Abstract
The occurrence of liver disease and its relation to HBV markers were investigated in ten children with AML who were given HDARAC as late consolidation therapy. None of them developed jaundice or biochemical evidence of cholestasis. During therapy, SGPT values were normal in 5/10 patients, while in the other 5 a sharp increase was noted. These enzyme elevations followed an unusual timing, peaking just before each infusion of HDARAC. Evidence of long-lasting hepatocellular necrosis after therapy withdrawal was found in 8/8 cases. One child died of fulminant type B hepatitis and HBsAg positivity was found in 2/10 patients during therapy and 3/8 after withdrawal of the drug. Three children developed HBV antibodies during the observation period. We conclude that the use of HDARAC in childhood leukemia is not associated with major evidence of direct drug hepatotoxicity while it clearly affects the natural outcome of viral hepatitis.
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