Remission in a person with RA can be defined as the absence of disease activity, such as swollen joints, pain, and stiffness.
In the 1980s, when the authors of this book began practicing medicine, physicians approached RA differently than they do today. Back then, physicians were mostly concerned with controlling patients' symptoms. Patients were treated with nonsteroidal anti-inflammatory drugs (NSAIDs), which relieved some of their pain and were felt to be relatively safe. Physicians avoided “aggressive therapy,” with its attendant risks, until a patient had uncontrollable symptoms or showed obvious signs of joint destruction and disability. Aggressive therapy, at that time, was defined as the use of methotrexate, gold compounds, and antimalarials. These drugs were more effective than NSAIDs, but had higher rates of serious side effects.
Antimalarials
Drugs normally used to treat malaria but that are sometimes effective in the treatment of rheumatoid arthritis. The most commonly used antimalarial is hydroxychloroquine sulfate (Plaquenil).
Over time, research revealed that delaying aggressive treatment resulted in joint destruction and disability in patients with RA. In fact, several studies showed that a majority of the joint destruction in RA occurs in the first two years after the onset of the disease. As a result of these studies, in the 1990s physicians concentrated on limiting the destruction of joints by treating patients with more effective drugs much earlier in the course of their disease. Methotrexate and sulfasalazine were considered first-line treatment during this decade.
Since then, the introduction of the tumor necrosis factor (TNF) inhibitors—such as Remicade, Enbrel, and Humira—has changed the treatment paradigm yet again. Physicians and patients now expect better control of pain and stiffness, as well as decreased disability as a result of RA. For the first time, a significant number of patients are achieving remission. Physicians noticed that there was a difference in the rate of remission between those patients who had been treated with TNF inhibitors early in their disease and those who had started TNF inhibitors after their disease was well established. In some studies, the difference in remission rate between the early-treated and late-treated patients was three- or fourfold. This information has encouraged physicians to identify patients with RA early and to treat them aggressively with TNF inhibitors to maximize the chance of disease remission and decrease the chance of early joint destruction.
Disease remission is not disease cure, however. The RA is always there, but is suppressed by the medication only as long as you take it. Patients who have achieved disease remission and then stopped taking their medication, for example, have found that their disease often returns. You can think about your arthritis medications in much the same way you would think about medications for high blood pressure or diabetes. They might work very well, but they work only as long as you take them. Unfortunately, when these patients who stopped taking their RA medications were placed back on their treatment regimens, many were unable to achieve remission again.
If you are on a treatment regimen and it is controlling your symptoms, stick with it as long as you can: Don't tamper with success. If you believe the medication is causing problems, discuss your concerns with your physician before deciding to stop taking the drug. Your physician may be able to improve your symptoms by changing the route of administration, altering the dose of the medication, or changing to another medication altogether.
If you are on a treatment regimen and it is controlling your symptoms, stick with it as long as you can: Don't tamper with success.
I have had periods of remission. I believe this is due to medication. When my medication is cut, I get back flare-ups of the arthritis. Weather changes in the fall and spring also can cause flare ups.
—Jim