Department of Medicine, University of Auckland, Auckland, New Zealand.
Department of Anatomy, University of Otago, Dunedin, New Zealand.
Lancet. 2021 May 15;397(10287):1843-1855. doi: 10.1016/S0140-6736(21)00569-9. Epub 2021 Mar 30.
Gout is a common and treatable disease caused by the deposition of monosodium urate crystals in articular and non-articular structures. Increased concentration of serum urate (hyperuricaemia) is the most important risk factor for the development of gout. Serum urate is regulated by urate transporters in the kidney and gut, particularly GLUT9 (SLC2A9), URAT1 (SLC22A12), and ABCG2. Activation of the NLRP3 inflammasome by monosodium urate crystals with release of IL-1β plays a major role in the initiation of the gout flare; aggregated neutrophil extracellular traps are important in the resolution phase. Although presenting as an intermittent flaring condition, gout is a chronic disease. Long-term urate lowering therapy (eg, allopurinol) leads to the dissolution of monosodium urate crystals, ultimately resulting in the prevention of gout flares and tophi and in improved quality of life. Strategies such as nurse-led care are effective in delivering high-quality gout care and lead to major improvements in patient outcomes.
痛风是一种由单钠尿酸盐晶体在关节和非关节结构中沉积引起的常见且可治疗的疾病。血清尿酸浓度升高(高尿酸血症)是痛风发展的最重要危险因素。血清尿酸由肾脏和肠道中的尿酸转运蛋白调节,特别是 GLUT9(SLC2A9)、URAT1(SLC22A12)和 ABCG2。单钠尿酸盐晶体激活 NLRP3 炎性体并释放白细胞介素-1β(IL-1β),在痛风发作的起始中起主要作用;聚集的中性粒细胞细胞外陷阱在缓解阶段很重要。尽管痛风表现为间歇性发作,但它是一种慢性疾病。长期降低尿酸治疗(例如别嘌醇)可导致单钠尿酸盐晶体溶解,最终预防痛风发作和痛风石形成,并提高生活质量。护士主导的护理等策略可有效地提供高质量的痛风护理,并可显著改善患者的预后。