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作 者:王洪涛[1] 杨威[1] 盛秋菊[1] 王韫秀[1] 刘卓刚[1] 李迎春[1] 廖爱军[1]
机构地区:[1]中国医科大学附属盛京医院血液病治疗中心,沈阳110022
出 处:《药物不良反应杂志》2008年第6期432-433,共2页Adverse Drug Reactions Journal
基 金:"辽宁省临床医学重点专科基金"资助项目[辽卫科教函(2007)1号]
摘 要:2例患者大剂量甲氨蝶呤(MTX)化疗导致急性肾衰竭。第1例为53岁女性,因非霍奇金淋巴瘤给予大剂量MTX化疗:先用MTX500mg0.5h时内静脉滴注、3500mg24h内泵入,然后用亚叶酸钙进行解救,首次剂量为30mg/m2,以后15mg/m2,每隔6h肌内注射1次,解救8次。患者无慢性肾脏病史,化疗前肾功能正常(SCr97.1μmol/L,BUN4.78mmol/L)。化疗后第4天,出现颜面及双手轻度水肿,尿量减少,SCr升至151μmol/L。给予甲泼尼龙、呋塞米和碳酸钙-维生素D3对症治疗,并碱化尿液,监测肾功能(SCr最高达275μmol/L)。化疗后第13天肾功能恢复至正常(SCr96μmol/L)。第2例为29岁男性,因急性淋巴细胞白血病给予大剂量MTX化疗:MTX500mg0.5h内静脉滴注、4500mg24h内泵入,解救方案同例1。患者无慢性肾脏病史,化疗前肾功能正常(SCr86.9μmol/L,BUN5.35mmol/L)。化疗后第3天出现全身水肿、尿量减少,SCr升至235μmol/L(最高达360μmol/L)。给予对症治疗,同例1。化疗后第30天肾功能恢复至正常(SCr89μmol/L)。Two atients receiving high-dose methotrexate chemotherapy developed acute renal failure. Patient 1, a 53-year-old woman with non-Hodgkin lymphoma, received high-dose methotrexate chemotherapy. Initially she was infused with methotrexate 500 mg intravenously within half an hour, followed by 3500 mg via infusion pump within 24 hours. Then calcium folinate was given for rescue. The first dose of calcium folinate was 30 mg/m^2, followed by 15 mg/m^2 intramuscularly once every 6 hours for 8 doses. The patient had no history of chronic renal disease. Her renal function was normal before chemotherapy ( SCr 97.1 μmol/L, BUN 4.78 mmol/L). On day 4 after chemotherapy, she developed mild edema of the face and both hands, and oliguria; her SCr increased to 151 μmol/L. Mcthylprednisolone, furosemide, and calcium carbonate and vitamin D3 were given; her urinary alkalinisation and monitoring of renal function were performed (a peak SCr level of 275 μmol/L). On day 13 after chemotherapy, her renal function returned to within normal range ( SCr 96 μmo]/L). Patient 2, a 29-year-old man with acute lymphoblastic leukemia, received high-dose methotrexate chemotherapy. Initially he was infused with methotrexate 500 mg intravenously within half an hour, followed by 4500 mg via infusion pump within 24 hours. The regimen of rescue was the same as patient I. The patient had no history of chronic renal disease. His renal function was normal before chemotherapy ( SCr 86.9 μmoL/L, BUN 5.35 μmol/L). On day 3 after chemotherapy, he developed generalized edema and oliguria; his SCr increased to 235 ~mol/L (peak level 360 μmol/L). The symptomatic treatment was given (the regimen was the same as patient 1 ). On day 30 after chemotherapy, his renal function returned to within normal range( SCr 89 μmol/L).
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