Puig J G, Mateos F, Buño A, Ortega R, Rodriguez F, Dal-Ré R
Division of Internal Medicine, La Paz University Hospital, Madrid, Spain.
J Hypertens. 1999 Jul;17(7):1033-9. doi: 10.1097/00004872-199917070-00021.
The influence of angiotensin II AT-1 receptor antagonists on uric acid metabolism, and the potential differences among them with regard to this effect, remains to be precisely established. This study was designed to compare the effects of losartan and eprosartan on uric acid metabolism in patients with mild to moderate essential hypertension.
Randomized, double-blind, parallel-group study in hypertensive patients.
Outpatient clinic.
Following a 2- to 3-week single-blind placebo run-in period, 60 patients with sitting diastolic blood pressure > or = 95 and < or = 114 mmHg were randomized. Fifty-eight patients completed the study.
Patients were randomized to receive losartan 50 mg or eprosartan 600 mg once daily for 4 weeks.
The primary endpoint was the change in the ratio of urinary uric acid/creatinine in the period 0-4 h of a 24 h urine collection after 4 weeks of treatment. Secondary endpoints included 24 h urinary uric acid excretion, as well as serum urate and anti-hypertensive efficacy.
Mean urinary uric acid/creatinine changes from baseline were 0.14 (day 1) and 0.11 (week 4) for losartan and -0.04 for eprosartan (at both day 1 and week 4; P < 0.01 between groups at both time-points). The mean increase in 24 h urinary uric acid excretion with losartan was 0.7 mmol/24 h (25% increase from baseline) at both day 1 and week 4. No significant difference was observed in the change of serum urate levels versus baseline between both treatment groups after 4 weeks (- 23.4 and - 19.5 micromol/l for losartan and eprosartan, respectively). Patients with hyperuricaemia in both treatment groups showed similar modifications of uric acid metabolism compared with non-hyperuricaemic subjects. Blood pressure control (sitting diastolic blood pressure < 90 mmHg or < 100 mmHg with a decrease of at least 10 mmHg from baseline) was achieved in 22 patients (73%) with eprosartan and in 16 (53%) with losartan.
Losartan increased uric acid excretion in hypertensive patients, whilst eprosartan did not Neither AT-1 receptor antagonist substantially modified serum urate concentrations.
血管紧张素II AT-1受体拮抗剂对尿酸代谢的影响以及它们在此效应方面的潜在差异仍有待确切确定。本研究旨在比较氯沙坦和依普罗沙坦对轻至中度原发性高血压患者尿酸代谢的影响。
对高血压患者进行随机、双盲、平行组研究。
门诊诊所。
经过2至3周的单盲安慰剂导入期后,60例坐位舒张压≥95且≤114 mmHg的患者被随机分组。58例患者完成了研究。
患者被随机分组,每天一次接受50 mg氯沙坦或600 mg依普罗沙坦治疗4周。
主要终点是治疗4周后24小时尿液收集0至4小时期间尿尿酸/肌酐比值的变化。次要终点包括24小时尿尿酸排泄、血清尿酸盐以及降压疗效。
氯沙坦组尿尿酸/肌酐从基线的平均变化在第1天为0.14,第4周为0.11;依普罗沙坦组在第1天和第4周均为-0.04(两组在两个时间点均P<0.01)。氯沙坦组在第1天和第4周24小时尿尿酸排泄的平均增加量均为0.7 mmol/24小时(较基线增加25%)。4周后,两个治疗组血清尿酸盐水平相对于基线的变化无显著差异(氯沙坦组和依普罗沙坦组分别为-23.4和-19.5 μmol/L)。与非高尿酸血症受试者相比,两个治疗组中的高尿酸血症患者尿酸代谢的变化相似。依普罗沙坦组22例患者(73%)和氯沙坦组16例患者(53%)实现了血压控制(坐位舒张压<90 mmHg或<100 mmHg且较基线至少降低10 mmHg)。
氯沙坦增加高血压患者的尿酸排泄,而依普罗沙坦则无此作用。两种AT-1受体拮抗剂均未显著改变血清尿酸盐浓度。