Arthritis Treatment: Can Rheumatoid Arthritis Be Cured With Treatment?

Rheumatoid arthritis (RA) is a relatively common, systemic, autoimmune disease. It affects approximately 2 million Americans.

There are multiple theories regarding how and why it develops. Up until the mid-1980's treatment for this disorder was primitive at best. Corticosteroids and non-steroidal anti-inflammatory drugs (NSAIDS) were used to treat symptoms. And medicines like hydroxychloroquine (Plaquenil), gold salts, d-penicillamine, sulfasalazine, azathioprine, and the like were used to slow down the progression of disease.

Most of these drugs had horrendous side effects that limited their utility.

Disease modifying drugs such as methotrexate and leflunomide (Arava) elevated the bar in the mid to late 1980's, allowing more control of RA. In addition the use of combination therapy employing methotrexate, hydroxychloroquine, and sulfasalazine (Azulfidine) was touted (and still is in some quarters) as being remission inducing.

However, recent data published in the Cochrane review has indicated that combination therapy probably has little to offer above and beyond methotrexate alone.

And proponents of triple therapy cite data indicating its effectiveness versus patients treated with a combination of methotrexate and a biologic therapy.

However, in my opinion, this latter group, the biologics, have truly revolutionized our approach to the treatment of RA. For the first time, as treating rheumatologists, we have been able to induce remission more often than not. The definition of remission is bandied about. However, simplistically speaking, it is the absence of clinical disease. That doesn't mean a patient can stop their drug. The drug needs to be continued. However, the fact that the disease is stopped in its tracks with no further destruction of joints or damage to internal organs is amazing.

The first biologics were the tumor necrosis factor (TNF) inhibitors. Tumor necrosis factor, along with interleukin 1, interleukin 6, and a few other cytokines (biological messengers made by inflammatory cells) appear to drive the RA process.

The bad news is... not every patient responds to TNF inhibitors. When that occurs, changes to drugs with different modes of action are used. These will include drugs that block interleukin 6 as well as medicines that affect T cell and B cells, other players in the RA process.

What is lacking is the ability to predict which drug a patient will respond to best with remission. Markers of disease activity (biomarkers) in the inflamed joints probably hold the answer. If that puzzle can be solved, then the possibility of a cure becomes a not only a probability but a certainty.