The metabolic consequences of imatinib mesylate: Changes on glucose, lypidic and bone metabolism

The therapeutic efficacy of imatinib mesylate is based on its specific inhibition of several tyrosine kinases (TKs) implicated in the disease pathogenesis. These enzymes include BCR/ABL in patients with chronic myeloid leukaemia, PDGF-R alpha and beta in patients with certain myeloproliferative disorders and dermatofibrosarcoma protuberans and c-KIT in patients with gastrointestinal tumors. Most patients tolerate the drug well and apparently no metabolic abnormalities are evidenced during treatment. However, different metabolic effects have been reported as a consequence of imatinib inhibition during treatment of patients with CML. The aim of this review is to report the changes caused by imatinib on glucose, lypidic and bone metabolism.