作者：Ruoff G, Edwards NL
翻譯：北京市海淀醫院（北醫三院海淀院區）費雅楠（feiyn@sina.cn）
校正：北京市海淀醫院 張舸
摘要： 痛風是一種進展的、痛苦的、使人衰弱的炎癥性關節炎。它是由血清尿酸（sUA）濃度升高而引起，導致高尿酸（SUA >6.8mg/dl）。持續升高的血尿酸可導致尿酸鈉（MSU）晶體沉積在關節和軟組織，可引起急性和慢性炎癥。在過去的幾十年里高尿酸血癥和痛風的患病率逐漸增加，可能是由于人口老齡化、生活方式和飲食結構的改變，而且痛風相關并發癥也在增加。痛風未經治療或治療不當可導致疾病的慢性癥狀，包括持續性炎癥，急性發作次數的增加，發展成痛風石和關節結構損傷。有數據表明，即使當時患者是無癥狀的，但在局部關節和系統會發生持續的炎癥和隨后的損害。痛風的長期治療的目標是降低血尿酸水平
附原文：Abstract Gout is a progressive, painful, debilitating form of inflammatory arthritis. It is caused by factors that elevate the concentration of serum uric acid (sUA), leading to hyperuricemia (sUA >6.8 mg/dL). Continued elevated sUA can result in monosodium urate (MSU) crystal deposition in joints and soft tissues, and can cause acute and chronic inflammation. The prevalence of hyperuricemia and gout has increased over the last few decades, likely due to an aging population, changes in lifestyles and diet, and an increase in gout-associated comorbidities. Untreated or improperly treated gout can lead to chronic manifestation of the disease, including persistent inflammation, increased number of flares, development of tophi, and structural joint damage. Data show that even when patients are asymptomatic, ongoing inflammation and subsequent damage occurs locally at the joint and systemically. The aim of long-term treatment of gout is to reduce sUA levels to
引自：Ruoff G1, Edwards NL2, Overview of Serum Uric Acid Treatment Targets in Gout: Why Less Than 6 mg/dL? Postgrad Med. 2016 Aug 25:1-10.
