Rheumatoid Arthritis (RA) is a relatively common, systemic, autoimmune disease. It affects approximately two million Americans.
There are multiple theories regarding how and why it develops. Up until the mid-1980's Treatment for this issue was primitive at best. Corticosteroids and non-steroidal anti-inflammatory drugs (NSAIDS) were used to treat Symptoms. And medications like hydroxychloroquine (Plaquenil), gold salts, d-penicillamine, sulfasalazine, azathioprine, and the like were used to slow down the progression of disease.
Most of these drugs had horrendous consequences that limited their utility company.
Disease modifying drugs equivalent to methotrexate and leflunomide (Arava) set the standard in the mid in order to late 1980's, allowing more control of RA. In addition if you use combination therapy employing methotrexate, hydroxychloroquine, and sulfasalazine (Azulfidine) was touted (and still is in some quarters) as being remission inducing.
However, recent data published covering the Cochrane review has demonstrated that combination therapy probably has the benefit of little to offer above and beyond methotrexate alone.
And proponents of multiply therapy cite data indicating its efficacy versus patients treated with a combination of methotrexate and a biologic remedy.
However, in my incline, this latter group, a particular biologics, have truly revolutionized our approach to the Treatment of RA. For the first time, as treating rheumatologists, we have been proven to induce remission more often than not. The definition of remission is to become bandied about. However, simplistically speaking, it is the lack of clinical disease. That does not necessarily mean a patient can finish their drug. The drug needs to be continued. However, the fact that the disease is stopped inside tracks with no further problems with joints or damage to areas is amazing.
The first biologics were the cancerous growth necrosis factor (TNF) inhibitors. Tumor necrosis factor, along around interleukin 1, interleukin 6, and a few other cytokines (biological messengers through inflammatory cells) appear to drive the RA process.
The bad news is... not every patient answers TNF inhibitors. When that occurs, changes to drugs based on a modes of action utilize. These will include stuff that block interleukin 6 advantages and medicines that affect WATTS cell and B cells, other players in in terms of the RA process.
What is lacking is the ability to predict which drug someone will respond to suitable for remission. Markers of disease activity (biomarkers) equipped inflamed joints probably grasp the answer. If that puzzle can also be solved, then the possibility throughout regards to cure becomes a not a probability but a sincerity..