Mechanism of impaired glucose metabolism during nilotinib therapy in patients with chronic myelogenous leukemia
| Autor: | Lucie Burešová, Daniela Zackova, Ludmila Malaskova, J. Drápalová, Filip Rázga, Jiri Mayer, Martina Palacková, Zdenek Racil, Martin Haluzik, Lukáš Semerád |
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| Jazyk: | angličtina |
| Rok vydání: | 2013 |
| Předmět: |
Oncology
Adult Blood Glucose Male medicine.medical_specialty Adipokine 030204 cardiovascular system & hematology Carbohydrate metabolism 03 medical and health sciences Myelogenous 0302 clinical medicine Insulin resistance hemic and lymphatic diseases Internal medicine Leukemia Myelogenous Chronic BCR-ABL Positive medicine Humans Adverse effect Aged business.industry Hematology Middle Aged Protein-Tyrosine Kinases medicine.disease 3. Good health Leukemia Endocrinology Glucose Pyrimidines Nilotinib Online-Only Articles 030220 oncology & carcinogenesis Female Insulin Resistance business medicine.drug Chronic myelogenous leukemia |
| Popis: | Hyperglycemia represents frequent adverse event reported in chronic myelogenous leukemia (CML) patients treated with nilotinib. In order to determine the major mechanism of glucose metabolism impairment, we performed a metabolic analysis using an oral glucose tolerance test as well as assessment of incretins and adipokines at baseline and after 3 months of nilotinib treatment in patients with CML. We proved that rapid insulin resistance, compensatory hyperinsulinaemia, and hypoadiponectinaemia develop after initiation of nilotinib therapy, which clarifies not only the mechanism of impaired glucose metabolism, but also explains the fast development of dyslipidaemia and peripheral artery occlusion in nilotinib-treated CML patients. |
| Databáze: | OpenAIRE |
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