Lin A C, Goldwasser E, Bernard E M, Chapman S W
Department of Medicine, University of Mississippi Medical Center, Jackson 39216-4505.
J Infect Dis. 1990 Feb;161(2):348-51. doi: 10.1093/infdis/161.2.348.
Amphotericin B causes a normochromic, normocytic anemia thought to be mediated by direct marrow toxicity or suppression of erythropoietin production. Serial hemoglobin, hematocrit, amphotericin B, and erythropoietin levels were determined before, during, and after completion of amphotericin B therapy for three patients without significant renal disease or active hematologic malignancy. Patients with systemic fungal diseases treated with itraconazole served as controls. Serum erythropoietin levels were determined by radioimmunoassay and amphotericin B by high-performance liquid chromatography. Despite anemia in all amphotericin B-treated patients, erythropoietin levels declined or remained relatively constant during therapy while erythropoietin levels in controls were appropriate for the degree of anemia. Within 2 weeks of completion of amphotericin B treatment, two patients had increasing erythropoietin levels in response to anemia. Amphotericin B appears to suppress but not abolish the erythropoietin response to anemia; this effect disappears quickly after discontinuation of the drug.
两性霉素B可导致正色素正细胞性贫血,推测其由直接的骨髓毒性或促红细胞生成素生成受抑制介导。在3例无严重肾脏疾病或活动性血液系统恶性肿瘤的患者接受两性霉素B治疗前、治疗期间及治疗结束后,测定了系列血红蛋白、血细胞比容、两性霉素B及促红细胞生成素水平。接受伊曲康唑治疗的系统性真菌病患者作为对照。血清促红细胞生成素水平通过放射免疫测定法测定,两性霉素B通过高效液相色谱法测定。尽管所有接受两性霉素B治疗的患者均出现贫血,但治疗期间促红细胞生成素水平下降或保持相对稳定,而对照组的促红细胞生成素水平与贫血程度相符。两性霉素B治疗结束后2周内,2例患者因贫血促红细胞生成素水平升高。两性霉素B似乎抑制但并未消除对贫血的促红细胞生成素反应;停药后这种效应很快消失。