Treatment of Rheumatoid Arthritis Flare
For an RA flare, immediately administer short-term systemic glucocorticoids (≤10 mg/day prednisone equivalent for <3 months) while simultaneously optimizing your DMARD regimen to achieve remission or low disease activity. 1
Immediate Flare Control
Administer low-dose systemic glucocorticoids (≤10 mg/day prednisone equivalent) for less than 3 months to bridge until DMARD optimization takes effect. 1 This provides rapid symptom relief while disease-modifying therapy is escalated.
For predominantly single-joint involvement, use intra-articular glucocorticoid injection for targeted relief rather than systemic therapy. 1, 2
Critical pitfall: Never use glucocorticoids beyond 1-2 years due to risks of cataracts, osteoporosis, fractures, and cardiovascular disease. 1, 2 The risk-benefit ratio only favors glucocorticoids when dose is low and duration is short.
Disease Activity Assessment Before Treatment Escalation
Measure disease activity using validated indices: SDAI >11 or CDAI >10 indicates moderate-to-high activity requiring aggressive escalation. 1, 2
Check inflammatory markers (CRP, ESR) and autoantibodies (rheumatoid factor, anti-CCP) to guide therapy selection. 1, 2
Reassess disease activity every 1-3 months during active disease—if no improvement by 3 months after treatment change, adjust therapy immediately rather than waiting for the 6-month maximal effect. 1, 3
DMARD Optimization Algorithm
Step 1: Optimize Methotrexate First
Escalate methotrexate to 20-25 mg/week (or maximum tolerated dose) before declaring treatment failure. 1, 2 This is the most common error—underdosing methotrexate leads to premature escalation to biologics.
Consider switching to subcutaneous methotrexate for better bioavailability if oral dosing is inadequate. 2
Step 2: Add Conventional DMARDs if MTX Optimization Fails
- Add sulfasalazine and hydroxychloroquine to create triple-DMARD therapy if methotrexate optimization fails to achieve low disease activity. 1, 2 The TEAR study demonstrated that step-up therapy achieves similar clinical and radiographic outcomes to immediate triple therapy when using treat-to-target principles. 4
Step 3: Add Biologic or Targeted Synthetic DMARD
If triple-DMARD therapy fails, add a biologic DMARD or targeted synthetic DMARD rather than continuing to adjust conventional DMARDs. 1
Tofacitinib at 5 mg twice daily demonstrated superior ACR20 response versus placebo (pooled OR 2.44,95% CI 1.97-3.02 at 24 weeks) and reduced radiographic progression in both early and established RA. 4
Biologic Switching Strategy for Persistent Flares
If a TNF inhibitor fails, switch to a different mechanism of action rather than trying another TNF inhibitor. 1, 2 This is critical—switching within the same class has lower success rates.
Options with different mechanisms include:
Seronegative patients with inadequate response to TNF inhibitors may respond better to abatacept or tocilizumab rather than rituximab. 2
Treatment Target and Monitoring
Target remission (SDAI ≤3.3, CDAI ≤2.8) or low disease activity (SDAI ≤11, CDAI ≤10) within 6 months. 1, 2 This treat-to-target strategy prevents irreversible joint damage in up to 90% of patients. 5
Aim for at least 50% reduction in disease activity within 3 months as an interim goal. 5
Clinical response to biologics typically begins within 4-6 weeks, with maximal efficacy often not seen until 24 weeks. 3
Common Pitfalls to Avoid
Do not underdose methotrexate—must reach 20-25 mg/week before concluding inadequate response. 1, 2 Prescribe with folic acid supplementation. 6
Do not use long-term glucocorticoids (>1-2 years)—adverse effects (osteoporosis, cataracts, cardiovascular disease) outweigh benefits. 1, 2
Do not switch within the same biologic class after first failure—change mechanism of action instead. 1, 2
Do not wait 6 months to adjust failing therapy—if no improvement by 3 months, escalate treatment immediately. 1, 3