Rheumatoid arthritis (RA) is a long-term autoimmune disorder that primarily affects joints (Wikipedia, n.d.).

If the general cause is over activity of inflammatory cytokines (Nalbant & Birlik, 2016), why do we just just manage RA with pain medications, steroids, non steroidal anti-inflammatory drugs (NSAIDs), and disease-modifying antirheumatic drugs (DMARDs) such as hydroxychloroquine and methotrexate?

Can we not deal with the cytokine over activity with immunosuppressants?


Nalbant, S. & Birlik, A. M. (2016). Cytokines in Rheumatoid Arthritis (RA). In: Sakkas, L. (Ed.) New Developments in the Pathogenesis of Rheumatoid Arthritis. doi: 10.5772/65893.

Wikipedia (n.d.). Rheumatoid arthritis. Retrieved from: https://en.wikipedia.org/wiki/Rheumatoid_arthritis


In treatment of rheumatoid arthritis, the following immunosuppressants, which are already in use, inhibit cytokines:

Biologic DMARDs are not the first choice in treatment of RA because they:

  • are expensive
  • cannot be taken by mouth (because they contain antibodies, which are proteins)
  • can have severe side effects (thrombosis, liver and kidney toxicity, demyelinating disorders...)
  • increase the risk of infections (pneumonia, skin infections, the reactivation of tuberculosis or hepatitis B...)
  • usually do not induce remission, unlike methotrexate and sulfasalazine (Emedicine)

Emedicine (free registering required) and John Hopkins Medicine cover drugs used in treatment of RA, including DMARDs, one by one in detail (mechanism of action, dosing, clinical effectiveness, side effects).

Most drugs mentioned here are included in 2015 American College of Rheumatology Guideline for the Treatment of Rheumatoid Arthritis.


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