Carboxypeptidase-G2, thymidine, and leucovorin rescue in cancer patients with methotrexate-induced renal dysfunction.
作者： B C Widemann , F M Balis , R F Murphy , J M Sorensen , M J Montello
DOI: 10.1200/JCO.1997.15.5.2125
关键词: Toxicity 、 Metabolite 、 Chemotherapy 、 Nephrotoxicity 、 Medicine 、 Internal medicine 、 Carboxypeptidase-G2 、 Glutamate carboxypeptidase 、 Glucarpidase 、 Pharmacology 、 Methotrexate 、 Endocrinology
摘要: PURPOSEMethotrexate nephrotoxicity can lead to delayed methotrexate elimination and the development of life-threatening toxicity, which may not be preventable with standard rescue agent leucovorin. In preclinical studies, we previously demonstrated that carboxypetidase-G2 (CPDG2) rapidly hydrolyzes nontoxic metabolites. A protocol for compassionate use CPDG2 in patients who develop while receiving high-dose was therefore developed. The pharmacologic clinical outcome administered thymidine leucovorin 20 is presented here.METHODSPatients methotrexate-induced renal dysfunction received one three doses CPDG2, 50 U/kg body weight intravenously (i.v.), 8 g/m2/d by continuous i.v. infusion, pharmacokinetically guided rescue. Plasma concentrations its inactive metabolite 4-deoxy-4-amino-N10-methylpteroic acid (DAMPA) were measured before aft...
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