489 were considered moderate smokers and 55 were classified as heavy smokers, consuming more than one pack per day.
Overall, the investigators found that the smokers and non-smokers had similar rates of progressive joint damage and functional disability.
Unexpectedly, they also found slower rates of progressive joint damage in the X-rays of heavy cigarette smokers compared with the moderate smokers and the non-smokers over the 3-year study.
These findings suggest that smoking is more influential in the development of rheumatoid arthritis than the progression of the disease over time, but further research is needed to fully understand the impact smoking has on disease progression.
Still, Finckh cautioned: "The cardiovascular hazards of smoking certainly outweigh the potential anti-inflammatory benefits of nicotine," so the health risks associated with smoking are much greater than any benefits people with rheumatoid arthritis may gain from smoking.
Additional study is needed to understand the influence of tobacco and nicotine on the body's immune system.
SOURCE: Annals of the Rheumatic Diseases, July 2007.
