Caravaca F, López-Minguez J R, Arrobas M, Cubero J, Pizarro J L, Cid M C, Sanchez-Casado E, Miranda M P
Servicio Nefrología, Hospital Infanta Cristina, Extremadura University, Badajoz, Spain.
Nephrol Dial Transplant. 1995;10(9):1720-4.
In a retrospective study, antiplatelet therapy has been shown to be associated with a decreased incidence of erythropoietin-induced hypertension. In order to ascertain the role of antiplatelet drugs in the haemodynamic response to the correction of anaemia by rHuEpo, 18 patients on chronic haemodialysis who started rHuEpo therapy were prospectively studied.
The subjects were randomly assigned to receive or not, one of the following antiplatelet drugs: ditazole (3 patients), ticlopidine (3 patients) or aspirin plus dipyridamole (3 patients). Cardiac index (CI) by echo-Doppler, total peripheral resistance (TPR) and mean arterial pressure (MAP) were determined at baseline 10 and 20 weeks following the initiation of rHuEpo therapy. rHuEpo therapy was administered subcutaneously at the same dose (40 U/kg thrice weekly) during the first 10 weeks. Ten uraemic patients on haemodialysis who had never received rHuEpo therapy served as the control group.
One patient in the group without antiplatelet drugs discontinued the study due to the development of severe hypertension after 12 weeks on rHuEpo therapy. There were no significant differences in the haemodynamic parameters at baseline. At 10 weeks, MAP was higher in patients without than with antiplatelet drugs or controls untreated with rHuEpo (128.5 +/- 28 versus 100.6 +/- 13.5 versus 98.7 +/- 14 mmHg respectively, P = 0.0047), TPR was also higher in patients without antiplatelet drugs than in the 2 other groups (1919 +/- 433 versus 1576 +/- 359 versus 1418 +/- 324 din.seg.cm-5m2 respectively, P = 0.0231), but CI did not differ among the three groups. At 20 weeks, MAP was still higher in patients without antiplatelet drugs than in patients with antiplatelet drugs or controls not on rHuEpo therapy respectively (112.9 +/- 24.6 versus 91.0 +/- 9.0 versus 101.7 +/- 14.1 mmHg respectively, P = 0.075), but at this stage TPR and Cl did not differ among the three groups.
These data reinforce the previous observation that antiplatelet therapy may prevent the development of rHuEpo-induced hypertension.
在一项回顾性研究中,抗血小板治疗已被证明与促红细胞生成素诱导的高血压发病率降低有关。为了确定抗血小板药物在重组人促红细胞生成素(rHuEpo)纠正贫血的血液动力学反应中的作用,对18例开始接受rHuEpo治疗的慢性血液透析患者进行了前瞻性研究。
将受试者随机分为接受或不接受以下抗血小板药物之一:双嘧达莫(3例患者)、噻氯匹定(3例患者)或阿司匹林加双嘧达莫(3例患者)。在开始rHuEpo治疗后的基线、10周和20周时,通过超声多普勒测定心脏指数(CI)、总外周阻力(TPR)和平均动脉压(MAP)。在最初的10周内,以相同剂量(40 U/kg,每周三次)皮下注射rHuEpo治疗。10例从未接受过rHuEpo治疗的尿毒症血液透析患者作为对照组。
未使用抗血小板药物组的1例患者在接受rHuEpo治疗12周后因发生严重高血压而退出研究。基线时血液动力学参数无显著差异。在10周时,未使用抗血小板药物的患者的MAP高于使用抗血小板药物的患者或未接受rHuEpo治疗的对照组(分别为128.5±28、100.6±13.5和98.7±14 mmHg,P = 0.0047),未使用抗血小板药物的患者的TPR也高于其他两组(分别为1919±433、1576±359和1418±324 dyn·sec/cm-5·m2,P = 0.0231),但三组之间的CI无差异。在20周时,未使用抗血小板药物的患者的MAP仍高于使用抗血小板药物的患者或未接受rHuEpo治疗的对照组(分别为112.9±24.6、91.0±9.0和101.7±14.1 mmHg,P = 0.075),但在此阶段,三组之间的TPR和CI无差异。
这些数据强化了先前的观察结果,即抗血小板治疗可能预防rHuEpo诱导的高血压的发生。