Schlesinger Naomi, Dalbeth Nicola, Perez-Ruiz Fernando
Division of Rheumatology Department of Medicine, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ 08903-0019, USA.
Expert Opin Pharmacother. 2009 Jun;10(8):1319-28. doi: 10.1517/14656560902950742.
There has been an increase in the incidence and prevalence of gout in the past several decades. A distinction needs to be made between the treatment of gout as an acute inflammatory disease and the lowering of the serum urate (SU) levels into a normal range. Treating acute gout attacks alone is not sufficient to prevent the disease from progressing. When treating gout one needs to treat acute attacks, and lower excess stores of uric acid to achieve dissolution of monosodium urate crystals through a long-term reduction of SU concentrations far beyond the threshold for saturation of urate and provide prophylaxis to prevent acute flares. The options available for the treatment of acute gout are NSAIDs, colchicine, corticosteroids, adrenocorticotropic hormone (ACTH) and intra-articular corticosteroids. The most important determinant of therapeutic success is not which anti-inflammatory agent is chosen, but rather how soon therapy is initiated and that the dose be appropriate. Prophylaxis should be considered an adjunct, rather than an alternative, to long-term urate-lowering therapy. For purposes of maintaining patient adherence to urate-lowering therapy, there is interest in improving prophylaxis of such treatment-induced attacks. The optimal agent, dose and duration for gout prophylaxis are unknown and require further investigation. The importance of long-term management of gout is the reduction and maintenance of SU in a goal range, usually defined as less than 6.0 mg/dL. Allopurinol and benzbromarone remain the cornerstone drugs for reducing SU levels lower than the saturation threshold to dissolve urate deposits effectively. Febuxostat and pegloticase help to optimize control of SU levels, especially in those patients with the most severe gout. Other agents, such as fenofibrate and losartan may be helpful as adjuvant drugs. Treatment for gout has advanced little in the last 40 years, until recently. The recent development of new therapeutic options promises to provide much needed alternatives for the many patients with gout who are intolerant of or refractory to available therapies. It is important to note that inappropriate use of medications as opposed to an apparent refractoriness to available therapies is not uncommon.
在过去几十年中,痛风的发病率和患病率均有所上升。需要区分将痛风作为一种急性炎症性疾病进行的治疗与将血清尿酸(SU)水平降至正常范围这两者。仅治疗急性痛风发作不足以防止疾病进展。治疗痛风时,需要治疗急性发作,降低过量的尿酸储存,通过长期将SU浓度降至远低于尿酸饱和阈值来实现尿酸单钠晶体的溶解,并提供预防措施以防止急性发作。治疗急性痛风的可用药物有非甾体抗炎药、秋水仙碱、皮质类固醇、促肾上腺皮质激素(ACTH)和关节内注射皮质类固醇。治疗成功的最重要决定因素不是选择哪种抗炎药,而是治疗开始的速度有多快以及剂量是否合适。预防应被视为长期降低尿酸治疗的辅助手段,而非替代手段。为了使患者坚持降低尿酸治疗,人们对改善对此类治疗引起的发作的预防很感兴趣。痛风预防的最佳药物、剂量和持续时间尚不清楚,需要进一步研究。痛风长期管理的重要性在于将SU降低并维持在目标范围内,通常定义为低于6.0mg/dL。别嘌醇和苯溴马隆仍然是将SU水平降低至低于饱和阈值以有效溶解尿酸盐沉积物的基石药物。非布司他和聚乙二醇化尿酸酶有助于优化SU水平的控制,尤其是在那些痛风最严重的患者中。其他药物,如非诺贝特和氯沙坦,作为辅助药物可能会有帮助。直到最近,痛风治疗在过去40年里进展甚微。新治疗选择的近期发展有望为许多对现有疗法不耐受或难治的痛风患者提供急需的替代方案。需要注意的是,与对现有疗法明显难治相反,不适当用药的情况并不少见。