• Demographic Factors;
  • NSAID;
  • Response;
  • Outcome;
  • Predictors;
  • Osteoarthritis


Objective.  Nonsteroidal anti-inflammatory drug (NSAID) responses in osteoarthritis (OA) are highly variable, often requiring multiple medication changes. We sought to determine pre-randomization predictors of response to NSAIDs in OA.

Methods.  Data were pooled from two identical 26-week double-blind, randomized flare design trials comparing etoricoxib 30 mg/day (N = 475), celecoxib 200 mg/day (N = 488), and placebo (N = 244) in patients with OA of the hip or knee. This analysis was limited to the 12-week placebo-controlled period. Response at Week 12 was defined using Outcome Measures in Rheumatology Clinical Trials and Osteoarthritis Research Society International (OMERACT–OARSI) criteria. Factors were analyzed using logistic regression and included age, race, gender, body mass index, index joint, screening (pre-washout) and baseline (post-washout) Western Ontario and McMaster Universities (WOMAC) Osteoarthritis Index pain, physical function, and stiffness, and patient global assessment of disease status, prior NSAID/coxib or acetaminophen use, American Rheumatology Association functional class, and disease duration.

Results.  We found that screening WOMAC physical function was the only factor that predicted response in all treatment groups; worse function was associated with lower odds of achieving an OMERACT–OARSI response at 12 weeks (odds ratio 0.84 placebo; 0.87 etoricoxib; 0.89 celecoxib; P < 0.05 for all). However, the differences in WOMAC physical function between responders and nonresponders were small (∼5 mm on a 100-mm scale). No factor discriminated between the ability to predict placebo response from active treatment response.

Conclusions.  Lower levels of physical function decreased the odds of a response to NSAID treatment in OA, although the clinical significance is unknown given the small differences between responders and nonresponders. No other measured baseline variables consistently predicted response in these studies, which may reflect the known individual variability in NSAID response.