Treatment of chronic gout. Can we determine when urate stores are depleted enough to prevent attacks of gout?
Treatment of chronic gout. Can we determine when urate stores are depleted enough to prevent attacks of gout?
复制标题
治疗慢性痛风。
DOI：
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发表时间：
2001
影响因子：
3.9
通讯作者：
H. Schumacher
中科院分区：
文献类型：
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作者：
J. Li;G. Clayburne;M. Sieck;Anna Beutler;Marina Rull;E. Eisner;H. Schumacher
目的
确定血清尿酸（SUA）浓度低于6 mg/dl或持续时间较长的SUA降低是否会导致膝关节尿酸盐结晶耗尽，并防止痛风进一步发作。
方法
10年前，费城退伍军人医疗中心开始了一项前瞻性研究，试图将晶体证实的痛风患者的SUA水平维持在< 6.0 mg/dl。我们召回了1999年期间所有可用的57名患者。患者分为2组：A组，SUA仍> 6 mg/dl，B组，SUA ≤ 6 mg/dl。要求所有无症状B组患者和许多A组患者进行膝关节穿刺。通过偏振光显微镜检查吸出物以鉴定晶体。
结果
两组之间在年龄、性别、痛风持续时间或血清肌酐方面没有差异。A组（n = 38）近年来平均痛风发作6次，痛风石发作次数最多。在该组同意膝关节抽吸的16名患者中，14名患者发现了尿酸盐（MSU）晶体，尽管当时他们没有症状。19名患者（B组）能够维持血清尿酸水平≤ 6 mg/dl> 12个月。近一半的人2年或2年以上没有痛风发作，整个组在过去一年中平均发作1次。在过去的一年里，三名发现痛风石的患者没有痛风的严重发作。对16例无症状患者进行膝关节穿刺。7例（44%）患者的膝关节中仍存在MSU晶体。预防性服用秋水仙碱的患者与停药数年的患者在滑液特征方面没有差异，尽管继续服用秋水仙碱的患者发作频率较低。
结论
当SUA水平保持在≤ 6 mg/dl数年时，大多数患者能够耗尽膝关节液中的尿酸盐晶体储存。在某些患者中持续存在的机制以及这种晶体是否具有临床意义尚不清楚。慢性痛风患者需要将血清尿酸盐浓度保持在较低水平，以防止进一步发作。
OBJECTIVE
To determine if lowering of serum uric acid (SUA) concentrations below 6 mg/dl or longer duration of lowered SUA will result in depletion of urate crystals from the knee joints and prevent further attacks of gout.
METHODS
A prospective study was initiated 10 years ago at Philadelphia VA Medical Center to attempt to maintain SUA levels of patients with crystal proven gout at < 6.0 mg/dl. We recalled all 57 patients who were available during 1999. Patients were divided into 2 groups: Group A, with SUA still > 6 mg/dl, and Group B, with SUA < or = 6 mg/dl. A knee joint aspirate was requested from all asymptomatic Group B patients and many in Group A. Aspirates were examined by polarized light microscopy for identification of crystals.
RESULTS
There were no differences between the groups in age, sex, duration of gout, or serum creatinine. Group A (n = 38) had a mean of 6 attacks of gout for the recent year, those with tophi having the most frequent attacks. Among the 16 patients in this group who agreed to knee aspiration, monosodium urate (MSU) crystals were found in 14, although they were asymptomatic at the time. Nineteen patients (Group B) were able to maintain serum urate levels < or = 6 mg/dl for > 12 months. Nearly half of them had no attack of gout for 2 or more years, with a mean of 1 attack in the last year for the whole group. Three patients in whom tophi were found did not have major flares of gout within the past year. Knee joint aspiration was done on 16 asymptomatic patients. Seven (44%) still had MSU crystals present in their knees. Patients in this group who were taking prophylactic colchicine did not differ with respect to the character of synovial fluid from those who had discontinued it for up to several years, although the frequency of attacks was less in those who continued colchicine.
CONCLUSION
A majority of patients were able to deplete urate crystal stores in their knee joint fluids when their SUA levels were kept to < or = 6 mg/dl for several years. The mechanisms for persistence in some patients, and whether such crystals have clinical implications, are not known. Patients with chronic gout need serum urate concentrations to be kept low to prevent further attacks.