Lioté F
Univ Paris Diderot, Sorbonne Paris Cité and AP-HP, Hôpital Lariboisière, Centre Viggo Petersen, Service de Rhumatologie, Paris, France.
Reumatismo. 2012 Jan 19;63(4):276-83. doi: 10.4081/reumatismo.2011.276.
Gout is a very common joint disease which is due to chronic hyperuricemia and its related articular involvements. Yet it can be cured when appropriately managed. Comprehensive management of gout involves correct identification and addressing all causes of hyperuricemia, treating and preventing attacks of gouty inflammation (using colchicine NSAIDs, and/or steroids), and lowering serum urate (SUA) to an appropriate target level indefinitely. The ideal SUA target is, at a minimum, less than 6 mg/dL (60 mg/L or 360 μmol/L), or even less than 5 mg/dL in patients with tophi. The SUA target should remain at less than 6 mg/dL for long in all gout patients, especially until tophi have resolved. Patient education and adherence to therapy are key point to the optimal management of gout, aspects which are often neglected. Adherence can be monitored in part by continuing, regular assessment of the SUA level. More difficult cases of gout often need a combination of urate lowering therapy (ULT) for both refractory hyperuricemia and chronic tophaceous arthritis. Chronic tophaceous gouty arthropathy which do not respond adequately to optimized oral ULT might benefit from the use of pegloticase, when this is available in, for example, Italy and other European countries. By contrast, in calcium pyrophosphate (CPP) crystal deposition disease (CPPD), as evidenced by pseudo gout attacks or chronic polyarthritis, similar anti-inflammatory strategies have been recommended, but there have as yet been no controlled trials. Of note, there is no treatment for the underlying metabolic disorders able to control the CPPD. Management of crystal-induced arthropathies (CIA) depends not only on clinical expression, namely acute attacks or chronic arthropathy, but also on the underlying metabolic disorder. We will mainly focus on gout as an archetype of CIA.
痛风是一种非常常见的关节疾病，由慢性高尿酸血症及其相关的关节受累引起。然而，通过适当管理可以治愈。痛风的综合管理包括正确识别和解决高尿酸血症的所有病因，治疗和预防痛风性炎症发作（使用秋水仙碱、非甾体抗炎药和/或类固醇），并将血清尿酸盐（SUA）无限期降低至适当的目标水平。理想的SUA目标至少应低于6mg/dL（60mg/L或360μmol/L），对于有痛风石的患者甚至应低于5mg/dL。在所有痛风患者中，SUA目标应长期保持低于6mg/dL，尤其是在痛风石消退之前。患者教育和坚持治疗是痛风最佳管理的关键点，而这些方面往往被忽视。坚持治疗情况可部分通过持续定期评估SUA水平来监测。痛风较难治疗的病例通常需要联合使用降尿酸治疗（ULT）来治疗难治性高尿酸血症和慢性痛风石性关节炎。对于优化口服ULT反应不佳的慢性痛风石性痛风性关节病，在例如意大利和其他欧洲国家有聚乙二醇尿酸酶可用时，使用该药可能有益。相比之下，在焦磷酸钙（CPP）晶体沉积病（CPPD）中，如假痛风发作或慢性多关节炎所证实的，已推荐了类似的抗炎策略，但尚未有对照试验。值得注意的是，对于能够控制CPPD的潜在代谢紊乱尚无治疗方法。晶体诱导的关节病（CIA）的管理不仅取决于临床表现，即急性发作或慢性关节病，还取决于潜在的代谢紊乱。我们将主要关注痛风作为CIA的一个典型例子。
