How You Can Beat Rheumatoid Arthritis Part 5: Putting It Into Remission

The options available for treatment have expanded greatly in the last 10 years.

Non steroidal anti inflammatory drugs: These help to reduce pain and improve function. They do not have an effect on the underlying disease. Examples include ibuprofen, naproxyn, sulindac, etodolac, nabumatone, celecoxib, and meloxicam.

These drugs are effective but they have potential side effects including peptic ulcer disease, kidney and liver damage, rashes, and fluid retention. Another problem associated with these drugs is the slight increase in cardiovascular events such as heart attack and stroke. These drugs require careful monitoring.

Corticosteroids: These drugs suppress inflammation but also have no effect on the underlying disease. Examples include prednisone, methylprednisolone, and prednisolone. Used long term they may have undesirable side effects including ulcers, cataracts, osteoporosis, adrenal gland suppression, thinning of the skin, and diabetes.

Disease-modifying anti-rheumatic drugs (DMARDS): These drugs slow down the progression of rheumatoid arthritis. Examples would be medicines such as methotrexate, sulfasalazine (Azulfidine), leflunomide (Arava), hydroxychloroquine (Plaquenil), and cyclosporine (Sandimmune).

Most DMARDS act slowly.

The workhorse of DMARDS is probably methotrexate. All DMARDS have the potential for significant side-effects and must be monitored slowly.

Biologics: Most recently, biologic therapies such as etanercept (Enbrel), adalimumab (Humira), infliximab (Remicade), and anakinra (Kineret) have helped tremendously.

These drugs target the cells and cytokines that are the primary cause of rheumatoid arthritis. These drugs work quickly. Etanercept, adalimumab, and infliximab are anti-TNF drugs. They block tumor necrosis factor- the major culprit in RA - and by doing so keep it from doing damage. These drugs have a slightly different mechanism of action from each other but they essentially all do the same thing. And they do it well. These drugs have revolutionized our approach to RA.

Rheumatologists are using this group of drugs earlier in the course of disease to hopefully prevent damage from occurring. There is also some evidence that early aggressive treatment may prevent some of the long term complications of rheumatoid arthritis such as lymphoma and cardiovascular events.

Potential side-effects of anti-TNF therapy include an increased susceptibility to infection, the reactivation of latent tuberculosis, and the development of lupus-like or MS-like syndromes.

Kineret, unfortunately, does not have the same salutary effect and is not used very often.

The second wave of biologic therapies are available and offers hope for patients who fail anti-TNF treatment. The two newest drugs are abatacept (Orencia) and rituximab (Rituxan).

Abatacept is a co-stimulatory blocker. This means it prevents T cells from being activated to produce cytokines. Rituximab is a B-cell depleter. It removes B cells from a patient's system. B-cells are felt to play a big role in the development of RA by some experts.

Both drugs are given by intravenous infusion. Side effects include infusion reactions and rashes. The long-term consequence of B-cell depletion is still uncertain.

More biologic therapies are on the horizon. These new drugs may prove to be more effective and safer than what is currently available.

In patients with more severe disease, a procedure where blood is passed through a special filter (Prosorba column) may be of use. As one might guess, it is not used very often.