The Johns Hopkins University School of Medicine, Division of General Internal Medicine, The Johns Hopkins Bloomberg School of Public Health, and The Welch Center for Prevention, Epidemiology and Clinical Research, Baltimore, Maryand, USA.
Am J Hypertens. 2017 Sep 1;30(9):871-875. doi: 10.1093/ajh/hpx113.
There is little evidence guiding selection of nondiuretic, antihypertensive agents with a goal of lowering uric acid (SUA) and minimizing gout risk.
In the African American Study of Kidney Disease and Hypertension (AASK) trial, African Americans with chronic kidney disease were randomly assigned to metoprolol (a beta-blocker), ramipril (an angiotensin-converting enzyme inhibitors [ACEi]), or amlodipine (a dihydropyridine calcium-channel blocker). SUA was measured at baseline and 12 months. Gout-related hospitalizations were based on ICD9 codes. Gout-related medication use (GRMs) was based on active prescriptions of allopurinol, colchicine, or probenecid during the baseline visit of the AASK cohort phase. We examined the effect of drug assignment on 12-month SUA (linear regression), gout-related hospitalization (Cox regression), and GRM (logistic regression).
Of the 630 participants, 40% were female with a mean age of 55 years (SD, 10), mean SUA of 8.2 mg/dl (2.0), and mean serum creatinine of 1.8 mg/dl (0.6). After 12 months, metoprolol increased SUA by 0.3 mg/dl, while ramipril or amlodipine had no effect on SUA. Compared to ramipril, metoprolol significantly increased 12-month SUA (0.40; 0.10, 0.70 mg/dl; P = 0.009), nonsignificantly increased risk of gout-related hospitalization (hazard ratio: 3.87; 0.82, 18.26; P = 0.09), and significantly increased the odds of GRM (odds ratio: 1.62; 1.03, 2.54; P = 0.04). While metoprolol was associated with a higher 12-month SUA compared with amlodipine (0.57; 0.18, 0.95; P = 0.004), there was no difference in gout-related hospitalizations or GRM.
Metoprolol increased SUA and GRM in African American adults. Health professionals treating patients with kidney disease at risk for gout should avoid metoprolol and possibly consider an ACEi.
Trial Number NCT00582777.
目前针对降低尿酸(SUA)和最小化痛风风险的非利尿剂降压药物选择,证据很少。
在非裔美国人肾脏病和高血压研究(AASK)试验中,患有慢性肾脏病的非裔美国人被随机分配至美托洛尔(β受体阻滞剂)、雷米普利(血管紧张素转换酶抑制剂[ACEi])或氨氯地平(二氢吡啶钙通道阻滞剂)。在基线和 12 个月时测量 SUA。痛风相关住院治疗基于 ICD9 编码。根据 AASK 队列阶段基线就诊时所有别嘌醇、秋水仙碱或丙磺舒的有效处方,确定痛风相关药物使用(GRM)。我们研究了药物分配对 12 个月 SUA(线性回归)、痛风相关住院治疗(Cox 回归)和 GRM(逻辑回归)的影响。
在 630 名参与者中,40%为女性,平均年龄 55 岁(标准差 10),平均 SUA 为 8.2mg/dl(2.0),平均血清肌酐为 1.8mg/dl(0.6)。12 个月后,美托洛尔使 SUA 增加了 0.3mg/dl,而雷米普利或氨氯地平对 SUA 无影响。与雷米普利相比,美托洛尔显著增加了 12 个月 SUA(0.40;0.10,0.70mg/dl;P=0.009),痛风相关住院治疗风险无显著增加(风险比:3.87;0.82,18.26;P=0.09),GRM 的几率显著增加(比值比:1.62;1.03,2.54;P=0.04)。虽然与氨氯地平相比,美托洛尔与 12 个月时更高的 SUA 相关(0.57;0.18,0.95;P=0.004),但痛风相关住院治疗或 GRM 无差异。
美托洛尔增加了非裔美国成年人的 SUA 和 GRM。治疗有痛风风险的肾脏病患者的医疗保健专业人员应避免使用美托洛尔,并可能考虑使用 ACEi。
试验编号 NCT00582777。