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.
Related projects:	Mutační analýza primitivních buněčných populací u chronické myeloidní leukémie: za hranicí BCR-ABL1