Insulin resistance is an underlying mechanism of impaired glucose metabolism during nilotinib therapy

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Authors

RÁČIL Zdeněk KORIŤÁKOVÁ Eva SACHA Tomasz KLAMOVA Hana BELOHLAVKOVA Petra FABER Edgar REA Delphine MALASKOVA Ludmila PROCHÁZKOVÁ Jiřina ŽÁČKOVÁ Daniela VOGLOVA Jaroslava WACLAW Joanna CETKOVSKY Petr ZAK Pavel MAYER Jiří

Year of publication 2018
Type Article in Periodical
Magazine / Source American Journal of Hematology
MU Faculty or unit

Faculty of Medicine

Citation
Doi http://dx.doi.org/10.1002/ajh.25232
Keywords nilotinib therapy
Description Impaired glucose metabolism (IGM) with hyperglycemia represents one of the most frequently observed adverse events (AE) during nilotinib therapy of chronic myeloid leukemia (CML). The exact mechanism of IGM remains controversial. Although a case report has shown a decrease in insulin secretion1 , our previous pilot data suggested development of insulin resistance as a possible mechanism.2 In this prospective study we aimed to confirm results from our pilot study using a larger cohort of CML patients treated with nilotinib and to compare results with data obtained on control groups receiving imatinib and dasatinib.
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