Apoptotic profiling of chronic myeloid leukaemia patients' platelets ex vivo before and after treatment with Imatinib.

Affiliation

Repsold L(1), Pool R(2), Karodia M(2), Tintinger G(3), Becker P(4), Joubert AM(1).
Author information:
(1)Department of Physiology, Faculty of Health Sciences, School of Medicine, University of Pretoria, Pretoria, South Africa.
(2)Department of Haematology, Faculty of Health Sciences, School of Medicine, University of Pretoria, Pretoria, South Africa.
(3)Department of Internal Medicine, Faculty of Health Sciences, School of Medicine, University of Pretoria, Pretoria, South Africa.
(4)Research Office, Faculty of Health Sciences, School of Medicine, University of Pretoria, Pretoria, South Africa.

Abstract

Chronic myeloid leukaemia (CML) is a malignancy of the haematopoietic stem cells. The first line of treatment for CML, especially in developing countries, remains the first-generation tyrosine kinase inhibitor, Imatinib. Patients with CML are frequently diagnosed with platelet abnormalities. However, the specific mechanism of platelet abnormalities in CML remains unclear and poorly understood. The aim of this study was therefore to determine the apoptotic profiles of CML patients ex vivo on platelets before and after treatment with Imatinib. Blood samples of healthy volunteers and CML patients at diagnosis and after 6 months treatment with Imatinib were collected. Platelet counts, viability and activation were determined. Results showed that CML patients' platelet counts were elevated upon diagnosis and these levels statistically significantly decreased after 6 months of treatment. Platelet activation was significantly increased after 6 months of treatment compared to levels at diagnosis (P-value < .05). Similarly, platelet apoptosis was also increased after 6 months of treatment. Abnormalities in platelet functioning found in this study may partly be due to clonal proliferation of haematopoietic cells in CML patients, specifically of megakaryocyte precursors as well as the inhibition of platelet tyrosine kinase's and the inhibition of platelet-derived growth factor.