A predictive model for remission and low disease activity in patients with established rheumatoid arthritis receiving TNF blockers

Cristina Pomirleanu, Codrina Ancuta, Smaranda Miu, Rodica Chirieac
Clinical Rheumatology 2013, 32 (5): 665-70
The objective of this study was to identify predictors for remission or low disease activity (LDA) in established rheumatoid arthritis (RA) at 12 months of anti-TNF-α therapy. We have performed a prospective observational study in 90 consecutive patients with active RA receiving TNF-α inhibitors. Baseline and standard assessments were done every 3 months, including individual parameters (clinical and biological) and composite activity scores (28-joint disease activity score, DAS28). The primary outcome measure was DAS28-based EULAR response criteria. The multivariate logistic regression was used to analyze the association between disease activity and several RA baseline characteristics. Of the RA, 78.8 % was classified as good responders based on the EULAR-DAS28 criteria, 44.4 % RA achieving remission (DAS28 ≤ 2.6) and 34.4 %, LDA (DAS28 ≤ 3.2). Parameters associated with an increased likelihood of remission and LDA were initial DAS28-erythrocyte sedimentation rate ≤ 7 (odds ratio (OR) 3.3, 95 % confidence interval (CI) 2.03-5.81; OR 1.8, 95 % CI 1.09-6.68), Health Assessment Questionnaire Disability Index ≤  2 (OR 7.0, 95 % CI 1.56-31.91; OR 1.3, 95 % CI 1.03-5.79), C-reactive protein level ≤ 20 mg/l (OR 1.5, 95 % CI 0.29-8.22; OR 0.5, 95 % CI0.08-2.97), rheumatoid factor ≤ 20 IU/ml (OR 18.9, 95 % CI 10.79-38.36; OR 32.9, 95 % CI 4.03-269), anti-cyclic citrullinated peptide antibodies ≤ 40 IU/ml (OR 3.5, 95 % CI 0.67-18.19; OR 1.2, 95 % CI 1.02-1.59), concurrent prednisolone (OR 0.2, 95 % CI 0.05-0.36; OR 0.2, 95 % CI 0.06-0.63), methotrexate or leflunomide (OR 1.6, 95 % CI 1.2-13.53; OR 2.9, 95 % CI 1.20-4.36). A predictive matrix for remission and LDA in established active RA patients receiving TNF-α inhibitors was proposed. Further studies are necessary to confirm the value of such matrix in particular RA settings, leading to optimization of the use of anti-TNF-α therapy.

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