Rheumatology Medical News about pack-year history of smoking;response to tumor necrosis factor antagonists;rheumatoid arthritis

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Relationship between pack-year history of smoking and response to tumor necrosis factor antagonists in patients with rheumatoid arthritis
Journal of Rheumatology, 06/16/09

Mattey DL et al. – Study demonstrates that rheumatoid arthritis (RA) patients with a history of smoking are more likely to show a poor response to TNF antagonists. Response failure was associated with the intensity of previous smoking, irrespective of smoking status at initiation of anti-TNF therapy.

Methods

Aim was to determine whether there is a quantitative relationship between smoking history and response to therapy with TNF antagonists
History of cigarette smoking was obtained from a questionnaire completed from pts (n=154) at the start of therapy
Demographic and clinical variables was recorded at baseline and at 3 and 12 mo
Extent of smoking was quantified in pack-yrs (py), with 1 py equivalent to 20 cigarettes/d for 1 year

Results

There was an increasing trend of no response at 3 and 12 mo with increasing py history
Change in DAS-28 over the first 3 mo was inversely associated with the number of py
The association of py history with response failure was independent of age, sex, disease duration, baseline DAS28, HAQ score, IgM RF and smoking at baseline
Most significant effect was seen in pts treated with infliximab

Exclusive Author Commentary
Derek Mattey, 06/17/09

Our study raises the question as to why smokers have a worse response to anti-TNF therapy. We do not currently know the reason but suggest several possible mechanisms: a) increased production of autoantibodies such as rheumatoid factor (RF) and anti-cyclic citrullinated antibodies (anti-CCP) in smokers. Patients with autoantibodies tend to have more severe disease, so may show a poorer response to TNF-alpha blockers. b) increased production of antibodies against TNF-alpha blockers. Such antibodies may interfere with the drug, leading to a reduced response. c) an alteration in the absorption of TNF-alpha blockers or more rapid clearance of the drug in smokers. d) higher levels of TNF? or other inflammatory mediators in smokers that make them more resistant to TNF-alpha blockers. e) a greater perception of pain in smokers. f) neuropschological or sociocultural differences in smokers that are reflected by differences in personality or illness behaviour such as a lower threshold for reporting pain and disability. These possibilities need not be mutually exclusive, and a number of mechanisms may be operating in individual patients. The fact that we see an effect in people who have given up smoking suggests that smoking has long lasting effects on patient physiology which may influence response. The amount that a patient has previously smoked seems to be more important than whether or not they are smoking at the time of starting anti-TNF therapy. Nevertheless, RA patients who smoke should be encouraged to give up because of the well recognised health benefits to smoking cessation. There are still questions that need to be addressed. Further investigation is needed to see whether patients treated at a much earlier stage of disease show a similar relationship between smoking history and poor response. Other ethnic populations also need to be studied to determine whether the relationship between smoking and anti-TNF response is a general finding in all RA populations.

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