Rheumatoid Arthritis: 20 Years Has Made a Big Difference in Treatment

Jonathan Kay, MD


September 20, 2015

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I am Dr Jonathan Kay, professor of medicine at the University of Massachusetts Medical School and director of clinical research in the Division of Rheumatology at the University of Massachusetts Memorial Medical Center, both in Worcester, Massachusetts.

I would like to congratulate Medscape on its 20th anniversary. This has prompted me to think about the advances in the treatment of rheumatoid arthritis (RA) over the past two decades.

Since the advent of Medscape, we have seen the introduction of targeted biological therapies. In 1998, 3 years after Medscape began, we saw the approval of infliximab and etanercept, the first two tumor necrosis factor (TNF) inhibitors introduced to treat RA. Subsequently, there have been three other TNF inhibitors introduced as well as an inhibitor of T-cell costimulation, a B-cell-directed therapy, an antibody directed against the interleukin-6 receptor, and an interleukin-1 receptor antagonist. These agents have allowed us now to aim for remission and not just to control disease activity and make a patient feel somewhat more comfortable. Treating to target now is the approach to treatment of RA, aiming to use a quantitative measure of disease activity to achieve low disease activity or remission—goals that were previously not achievable before 1998 or the past decade or so.

We also have seen the introduction of new markers of RA. Antibodies against citrullinated peptides (or anti-CCP antibodies or ACPA) have been introduced over the past two decades to identify patients with RA, especially those with poor prognostic indicators. This has allowed us not only to identify patients with early RA and to aim treatment at early disease, but also to look for patients perhaps at risk for the development of RA. Studies looking at first-degree relatives of patients with RA, who also have antibodies to cyclic citrullinated peptides, show that they are potentially at risk for RA. And now they are the subject of clinical trials to not only treat but actually prevent RA. Studies of the microbiome over the past several years have pointed to pathogenic mechanisms that may prompt other treatments to prevent the development of RA.


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