Rheumatoid Arthritis (RA) is mostly a relatively common, systemic, autoimmune disorder. It affects approximately only two million Americans.
There are multiple theories regarding how and why it develops. Up until the mid-1980's Treatment for this problem was primitive at top. Corticosteroids and non-steroidal anti-inflammatory drugs (NSAIDS) were used to treat Symptoms. And medications like hydroxychloroquine (Plaquenil), diamonds salts, d-penicillamine, sulfasalazine, azathioprine, yet others were used to slow down the progression of disease.
Most for the drugs had horrendous side effects that limited their ability.
Disease modifying drugs act like methotrexate and leflunomide (Arava) set the standard in the mid spanning late 1980's, allowing more control of RA. In addition the use of combination therapy employing methotrexate, hydroxychloroquine, and sulfasalazine (Azulfidine) was touted (and still is in some quarters) like an remission inducing.
However, recent data published able to Cochrane review has demonstrated that combination therapy probably bears little to offer far above methotrexate alone.
And proponents of three times the therapy cite data indicating its effectiveness versus patients treated with a little methotrexate and a biologic treatment.
However, in my imagined, this latter group, can be biologics, have truly revolutionized our technique of the Treatment of RA. The very first time, as treating rheumatologists, we have been willing to induce remission that the. The definition of remission is one other bandied about. However, simplistically conversational, it is the lack of clinical disease. That doesn't mean a patient can quit their drug. The drug shall be continued. However, the need for the disease is stopped in tracks with no further scratches to joints or damage to organs is amazing.
The most notably biologics were the tumour necrosis factor (TNF) inhibitors. Cancer malignancy necrosis factor, along featuring interleukin 1, interleukin 6, and a few other cytokines (biological messengers made by inflammatory cells) appear to run the RA process.
The bad news is... not every patient answers TNF inhibitors. When that happens, changes to drugs based on a modes of action are used. These will include meds that block interleukin 6 and gratifaction medicines that affect N cell and B body, other players in a directory of RA process.
What is lacking is having the capacity to predict which drug an individual will respond to appropriate for remission. Markers of disease activity (biomarkers) with a inflamed joints probably hold the answer. If that puzzle additional details solved, then the possibility out from the cure becomes a not only a probability but a guarantee..