Article Text

FRI0175 The influence of smoking on clinical response to etanercept therapy in patients with rheumatoid arthritis
  1. S. Zivojinovic1,
  2. N. Pilipovic1,
  3. M. Sefik Bukilica1,
  4. L. Kovacevic1,
  5. N. Roganovic1,
  6. I. Jeremic1,
  7. N. Damjanov2
  1. 1Institute of Rheumatology, Belgrade, Serbia
  2. 2Head office, Institute of Rheumatology, Belgrade, Serbia


Background Many recent studies have suggested that smoking is an important risk factor for rheumatoid arthritis (RA), particulary IgM rheumatoid factor (IgM-RF) and antibodies to citrullinated peptide (ACPA) positive RA, as well as a predictor of severe disease. However, there is lack of data on relationship between history of smoking and response to tumor necrosis factor antagonists in patients with RA.

Objectives To determine whether cigarette smoking influences the response to etanercept treatment in patients with RA.

Methods A history of cigarette smoking was obtained from a questionnaire completed by each patient starting therapy with etanercept since 2008 (n=136). A core set of demographic and clinical variables was recorded at baseline and at 3 and 12 months. The extent of smoking was quantified in pack-years (py), with 1 py equivalent to 20 cigarettes per day for 1 year. The influence of cigarette smoking (current or past) on the response to therapy was evaluated by logistic regression, with never smokers as the referent group. Response to therapy was defined according to the European League Against Rheumatism improvement criteria, based on their 3 or 12-month Disease Activity Score (DAS28) and absolute change in DAS28 from baseline.

Results A history of smoking was found in 68/136 (50%) patients. Of these, 50/136 (36.8%) were current smokers at the start of etanercept therapy. There was no significant difference in age, age of onset, sex and disease duration between nonsmokers, past smokers and current smokers. However, there was an increase in the frequency of patients with IgM-RF and ACPA who had smoked, although this did not achieve statistical significance. Compared with never smokers, current smokers were less likely to achieve a good response at 3 months following the start of etanercept therapy (27% versus 41%; p<0.05). Past smoking did not affect the chance of good response to etanercept therapy. The lower likelihood of a good response remained at later followup visits. Evaluating remission or joint counts yielded similar findings. The change in DAS28 over the first 3 months was inversely associated with the number of py (r=-0.31; p<0.05). The association of py history with response failure was independent of age, sex, disease duration, baseline DAS28, Health Assessment Questionnaire score and IgM-RF at baseline.

Conclusions RA patients with a history of smoking were more likely to show a poor response to etanercept. Response failure was associated with the intensity of smoking.

  1. G. Westhoff, et al. Rheumatoid arthritis patients who smoke have a higher need for DMARDs and feel worse, but they do not have more joint damage than non-smokers of the same serological group. Rheumatology 2008; 47:849-854

Disclosure of Interest None Declared

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