Donnelly S M, Smith E K
Department of Medicine, Faculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada.
Am J Kidney Dis. 1990 Nov;16(5):487-90. doi: 10.1016/s0272-6386(12)80065-5.
The quantitative variation among patients in their response to erythropoietin can be explained, in part, by factors that can independently cause anemia in patients with end-stage renal disease. Aluminum can blunt the effect of erythropoietin, in part by interfering with iron bioavailability. This inhibitory effect cannot be completely overcome by aggressive ferrotherapy, but can be reversed with aluminum chelation therapy. A patient is described who developed hematological evidence of aluminum excess after being treated with erythropoietin. The biochemical evidence of functional iron deficiency and the response to aluminum chelation therapy support the hypothesis that the inhibitory effect of aluminum on erythropoiesis is mediated by the interference of aluminum with the bioavailability of iron.
患者对促红细胞生成素反应的定量差异，部分可由终末期肾病患者中能独立导致贫血的因素来解释。铝可削弱促红细胞生成素的作用，部分原因是其干扰铁的生物利用度。这种抑制作用不能通过积极的铁疗法完全克服，但可通过铝螯合疗法逆转。本文描述了一名患者，在用促红细胞生成素治疗后出现了铝过量的血液学证据。功能性缺铁的生化证据以及对铝螯合疗法的反应支持了这样一种假说，即铝对红细胞生成的抑制作用是由铝干扰铁的生物利用度介导的。
