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Quick links
- Lifestyle changes
- Secondary complications in established rheumatoid arthritis
- Conventional synthetic disease-modifying antirheumatic drugs
- Drug adherence
- Management of flares
- Pretreatment screening
- Choice of biologic or targeted synthetic disease-modifying antirheumatic drug therapy
- Complications of treatment with biologic or targeted synthetic disease-modifying antirheumatic drugs (b/tsDMARDs)
- Conclusion
- References
Abstract
The aim of treating established rheumatoid arthritis is sustained disease remission and prevention of joint destruction. In addition to modifying lifestyle factors such as diet and exercise, remission is usually achievable with combination therapy using conventional synthetic disease-modifying antirheumatic drugs (DMARDs) and biologic DMARDs or newer, oral, targeted synthetic DMARDs.
Key Points
- The aim of treating established rheumatoid arthritis (RA) is sustained clinical remission (absence of clinically inflamed joints and normal inflammatory markers) and prevention of joint destruction.
- Clinicians should be aware of how to manage disease and treatment-related complications.
- Lifestyle factors such as diet and exercise should be addressed to improve symptoms, maximise physical function, enhance treatment response and reduce cardiovascular risk.
- Disease remission is usually achievable with combination therapy using disease-modifying antirheumatic drugs (DMARDs) – conventional synthetic DMARDs and biologic DMARDs or newer, oral, targeted synthetic DMARDs.
- Clinicians should be aware of the increased risk of infection with DMARDs and implement measures such as early treatment of infection and timely vaccination.
- Patients with established RA also experience noninflammatory pain, including mechanical, neuropathic and fibromyalgia-related pain.
- Mental health issues such as depression are more common among patients with chronic disease and should be considered an important part of overall management.
Rheumatoid arthritis (RA) is a chronic systemic inflammatory condition that affects 1.9% of Australians, predominantly middle-aged females.1 It is associated with pain, physical disability, fatigue and sleep disturbance. Prolonged active disease leads to progressive irreversible joint damage, functional deterioration and increased mortality from accelerated cardiovascular (CV) disease.2
Although the exact cause of RA is unknown, understanding the molecular pathogenesis has allowed development of targeted treatment using biologic disease-modifying antirheumatic drugs (bDMARDs) such as etanercept and adalimumab and targeted synthetic DMARDs (tsDMARDs) such as tofacitinib and baricitinib. This has revolutionised the management of RA and resulted in disease remission (no clinically inflamed joints and normal systemic inflammatory markers) being achievable in many patients using early intensive therapy. Although this has resulted in significantly less morbidity, the likelihood of disease remission is lower in patients with established disease compared with those with early disease.3,4 It is therefore crucial to start conventional synthetic DMARD (csDMARD) therapy as early as possible and escalate to b/tsDMARDs, if appropriate (Case vignette: Part 1).
