Gout
Gout
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DOI：
10.1038/s41572-019-0115-y
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发表时间：
2019-09-26
影响因子：
81.5
通讯作者：
Stamp, Lisa K.
中科院分区：
文献类型：
--
作者：
Dalbeth, Nicola;Choi, Hyon K.;Stamp, Lisa K.
痛风是一种由尿酸钠（MSU）晶体沉积引起的慢性疾病。痛风通常表现为一种影响下肢关节的急性、自限性炎症性单关节炎。血清尿酸水平升高（高尿酸血症）是 MSU 晶体沉积和痛风发展的主要危险因素。尽管传统上被认为是嘌呤代谢紊乱，但肠道和肾脏中尿酸盐转运的改变在高尿酸血症的发病机制中起着关键作用。抗炎药，如皮质类固醇、非甾体抗炎药和秋水仙碱，广泛用于治疗痛风发作；认识到 NLRP3 炎性体激活和生物活性 IL-1 β 释放在痛风发作起始中的重要性，导致了针对痛风发作的抗 IL-1 β 生物疗法的开发。使用降尿酸疗法持续降低血清尿酸水平对于痛风的长期治疗至关重要，其目的是溶解 MSU 晶体、抑制痛风发作并解决痛风石。别嘌呤醇是一线降尿酸治疗，应从小剂量开始，逐渐增加剂量。低剂量抗炎治疗可以在降尿酸治疗开始期间减少痛风发作。护理模式，例如以护士为主导、注重患者参与和教育的策略，大大改善了临床结果，现在代表了痛风管理的最佳实践。
Gout is a chronic disease caused by monosodium urate (MSU) crystal deposition. Gout typically presents as an acute, self-limiting inflammatory monoarthritis that affects the joints of the lower limb. Elevated serum urate level (hyperuricaemia) is the major risk factor for MSU crystal deposition and development of gout. Although traditionally considered a disorder of purine metabolism, altered urate transport, both in the gut and the kidneys, has a key role in the pathogenesis of hyperuricaemia. Anti-inflammatory agents, such corticosteroids, NSAIDs and colchicine, are widely used for the treatment of gout flare; recognition of the importance of NLRP3 inflammasome activation and bioactive IL-1 beta release in initiation of the gout flare has led to the development of anti-IL-1 beta biological therapy for gout flares. Sustained reduction in serum urate levels using urate-lowering therapy is vital in the long-term management of gout, which aims to dissolve MSU crystals, suppress gout flares and resolve tophi. Allopurinol is the first-line urate-lowering therapy and should be started at a low dose, with gradual dose escalation. Low-dose anti-inflammatory therapies can reduce gout flares during initiation of urate-lowering therapy. Models of care, such as nurse-led strategies that focus on patient engagement and education, substantially improve clinical outcomes and now represent best practice for gout management.