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-1β release in initiation of the gout flare has led to the development of anti-IL-1β 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.

中文翻译：

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痛风。

痛风是一种由尿酸钠（MSU）晶体沉积引起的慢性疾病。痛风通常表现为影响下肢关节的急性自限性炎性单关节炎。血清尿酸盐水平升高（高尿酸血症）是MSU晶体沉积和痛风发展的主要危险因素。尽管传统上认为嘌呤代谢紊乱，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理中起着关键作用。消炎药，例如皮质类固醇，NSAID和秋水仙碱，被广泛用于治疗痛风发作。认识到在痛风发作中NLRP3炎性体激活和生物活性IL-1β释放的重要性已经导致了针对痛风发作的抗IL-1β生物疗法的发展。使用降低尿酸盐的疗法持续降低血清尿酸盐水平对于痛风的长期治疗至关重要，该疾病的目的是溶解MSU晶体，抑制痛风发作和解决痛风石。别嘌醇是一线降低尿酸盐的疗法，应从低剂量开始，逐渐增加剂量。小剂量抗炎治疗可以在降低尿酸盐的治疗过程中减少痛风发作。护理模式（例如专注于患者参与和教育的以护士为主导的策略）大大改善了临床效果，现在代表痛风管理的最佳实践。随着剂量逐步增加。小剂量抗炎治疗可以在降低尿酸盐的治疗过程中减少痛风发作。护理模式（例如专注于患者参与和教育的以护士为主导的策略）大大改善了临床效果，现在代表痛风管理的最佳实践。随着剂量逐步增加。小剂量抗炎治疗可以在降低尿酸盐的治疗过程中减少痛风发作。护理模式（例如专注于患者参与和教育的以护士为主导的策略）大大改善了临床效果，现在代表痛风管理的最佳实践。