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Diagnosis difficulties are common for ankylosing spondylitis (AS) patients, leading to inadequate and inconsistent treatment. We evaluated the national and geographic variability in disease diagnosis and treatment in the United States.This retrospective, cross-sectional analysis utilized the IBM® MarketScan® Administrative Claims Database from 2014 to 2019. AS patients ≥ 18 years of age with continuous medical and pharmacy enrollment during the calendar year and complete geographic information during the study period were included. Patient cohorts assessed were D1 (≥ 1 AS diagnoses within each calendar year of assessment between 2014 and 2019), D2 (≥ 2 non-rheumatologist AS diagnoses), and D3 (≥ 2 rheumatologist AS diagnoses). For D2 and D3, diagnoses were ≥ 6 months apart, but within 18 months. Annual AS diagnostic prevalence and treatment rates were determined from 2014 to 2019 nationally and per state in 2019. Treatments assessed were disease-modifying antirheumatic drugs (DMARDs), opioids, nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and methotrexate.Nationally, AS diagnostic prevalence increased from 2014 to 2019, with 2019 rates of 9.6 (D1), 5.1 (D2), and 3.5 (D3) per 10,000 persons. Diagnostic prevalence varied between states, which was not explained by age, sex, racial distribution, or rheumatologists per capita. Nationally, a greater percentage of D3 patients vs. D1 and D2 patients received biologic/targeted synthetic DMARDs (bDMARD/tsDMARDs) and conventional synthetic DMARD. Opioid use ranged from 37 to 40% in 2019 and decreased from 2014 for all cohorts. Corticosteroid and methotrexate use decreased slightly, while NSAID and bDMARD/tsDMARD use generally increased from 2014 to 2019.AS diagnostic prevalence is increasing nationally, though it remains low among some states. bDMARD/tsDMARDs use was more common among patients treated by rheumatologists. Opioid and corticosteroid use is decreasing, though national rates remain high with significant state variability. Further education is needed, particularly in states with low prevalence and inadequate treatment, to improve diagnosis and treatment.

Spondyloarthritis (SpA) comprises a group of chronic inflammatory diseases with overlapping clinical, genetic and pathophysiological features including back pain, peripheral arthritis, psoriasis, enthesitis and dactylitis. Several cytokines are involved in the pathogenesis of SpA, variously contributing to each clinical manifestation. Many SpA-associated cytokines, including IL-23, IL-17, IL-6, type I/II interferon and tumour necrosis factor signal directly or indirectly via the Janus kinase (JAK)–signal transducer and activator of transcription pathway. JAK signalling also regulates development and maturation of cells of the innate and adaptive immune systems. Accordingly, disruption of this signalling pathway by small molecule oral JAK inhibitors can inhibit signalling implicated in SpA pathogenesis. Herein we discuss the role of JAK signalling in the pathogenesis of SpA and summarize the safety and efficacy of JAK inhibition by reference to relevant SpA clinical trials.