Gout
Gout
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DOI：
10.1038/s41572-019-0124-x
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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.
痛风是一种由尿酸盐（MSU）结晶沉积引起的慢性疾病。痛风通常表现为急性、自限性炎症性单关节炎，影响下肢关节。血清尿酸盐水平升高（高尿酸血症）是MSU晶体沉积和痛风发生的主要危险因素。虽然传统上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关键作用。抗炎剂，如皮质类固醇、NSAID和秋水仙碱，被广泛用于治疗痛风发作;认识到NLRP 3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，导致开发了用于痛风发作的抗IL-1 β生物疗法。使用降尿酸治疗持续降低血清尿酸水平在痛风的长期管理中至关重要，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，应开始低剂量，逐渐剂量递增。低剂量抗炎治疗可以减少痛风发作在开始降尿酸治疗。护理模式，如护士主导的战略，重点是病人的参与和教育，大大改善临床结果，现在代表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.