Sounak Majee and Bapi Paul*


In 1929 rheumatoid arthritis (RA) patients frequently prioritized pain as a major symptom and it was a prevalent disease among Egyptians. RA treatment is expected to include pain management as part of inflammation control, intuitively, RA-related pain is frequently regarded as a natural consequence of peripheral inflammation. However, there can be a low correlation between objective measures of inflammation and pain in RA patients. Systemic inflammatory disease's pathogenesis relies heavily on the potent pro-inflammatory interleukin (IL)-6. Since IL-6 is necessary for both the destruction of joints and the manifestation of the disease throughout the body, it seems like a promising strategy to target this pathway in RA. To this point, data on efficacy show that Interleukin-6 inhibition performs better than placebo, conventional anti- rheumatic drugs like methotrexate, and TNF inhibition. In addition, even though the safety profile differs significantly from that of TNF inhibition (such as hyperlipidemia and neutropenia), these safety concerns have not been found to cause clinically significant side effects as of yet. Infection and malignancy rates, among other safety parameters, were found to be comparable between TNF inhibition and IL-6 inhibition. The biology and clinical applications of IL-6 inhibition in the treatment of rheumatoid arthritis are examined in this review.

Keywords: Rheumatoid arthritis, Osteoarthritis, DMARD, Tumor necrosis factor-alpha Inhibitors, IL-6 inhibitors, Autoimmunity, Cytokine Receptor, Inflammation, Interleukin-1, Interleukin-17, Interleukin-10, and GM-CSF.

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