Hepatotoxicity from arsenic trioxide for pediatric acute promyelocytic leukemia.

The aim of this study was to investigate the hepatotoxicity induced by arsenic trioxide (As2O3) at a therapeutic dose for pediatric acute promyelocytic leukemia (APL). A total of APL patients received As2O3 treatment by IV drip. Hepatotoxicity was monitored based on the observations of the dynamic changes in liver function and treatment responses. The influencing factors of hepatotoxicity were further analyzed. Liver impairment occurred in 24.4% of the patients, most of which was mild and moderate in severity. Liver impairment was primarily manifested by increases in alanine aminotransferase, aspertate aminotransferase, and γ-glutamyl transferase, and these increases mostly occurred within 1 to 3 weeks and then returned to normal levels after 4 weeks. Patients' ages, sex, disease time, hepatomegaly and liver dysfunction, and disseminated intravascular coagulation did not show correlations with hepatotoxicity. Their hemogram and lactate dehydrogenase numerical values obtained from preliminary diagnosis did not show significant correlations with hepatotoxicity. Aggravated hepatotoxicity was not observed in patients receiving marcellomycin for the sake of complete remission. Changes in short-term cumulative dose of As2O3 did not exhibit a correlation with hepatotoxicity. However, patients suffering from differentiation syndrome were more likely at the risk of hepatotoxicity. Liver impairment improved after the suspension of As2O3 and liver protection treatment. No patient died of liver failure. Hepatotoxicity induced by As2O3 at a therapeutic dose for pediatric APL is mild and temporary. The first to the third week of the remission induction is the important period for monitoring. Great attention should be given to differentiation syndrome as it may worsen hepatotoxicity.