Mazzali M, Filho G A
Internal Medicine Department, Faculty of Medical Sciences, State University of Campinas, São Paulo, Brazil.
Transplantation. 1998 Jun 15;65(11):1461-4. doi: 10.1097/00007890-199806150-00009.
Posttransplant polycythemia (PTP) affects 6-30% of renal transplant recipients and can result in thromboembolic disease. The pathogenesis of PTP remains unknown and may be multifactorial. Although phlebotomy has previously been the treatment for PTP, drugs such as adenosine receptor antagonists or angiotensin-converting enzyme inhibitors can be used to control PTP.
The authors performed a prospective study of two different drugs to treat PTP: aminophylline and enalapril. Twenty-seven patients with PTP lasting more than 6 months were evaluated. During phase 1, aminophylline was compared with enalapril. The patients sequentially received aminophylline and enalapril during 12-week periods, intercalated by 12-week periods of no drugs. During phase 2, enalapril was administered for 12 weeks.
From January 1984 to December 1993, 110 of 333 patients with PTP lasting more than 6 months (33%) developed polycythemia, and 27 patients were included in the present study. In phase 1, aminophylline had no effect on PTP. Enalapril promoted an erythropoiesis inhibition, characterized by a decrease in hematocrit and an increase in iron stores and ferritin levels. After withdrawal of enalapril, the hematocrit increased and the iron stores decreased. In phase 2, there was a progressive reduction in hematocrit after the 4th week of therapy. The lowest hematocrit was observed in the 12th week and then enalapril was stopped, leading to a subsequent rise in hematocrit. Erythropoietin levels and renal function remained constant during all periods of both phases of the study.
The use of adenosine antagonists was ineffective to treat PTP in our series. However, treatment with enalapril promoted an erythropoiesis inhibition, demonstrated by a reduction in hematocrit, hemoglobin, red blood cell count, and reticulocyte count, associated with an increase in iron stores. This response occurred independently from erythropoietin levels or hemodynamic graft changes.
移植后红细胞增多症（PTP）影响6% - 30%的肾移植受者，并可导致血栓栓塞性疾病。PTP的发病机制尚不清楚，可能是多因素的。尽管放血疗法以前一直是治疗PTP的方法，但腺苷受体拮抗剂或血管紧张素转换酶抑制剂等药物也可用于控制PTP。
作者对两种治疗PTP的不同药物进行了前瞻性研究：氨茶碱和依那普利。对27例持续超过6个月的PTP患者进行了评估。在第1阶段，将氨茶碱与依那普利进行比较。患者在12周期间依次接受氨茶碱和依那普利治疗，中间穿插12周的无药物治疗期。在第2阶段，给予依那普利治疗12周。
从1984年1月至1993年12月，333例持续超过6个月的PTP患者中有110例（33%）发生红细胞增多症，本研究纳入了27例患者。在第1阶段，氨茶碱对PTP无效。依那普利促进红细胞生成抑制，表现为血细胞比容降低、铁储备增加和铁蛋白水平升高。停用依那普利后，血细胞比容升高，铁储备减少。在第2阶段，治疗第4周后血细胞比容逐渐降低。在第12周观察到最低血细胞比容，然后停用依那普利，导致随后血细胞比容升高。在研究的两个阶段的所有时期，促红细胞生成素水平和肾功能均保持恒定。
在我们的系列研究中，使用腺苷拮抗剂治疗PTP无效。然而，依那普利治疗促进了红细胞生成抑制，表现为血细胞比容、血红蛋白、红细胞计数和网织红细胞计数降低，同时铁储备增加。这种反应独立于促红细胞生成素水平或移植肾血流动力学变化而发生。
