A COMPARATIVE STUDY BETWEEN OUTCOME OF JAK INHIBITORS (TOFACITINIB) AND NSAIDS ON PATIENTS WITH AXIAL SPONDYLOARTHROPATHIES

Ankylosing spondylitis (AS), also called radiographic axial spondyloarthropathy is a chronic inflammatory disease of the axial skeleton that can result in serious impairment of spinal mobility and reduced quality of life. The incidence of AS is 0.4-15.0 per 100000 patient-years, varying by region. The Assessment of SpondyloArthritis international Society (ASAS)/European League Against Rheumatism and American College of Rheumatology/Spondylitis Association of America/ Spondyloarthritis Research and Treatment Network treatment guidelines recommend several pharmacological treatments for AS management as well as physical therapy. Non-

steroidal anti-inflammatory drugs (NSAIDs) are recommended as first-line treatment, followed by biologic disease-modifying antirheumatic drugs (bDMARDs), such as tumour necrosis factor inhibitors (TNFi). No evidence exists to support the efficacy of conventional synthetic disease-modifying anti rheumatic drugs (csDMARDs) for treating purely axial disease. Therefore,treatment options are limited for patients with an inadequate response or intolerance (IR) to NSAIDs. Furthermore,given that bDMARDs are administered parenterally, there is an unmet need for oral therapies with alternative mechanisms of action to treat ASJanus kinase (JAK) inhibitors, also known as JAKi or JAKinibs, are the latest class of synthetic (non-biologic) disease-modifying anti-rheumatic drugs (DMARDs) that have been proven effective in clinical trials in the treatment of multiple forms of arthritis, including psoriatic arthritis (PsA) and ankylosing spondylitis These medications specially target the JAK family of enzymes, namely JAK1, JAK2, JAK3 and tyrosine kinase 2 (TYK2), each of which are involved in the initiation of the signal for a cell to make more than 60 different cytokines and growth factors. Unlike biologics, which inhibit the effects of one single cytokine, JAKi can block the effects of multiple cytokines that are implicated in the pathogenesis (development) of many immune-mediated rheumatic diseases, including AS. They have a shorter half-life compared to biologics, meaning they are active in the body for less time, which means if they are discontinued, any side effects will disappear in a swifter fashion.