Guidelines for Complications of Cancer Treatment Vol VIII Part B

metabolism for activity, cyclophosphamide is an uncommonhepatic toxin, and only a few reports of elevated hepaticenzymes are attributed to the drug (3). Ifosfamide is analkylator and elevations of hepatic enzymes have rarely beenreported during therapy. Rodriquez et al. showed that 7 of 32patients who were being treated with ifosfamide in doses of600 to 1,200 mg per m 2 developed elevations of thetransaminases and these were transient (4).Melphalan is rapidly hydrolyzed in plasma, and approximately15% is excreted unchanged in the urine. At usual doses, it isnot associated with hepatotoxicity, but it produce transientabnormalities in liver function tests at the high doses used inhematopoietic stem cell transplantation (HSCT) (5).Busulfan after administration is rapidly cleared from the blood.Hepatic metabolism is apparently not important. In standarddoses, busulfan rarely causes hepatic dysfunction but has beenimplicated to cholestatic hepatitis (6). As a group, the alkylatingagents are seldom implicated as hepatotoxins and can usuallybe given in the face of altered liver function with relative safety.The possible exception to this is cyclophosphamide, whichrequires adequate liver function for activation to its activemetabolites (7). Antimetabolites :Most commonly used antimetabolites are cytosine arabinoside(ara-C), 5-fluorouracil (5-FU), 6- mercaptopurine (6-MP),azathioprine (AZ), 6-thioguanine, fludarabine, pentostatin,gemcitabine and MTX.Ara-C induced liver toxicity includes increased SGOT/PT ,cholestatic jaundice and intrahepatic cholestasis and thisusually reversible (8).Fludarabine is a purine antimetabolite .Reversible elevation of the serum transaminases to two to threetimes normal has been described (9).5 Flurouracil commonly causes steatosis which usually remainssubclinical. Hepatotoxicity is rare (10).463