Wednesday, July 31, 2013

Arthritis Treatment: Evolution of Treatment for Rheumatoid Arthritis Today

Rheumatoid arthritis (RA) is the most common form of inflammatory arthritis, affecting approximately two million Americans. It is a chronic, systemic, autoimmune driven disease for which there is no cure.

Among the multisystem features of the disease is the ability to attack and destroy not only joint tissue, but also other organ systems such as the eye, bone marrow, lungs, peripheral nervous system as well as heighten the incidence of cardiovascular events such as heart attack and stroke.

While the disease, if not diagnosed and treated aggressively, can still cause significant problems, major advances in treatment have developed in the last 25 years.

The drug of choice remains methotrexate. We now have more than 30 years of experience with this medication and are familiar with its side effect profile which is much more benign than we used to believe.

Roughly, 25% to 30% of patients will go into remission or near remission on methotrexate alone, and many of those patients will sustain that response for up to a year or more.

So how is response defined?

Response occurs when a patient has no clinical signs of disease activity, no elevated acute phase reactants, which are blood tests that measure inflammation. The two most commonly used tests are the erythrocyte sedimentation rate ("sed rate") and CRP. And they have no functional deficit from their disease.

In patients who don't achieve remission or lose their remission, we now add on a tumor necrosis factor (TNF) inhibitor. These are a category of biologic drugs. These medicines that act like a laser beam against the immunologic disturbances that are responsible for RA.

While many patients respond to the combination of methotrexate and TNF inhibitor, some either don't respond initially or lose their response over time. In these patients we will try a second TNF inhibitor.

Fortunately, there are alternatives. We have three other biologic medicines that are all useful in the event a patient fails two TNF inhibitors. There is Orencia, which is a T-cell costimulatory modulator. T cells are felt to be a key player in the inflammation of RA. The second is Rituxan. This is a drug that was initially used to treat non-Hodgkins lymphoma. It is an antibody directed against B-cells, which are also a major contributor to chronic inflammation in RA. Finally, there is Actemra, which is an antibody drug directed against the interleukin-6 receptor.

Interleukin-6 is a protein messenger that is pivotal in perpetuating RA activity.

All of these have been shown to be effective in rheumatoid arthritis, and all have been shown to be effective in patients who have failed a TNF inhibitor.

With this arsenal of drugs there is better than a 50 per cent chance of getting a patient with new-onset RA into remission within six to twelve months.

And the good news is that newer therapies are being developed that may be even more effective.

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