If your mother or grandmother had rheumatoid arthritis in the 1930s and 40s, she was probably prescribed bed-rest and heavy doses of aspirin. As one doctor puts it, patients were given so much aspirin “their ears rang.”1
In the late 40s and early 50s things got a little better, and most patients were given cortisone to help control pain and inflammation. However, cortisone didn’t slow down the rate of joint deterioration, so the long-term outlook was still grim.
The big breakthrough came in the 1980s when methotrexate, a drug that was already being used in higher doses to treat leukemia, became the standard treatment for RA patients.
Current RA treatment
Today, if you're a newly diagnosed rheumatoid arthritis patient, you are treated almost like a cancer patient, with a cocktail of medications to fight the disease from many different angles at once. Methotrexate is still at the core of most treatment regimens, along with other disease-modifying antirheumatic drugs (DMARDs) and glucocorticosteriods (like prednisolone).
Potential RA treatments and prevention
New studies point to the future of RA treatment and possible prevention. Just last week the Annals of Rheumatic Diseases published a study showing one way rheumatoid arthritis is biochemically triggered in patients who are genetically predisposed to the disease.2
The hallmark of RA is the swelling and inflammation of a joint’s lining, or synovium. This swelling and inflammation occurs when different cells collect in the joint. These cells need oxygen to live, requiring the formation of abnormal blood vessels.
The study’s researchers say that when two proteins, CCL28 and its receptor CCR10, are present in a joint and marry together they promote the formation of abnormal blood vessels.
These new blood vessels set the stage for the amassing of cells, swelling and inflammation associated with rheumatoid arthritis.
What does this mean for future RA treatment? Doctors hope that if they can prevent the two proteins from ever meeting, they can prevent the cascade of events that lead to RA.
Preventing rheumatoid arthritis before it begins? That beats the heck out of aspirin and bed rest.
1 University of California Television (UCTV). June 12, 2008. Rheumatoid Arthritis: Part I, The Coming of Age Lecture Series (lecture with Dr. Michael Weisman, Show ID: 14860). Retrieved May 23, 2014 from https://www.youtube.com/watch?v=djZfEi-ztVQ
2 Chen Z, Kim SJ, Essani AB, Volin MV, Vila OM, Swedler W, Arami S, Volkov S, Sardin LV, Sweiss N, et al. Characterising the expression and function of CCL28 and its corresponding receptor, CCR10, in RA pathogenesis. Ann Rheum Dis. 2014 May 15. pii: annrheumdis-2013-204530. doi: 10.1136/annrheumdis-2013-204530. [Epub ahead of print] PubMed PMID: 24833787.