How tyrosine kinase inhibitors impair metabolism and endocrine system function: A systematic updated review

• Published in: Leukemia research Vol. 38; no. 12; pp. 1392 - 1398
• Main Authors: Breccia, Massimo, Molica, Matteo, Alimena, Giuliana
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.12.2014
• Subjects: Disease-Free Survival; Endocrine; Endocrine System - metabolism; Endocrine System - pathology; Endocrine System Diseases - chemically induced; Endocrine System Diseases - metabolism; Hematology, Oncology and Palliative Medicine; Humans; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy; Leukemia, Myelogenous, Chronic, BCR-ABL Positive - mortality; Metabolic; Protein Kinase Inhibitors - adverse effects; Protein Kinase Inhibitors - therapeutic use; Receptor Protein-Tyrosine Kinases - antagonists & inhibitors; Survival Rate; Tyrosine kinase inhibitors; Endocrine; Metabolic; Tyrosine kinase inhibitors
• ISSN: 0145-2126; 1873-5835; 1873-5835
• DOI: 10.1016/j.leukres.2014.09.016

•TKIs treatment could be associated to metabolic or endocrine side effects.•Fasting glucose may decrease with imatinib.•Nilotinib has been associated to hyperglycaemia and hypercholesterolemia.•Bone metabolism modification has been observed with all available TKIs. Tyrosine kinase inhibitors (TKIs) advent has deeply changed the outcome of chronic myeloid leukemia (CML) patients, with improved rates of response and overall survival. However, for this success some patients paid the price of a number of peculiar side effects, the so-called off-target side effects, specific for each one TKI. These effects are due to non-selective inhibition of other tyrosine kinase receptors, such as PDGFR, c-KIT, Src, VEGF. Consequences of this inhibition, some metabolic changes during the treatment with TKIs are reported. Aim of present review is to report metabolic changes and potential mechanisms involved in the pathogenesis related to imatinib, second (nilotinib and dasatinib) and third generation (bosutinib and ponatinib) TKIs.