Differentiating the new rheumatoid arthritis biologic therapies

Abstract

Current understanding of the mechanisms behind the pathogenesis of rheumatoid arthritis (RA) has led to the development of therapies involving biologic agents that target specific mediators of the disease process. Although the biologic agents used to treat RA share the ability to alter the cytokine cascade, they differ in ways that are clinically important. For example, they vary with regard to how they block cytokine activity (ie, as receptors, as receptor blockers, or as anticytokine antibodies) and the particular cytokine they target (eg, tumor necrosis factor [TNF] versus interleukin-1). Biologic therapies for RA also differ in mode of administration. Several are administered subcutaneously, whereas others are given intravenously. They also have molecular dissimilarities that result in differences in pharmacokinetics (ie, long versus medium half-life) and that may influence their safety profiles.Some biologic agents, such as the TNF inhibitors etanercept and infliximab, have been rigorously examined for long-term safety and efficacy, whereas other agents, like the TNF inhibitor adalimumab, have not. Differences between the various biologic agents may relate to the usefulness of each individual drug as a long-term treatment in RA. For example, the need for physician visits may impact the practicality of drugs that are administered intravenously. Also, physicians should be aware that use of cytokine inhibitors increases the risk of infection. The prevalence of tuberculosis during therapy with infliximab exceeds the background rate in patients with RA. Accordingly, physicians should be familiar with the updated warnings in the package inserts that accompany these drugs.