Thiazide diuretics and the initiation of anti-gout therapy
Thiazide diuretics and the initiation of anti-gout therapy
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DOI：
10.1016/s0895-4356(97)00101-7
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发表时间：
1997-08-01
影响因子：
7.2
通讯作者：
Avorn, J
中科院分区：
文献类型：
--
作者：
Gurwitz, JH;Kalish, SC;Avorn, J
虽然生理学和流行病学证据将利尿剂治疗与高尿酸血症联系起来，但以前没有研究量化服用噻嗪类利尿剂的老年患者开始高尿酸血症或痛风治疗的风险。我们对新泽西医疗补助计划的9249名65岁或以上的参与者进行了一项回顾性队列研究，这些参与者从1981年11月至1989年2月新开始使用抗高血压药物，并且在前一年期间没有使用过抗痛风治疗（别嘌呤醇、秋水仙碱或尿酸排泄剂）。我们使用考克斯比例风险分析来确定使用各种抗高血压治疗方案的患者相对于未使用抗高血压药物的患者开始痛风治疗的风险。患者随访时间延长至2年。在整个随访期间，根据以下类别描述抗高血压药物暴露的特征：单独使用噻嗪类利尿剂治疗;非噻嗪类抗高血压药物治疗;噻嗪类利尿剂治疗联合任何非噻嗪类抗高血压药物治疗;以及未使用抗高血压药物。将抗高血压药物暴露作为随时间变化的协变量输入模型。对年龄、性别、种族、疗养院居住地、处方数量、医生用药强度、住院史和开始抗高血压治疗的年份进行了校正。开始抗痛风治疗的校正相对风险为：单独非噻嗪类降压治疗为1.00（95% CI，0.65 - 1.53），噻嗪类利尿剂治疗为1.99（95% CI，1.21 - 3.26），噻嗪类利尿剂治疗联合任何非噻嗪类药物为2.29（95% CI，1.55 - 3.37）。噻嗪类药物剂量大于或等于25 mg/天（氢氯噻嗪当量）时，抗痛风治疗的风险显著增加;较低剂量时未观察到风险显著增加。我们的结论是，使用噻嗪类利尿剂的剂量为25毫克/天或更高的是与显着增加的风险开始抗痛风治疗。这种治疗可能反映了利尿剂引起的高尿酸血症的临床后遗症或无症状高尿酸血症的治疗不当。(C)1997年爱思唯尔科学公司
While physiologic and epidemiologic evidence link diuretic therapy with hyperuricemia, no previous study has quantified the risk for initiation of treatment specific for hyperuricemia or gout among elderly patients taking thiazide diuretics. We performed a retrospective cohort study of 9249 enrollees aged 65 or older in the New Jersey Medicaid program who were newly started on an antihypertensive medication from November 1981 through February 1989 and who had no prior use of anti-gout therapy (allopurinol, colchicine, or a uricosuric) during the preceding one-year period. We used Cox proportional hazards analysis to determine the risk for the initiation of and gout therapy in patients using various antihypertensive treatment regimens relative to no antihypertensive exposure. Patient follow-up extended for up to two years. Antihypertensive exposure was characterized over the entire period of follow-up according to the following categories: thiazide diuretic therapy alone; non-thiazide antihypertensive therapy; thiazide diuretic therapy in combination with any non-thiazide antihypertensive agent(s); and no antihypertensive use. Antihypertensive exposure was entered into the model as a time-varying covariate. Estimates of risk were adjusted for age, sex, race, nursing home residence, number of prescriptions filled, intensity of physician use, hospitalization history, and year of antihypertensive treatment initiation. The adjusted relative risk for the initiation of anti-gout therapy was 1.00 (95% CI, 0.65-1.53) for non-thiazide antihypertensive therapy alone, 1.99 (95% CI, 1.21-3.26) for thiazide diuretic therapy, and 2.29 (95% CI, 1.55-3.37) for thiazide diuretic therapy in combination with any non-thiazide agent(s). Risk for antigout therapy was significantly increased for thiazide doses of greater than or equal to 25 mg/day (in hydrochlorothiazide equivalents); no significant increase in risk was seen for lower doses. We conclude that use of thiazide diuretics in doses of 25 mg/day or higher is associated with a significantly increased risk for initiation of anti-gout therapy. Such treatment may reflect the occurrence of clinical sequelae of diuretic-induced hyperuricemia or the inappropriate treatment of asymptomatic hyperuricemia. (C) 1997 Elsevier Science Inc.