Rheumatologists usually use non-steroidal anti inflammatory drugs (NSAIDS) or low doses of corticosteroids to help with symptoms. To slow down disease, they employ disease-modifying anti-rheumatic drugs (DMARDS). Examples of DMARDS are drugs such as hydroxychloroquine (Plaquenil), sulfasalazine (Azulfidine), leflunomide (Arava), and methotrexate. By far, the “workhorse” DMARD is methotrexate.

In recent years, biologic drugs have been added to the therapeutic armamentarium. Biologic drugs are laser-like drugs that target the immune pathway abnormalities in RA. Medicines that target tumor necrosis factor, a particularly important instigator of chronic inflammation include drugs such as etanercept (Enbrel), infliximab (Remicade), and adalimumab (Humira).

Other biologic therapies target B-cells (Rituxan) or T-cells (Orencia).

What many of these biologic therapies have in common is the ability to shut down the production of cytokines, the chemical messengers that promote inflammation. Tumor necrosis factor is a prime example of a cytokine that perpetuates inflammation. There are many other cytokines that also play important roles in inflammation.

Interleukin-6 (IL-6) is a cytokine that also appears to play a pivotal role in the inflammation of rheumatoid arthritis. new potentially very effective treatment. IL-6 is ubiquitous inside the joint and is expressed by almost 20 per cent of cells inside the synovial capsule (lining of the joint). It appears to be pivotal in the transition from acute inflammation to chronic inflammation. IL-6 seems to do this by stimulating B-cells, T-cells, and attracting cells that aggravate inflammation into the synovium. IL-6 also transforms cells from a less aggressive state into a more aggressive state.

Even more interesting is the theory advanced by Dr. Gary Firestein at the University of California, San Diego, who posits that “IL-6 plays a significant role in a primitive broad-based immune response.”

A substantial role for IL-6 involvement in the development of diabetes, obesity, cardiovascular disease, infections, and even cancer has been demonstrated. The presence of an IL-6 footprint in all these disorders implicates immunity as a causative factor and secondarily points out the key role that IL-6 plays in these diseases.

Another interesting note is the effect IL-6 plays in anemia. It apparently decreases the absorption of iron from the bowel and affects the storage of iron. This may explain why patients with severe inflammatory disorders such as rheumatoid arthritis often develop what is called the anemia of chronic disease. Unlike iron deficiency anemia which is due to lack of iron and which may be due to side effects of drugs, the anemia of chronic disease is due to the inflammation stemming from RA.

Attempts to target IL-6 have recently been successful with the use of an antibody directed against receptors for IL-6. In other words, the linking sites for IL-6 on different cells are blocked by an antibody. This prevents the IL-6 from attaching to different cells and causing damage.

The most prominent IL-6 receptor antibody that has been studied is a drug called tociluzumab (Actemra).

Clinical trials are ongoing at the time of this article (late 2007).

Where IL-6 will fall as far as treatment for RA is still unknown at this time but it will be a useful addition to the arsenal of the clinical rheumatologist.