Current opinion in rheumatology · 2026
Choosing NSAID treatment in axial spondyloarthritis: factors guiding clinical decision-making.
СтатьяОбзорНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Gensler Lianne S, McKay Cailean E, Mayer Adam S
Аннотация
PURPOSE OF REVIEW: Nonsteroidal anti-inflammatory drugs (NSAIDs) are first-line therapy for axial spondyloarthritis (axSpA), improving pain, function, and disease activity. This review evaluates evidence for NSAID efficacy, potential disease modification, and safety considerations in patients with axSpA, particularly those with inflammatory bowel disease (IBD) or elevated cardiovascular risk.
RECENT FINDINGS: Evidence for NSAID-mediated disease modification remains inconsistent. In patients with IBD, contemporary data suggest variable risk of disease exacerbation depending on NSAID selectivity and exposure patterns. Established gastrointestinal toxicities persist outside the IBD context, though risk-mitigation strategies are available. While general-population studies demonstrate increased cardiovascular risk with certain NSAIDs, emerging axSpA-specific observational data suggest a smaller excess risk of major adverse cardiovascular events, potentially reflecting the counterbalancing effect of inflammation control. Pharmacogenomic data increasingly support CYP2C9 variation as a determinant of NSAID exposure and toxicity.
SUMMARY: NSAIDs remain foundational in axSpA management, but long-term use requires individualized assessment of gastrointestinal, cardiovascular, and IBD-related risks. Pharmacogenomic considerations may further refine patient selection and dosing strategies.
RECENT FINDINGS: Evidence for NSAID-mediated disease modification remains inconsistent. In patients with IBD, contemporary data suggest variable risk of disease exacerbation depending on NSAID selectivity and exposure patterns. Established gastrointestinal toxicities persist outside the IBD context, though risk-mitigation strategies are available. While general-population studies demonstrate increased cardiovascular risk with certain NSAIDs, emerging axSpA-specific observational data suggest a smaller excess risk of major adverse cardiovascular events, potentially reflecting the counterbalancing effect of inflammation control. Pharmacogenomic data increasingly support CYP2C9 variation as a determinant of NSAID exposure and toxicity.
SUMMARY: NSAIDs remain foundational in axSpA management, but long-term use requires individualized assessment of gastrointestinal, cardiovascular, and IBD-related risks. Pharmacogenomic considerations may further refine patient selection and dosing strategies.