الفهرس 
CHRONIC MYELOGENOUS LEUKEMIAOnly 14 pages are availabe for public view
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Abstract
C
hronic myelogenous leukemia (CML) is a clonal disorder caused by the malignant transformation of pluripotent hematopoietic stem cells. Cytogenetically, CML is characterized by the Philadelphia (Ph) chromosome, which arises from the reciprocal translocation t (9; 22)(q34;q11).
Tyrosine kinases regulate many cellular processes, including growth and survival, and deregulated activity of these enzymes has been implicated in malignant transformation in various neoplasms. Therefore, specific inhibitors of tyrosine kinases are attractive therapeutic agents.
In the present study we give major concern about cardiotoxicity caused by tyrosine kinase inhibitors in 60 patients with chronic phase chronic myeloid leukaemia, aiming at evaluation of cardiac function by echocardiography, incidence of de-novo systemic hypertension, QT prolongation and screening of serum troponin-I levels.
The E.F of patients estimated using 2-D echocardiography (mean 64.8% + 3.9 SD) with 28% decrease from base line E.F, with no significant differences between different drug groups. Evident development of congestive heart failure and fluid retension in patients on imatinib was observed in our research.
De-novo systemic hypertension in patients on imatinib and nilotinib discovered with no significantly different ratios between these 2 drugs.
QT prolongation was observed in patients on imatinib and nilotinib (significant P value 0.02) with considerable number of patients with QTc >500 milliseconds.
We found in our study that cardiovascular adverse effects of TKIs is significantly present in our patients, especially those on imatinib and nilotinib.