{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,31]],"date-time":"2026-10-31T02:05:10Z","timestamp":1793412310419,"version":"4.5.0"},"reference-count":102,"publisher":"American Medical Association (AMA)","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAMA"],"published-print":{"date-parts":[[2025,2,4]]},"abstract":"<jats:sec id=\"ab-jrv240028-1\">\n                    <jats:title>Importance<\/jats:title>\n                    <jats:p>Axial spondyloarthritis is an immune-mediated inflammatory condition involving the sacroiliac joints, spine, and peripheral joints. It affects approximately 1% of adults in the US and is associated with impaired physical function and reduced quality of life.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-jrv240028-2\">\n                    <jats:title>Observations<\/jats:title>\n                    <jats:p>Inflammatory chronic back pain characterized by gradual onset starting before age 45 years, prolonged morning stiffness, improvement with exercise, and lack of improvement with rest is the most common symptom of axial spondyloarthritis and affects more than 80% of patients. Patients with axial spondyloarthritis may also have inflammatory arthritis in large peripheral joints (most commonly knees) in an oligoarticular, asymmetric fashion; inflammation at tendon insertions (enthesitis); inflammatory eye disease (uveitis); psoriasis; and inflammatory bowel disease. The pathogenesis of axial spondyloarthritis may involve genetic predisposition, gut microbial dysbiosis, and entheseal trauma, with immune cell infiltration of the sacroiliac joints and entheseal insertion areas in the spine. There are currently no diagnostic criteria for axial spondyloarthritis. The diagnosis, often delayed 6 to 8 years after symptom onset, is based on history (ie, inflammatory back pain [sensitivity, 74%-81%; specificity, 25%-44%]), laboratory findings (human leukocyte antigen B27\u2013positive [sensitivity, 50%; specificity, 90%] and elevated C-reactive protein level [sensitivity, 35%; specificity, 91%]), and imaging findings consisting of sacroiliitis on plain radiography (sensitivity, 66%; specificity, 68%) or magnetic resonance imaging (sensitivity, 78%; specificity, 88%). First-line treatments are physical therapy and nonsteroidal anti-inflammatory drugs (NSAIDs). However, less than 25% of patients achieve complete symptom control with NSAIDs. Approximately 75% of patients require biologic drugs (tumor necrosis factor inhibitors [anti-TNF agents], interleukin 17 inhibitors [anti\u2013IL-17 agents]) or targeted synthetic disease-modifying antirheumatic agents (Janus kinase [JAK] inhibitors) to reduce symptoms, prevent structural damage, and improve quality of life. Clinical trials reported that anti-TNF agents significantly improved ASAS20 (measure of pain, function, and inflammation) in 58% to 64% of patients compared with 19% to 38% for placebo. Similar outcomes were attained with anti\u2013IL-17 agents (48%-61%, vs 18%-29% with placebo) and JAK inhibitors (52%-56%, vs 26%-29% with placebo). Anti-TNF agents, anti\u2013IL-17 agents, and JAK inhibitors have been associated with reduced radiographic progression of axial spondyloarthritis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-jrv240028-3\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Axial spondyloarthritis predominantly affects the sacroiliac joints and spine but is also associated with extraskeletal manifestations such as uveitis, psoriasis, and inflammatory bowel disease. Physical therapy and NSAIDs are first-line treatments, but most patients require therapy with biologics (anti-TNF or anti\u2013IL-17 agents) or JAK inhibitors to achieve improvement in signs and symptoms, inflammation control, and reduced progression of structural damage.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1001\/jama.2024.20917","type":"journal-article","created":{"date-parts":[[2024,12,4]],"date-time":"2024-12-04T11:00:33Z","timestamp":1733310033000},"page":"408","source":"Crossref","is-referenced-by-count":104,"title":["Axial Spondyloarthritis"],"prefix":"10.1001","volume":"333","author":[{"given":"Mohamad","family":"Bittar","sequence":"first","affiliation":[{"name":"Division of Arthritis and Rheumatic Diseases (OP09), Oregon Health & Science University, Portland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Atul","family":"Deodhar","sequence":"additional","affiliation":[{"name":"Division of Arthritis and Rheumatic Diseases (OP09), Oregon Health & 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