Hwang T L, Yung W K, Lee Y Y, Borit A, Fields W S
J Neurooncol. 1986;3(4):335-9. doi: 10.1007/BF00165582.
Two patients with acute myelomonocytic leukemia in central nervous system relapse developed clinical signs and computerized tomographic evidence of leukoencephalopathy five to seven days after intravenous high dose Ara-C therapy. The first patient had received 30 gm of intravenous Ara-C with cranial irradiation (1680 rad in 2 fractions) and intrathecal Ara-C (100 mg X twice) for an intracerebral chloroma and leptomeningeal leukemia. In this patient the leukoencephatlopathy was probably a result of a synergistic effect of the concomitant triple therapy. The second patient had received intrathecal administration of Ara-C and methotrexate for five and one-half months prior to intravenous Ara-C therapy. He developed altered mental status after 24 gm of intravenous Ara-C infusion. CT scan showed changes in the white matter compatible with leukoencephalopathy. In this patient the intravenous Ara-C probably was the precipitating factor of the development of leukoencephalopathy. The possible mechanism of the Ara-C induced leukoencephalopathy is discussed.
两名急性粒单核细胞白血病中枢神经系统复发患者在静脉高剂量阿糖胞苷治疗后5至7天出现了白质脑病的临床症状和计算机断层扫描证据。第一名患者因脑内绿色瘤和软脑膜白血病接受了30克静脉阿糖胞苷治疗,并联合颅脑照射(分2次共1680拉德)及鞘内注射阿糖胞苷(100毫克,2次)。该患者的白质脑病可能是三联疗法协同作用的结果。第二名患者在静脉阿糖胞苷治疗前五个半月接受了鞘内注射阿糖胞苷和甲氨蝶呤。在输注24克静脉阿糖胞苷后,他出现了精神状态改变。CT扫描显示白质改变符合白质脑病表现。在该患者中,静脉阿糖胞苷可能是白质脑病发生的诱发因素。本文讨论了阿糖胞苷诱导白质脑病的可能机制。