Arthritis Under Arrest

For most victims arthritis simply means pain and stiffness in the joints--sometimes moderate, sometimes severe, usually responsive to treatment with one of a number of drugs. Pain can be just the beginning, though, for the more than 2 million Americans who suffer from the variant of the disease known as rheumatoid arthritis. This unfortunate minority may experience not just discomfort but also joint deformities, fatigue, nodules of tissue under the skin and inside internal organs and, in rare cases, inflammation of the membranes surrounding the heart and lungs.

Unfortunately, even the most powerful existing medications, like Methotrexate, either carry unacceptable side effects or are ineffective against rheumatoid arthritis, or both. Clinicians are understandably a bit giddy, therefore, at the news that after more than a decade of no progress, not just one but a number of new treatments are all at once streaming out of research labs.

Last week, for example, an FDA advisory panel recommended that the agency approve a new drug called Enbrel. The week before, the full FDA had given the nod to another anti-rheumatoid arthritis drug called Arava. Next month the agency will assess a promising blood-filtration device that clears the body of arthritis-promoting substances the same way kidney dialysis cleans the blood of toxins. Within a few months the FDA will also consider a new class of anti-inflammatories called COX-2 inhibitors (a.k.a. "super aspirin") that will attack arthritis pain. Says Steven Abramson, an FDA adviser and chief of rheumatology at New York University's Hospital for Joint Diseases: "This is the most exciting time I've witnessed."

The excitement began with a growing understanding of how rheumatoid arthritis works. Unlike its more common cousin, osteoarthritis, which causes pain in more than 20 million mostly older Americans through simple deterioration of joint cartilage, rheumatoid arthritis is a complex disease involving an immune system gone awry.

Most experts believe the trigger for rheumatoid arthritis is an ordinary infection in a joint, to which the immune system mounts an ordinary response. Then, for some unknown reason, the white blood cells that are fighting invading microbes attack the joint itself--specifically the synovial sac, which acts as both a cushion that keeps bones from banging together and a source of lubricating fluid. Even as the white cells attack, they send out signals, in the form of hormones called cytokines, that rally more troops to their aid. Meanwhile, the besieged synovial cells secrete prostaglandins, which cause inflammation. All this makes the joint redden and become sore.