Managing Rheumatoid Arthritis Flares
Initiate low-dose glucocorticoids (≤10 mg/day prednisone or equivalent) immediately for rapid symptom control, then optimize your current DMARD therapy to maximum doses before escalating treatment. 1
Immediate Flare Management
Start short-term glucocorticoids (≤10 mg/day prednisone equivalent) for less than 3 months to rapidly suppress inflammation during the acute flare. 1 This provides the most favorable benefit-risk ratio when kept at low doses and short duration. 1
Glucocorticoids can be administered via different routes (oral, intramuscular, or intra-articular) depending on the distribution of joint involvement. 2
Taper glucocorticoids as rapidly as clinically feasible once disease control is achieved. 2
Optimize Current DMARD Therapy
Before declaring treatment failure, ensure methotrexate is optimized to 20-25 mg weekly (oral or subcutaneous route). 1 Many patients are undertreated with suboptimal methotrexate dosing.
If the patient is on methotrexate monotherapy and experiencing a flare, this represents inadequate disease control requiring treatment escalation. 1
For patients already on combination conventional synthetic DMARDs who flare, proceed directly to biologic therapy rather than adjusting conventional DMARDs further. 2
Treatment Escalation Algorithm
For Patients with Poor Prognostic Factors:
Poor prognostic factors include: positive RF or anti-CCP antibodies, very high disease activity (SDAI >26 or CDAI >22), early joint damage on imaging, or failure of 2 conventional synthetic DMARDs. 1
Add a biologic DMARD combined with methotrexate as the preferred next step. 1
First-line biologic options: TNF inhibitors (adalimumab, etanercept, infliximab) combined with methotrexate. 1 TNF inhibitors demonstrate superior efficacy when combined with methotrexate compared to monotherapy. 1, 3
Alternative first-line biologics include IL-6 inhibitors (tocilizumab, sarilumab), which may be preferred if methotrexate cannot be used as comedication. 1, 2
For Patients Without Poor Prognostic Factors:
Consider adding combination conventional synthetic DMARDs (triple therapy: methotrexate + sulfasalazine + hydroxychloroquine) before advancing to biologics. 2
If triple-DMARD therapy fails, then proceed to biologic therapy as outlined above. 2
Monitoring and Treatment Adjustment
Reassess disease activity every 1-3 months during active disease using validated composite measures (SDAI, CDAI, or DAS28). 1, 2
If no improvement occurs by 3 months, adjust therapy immediately. 2, 1
If the treatment target is not reached by 6 months, escalate therapy. 2, 1
Treatment Targets:
Primary target: Clinical remission (SDAI ≤3.3 or CDAI ≤2.8). 2, 1
Acceptable alternative: Low disease activity (SDAI ≤11 or CDAI ≤10), particularly in patients with long-standing disease. 2, 1
If First Biologic Fails
Switch to either a different TNF inhibitor (50-70% response rate expected) or a non-TNF biologic with a different mechanism of action. 1
Non-TNF options after TNF inhibitor failure: abatacept (CTLA4-Ig), rituximab (anti-CD20), or tocilizumab (IL-6 inhibitor). 2, 1
After failure of one TNF inhibitor, switching to a non-TNF biologic may provide better outcomes than switching to another TNF inhibitor, though either approach is acceptable. 2
Critical Pitfalls to Avoid
Never combine multiple biologic agents simultaneously due to significantly increased infection risk without added benefit. 3, 4
Do not use TNF inhibitors with anakinra or abatacept as combination therapy increases serious infection rates (7% vs 0%) without improving efficacy. 4
Avoid declaring methotrexate failure if the dose is below 20-25 mg weekly or if the patient has not tried subcutaneous administration after oral intolerance. 1
Do not continue ineffective therapy beyond 3 months hoping for delayed response—this allows irreversible joint damage to progress. 2, 5
After starting glucocorticoids, do not continue beyond 3 months at doses >10 mg/day due to cumulative toxicity including osteoporosis, cardiovascular disease, and cataracts. 2, 6
Shared Decision-Making
All treatment decisions must be made jointly between patient and rheumatologist, incorporating discussion of disease risks, treatment benefits, potential adverse effects, and individual patient factors including comorbidities. 2