Vol 1, No 3 (2010)
Case report
Published online: 2010-07-27

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Imatinib-induced toxic liver failure in patients with chronic myeloid leukemia

Agnieszka Kołkowska-Leśniak, Katarzyna Budziszewska, Ilona Seferyńska, Krzysztof Warzocha
Hematologia 2010;1(3):254-260.

Abstract

Imatinib (IM) selectively inhibits the activity of some tyrosine kinases, including BCR-ABL1 and c-KIT. Mainly because of this mode of action, it has been registered as the first line treatment option for patients with chronic myeloid leukemia (CML) in the chronic, accelerated and blast crisis phases, patients with inoperable and disseminated gastrointestinal stromal tumors (GIST) and in the other rare malignancies with genetic abnormalities related to platelet-derived growth receptor, e.g. chronic myeloproliferative neoplasms with t(5;12) or hypereosinophilic syndrome. Although the treatment is generally well tolerated, about 2–5% of IM-treated patients may develop toxic liver failure. Herein, we report two clinical cases of hepatotoxicity induced by IM at the standard dose 400 mg/day. In both cases, cessation of IM treatment resulted in normalization of liver function, however with concomitant lost of cytogenetic and hematologic response. Subsequent treatment with the 2nd generation inhibitor of tyrosine kinase - dasatinib at a dose 100 mg/day allowed to achieve again cytogenetic and hematologic response without any signs of hepatotoxicity. These cases underscore the potential IM-induced liver failure and emerge for regular monitoring of liver function throughout the treatment. Hematologia 2010; 1, 3: 254-260

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Hematology in Clinical Practice