Rheumatoid arthritis is a systemic disease that is most characterised by a progressive destructive joint disease that is traditionally managed with disease modifying drugs. If these fail to control the disease, then patients are either switched to monoclonal drugs that target the TNF receptor - either soluble or membrane bound, or both.

Alternatives to anti-TNF drugs include Rituximab which is an monoclonal directed against CD20 lymphocytes, and Tocilizumab which is an IL-6 inhibitor. And there are others.

What biological factors influence the choice of either an TNF-i or the alternatives after DMARD failure (methotrexate, sulfasalazine, leflunomide)?

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