Does platelet aggregation differ among chronic myeloid leukemia-chronic phase (CML-CP) patients on tyrosine kinase inhibitors (TKIs)? A tertiary center experience

Abstract

Abstract Background Tyrosine kinase inhibitors (TKIs) have improved the prognosis of chronic myeloid leukemia (CML) by inhibiting the BCR-ABL kinase. There are concerns regarding the effect of TKI on hemostasis by inhibiting platelet aggregation; the possible reason for this is yet unclear. Objectives To study platelet aggregation response to different agonists [(adenosine diphosphate (ADP), collagen, and arachidonic acid (AA)] using platelet aggregometry in 75 CML-chronic phase (CML-CP) patients on TKI therapy, in complete hematologic response (CHR). Patients and methods This study included 75 CML patients of both sexes of age 32–66 years. A detailed medical history, clinical examination, and platelet aggregation by PAP-4 platelet aggregometer were done for all patients. Results Imatinib-treated CML patients had a lower platelet aggregation response to AA (less than 50% aggregation) than those on nilotinib either first- or second-line treatment, in a statistically significant manner (P=0.001, P=0.025) for both comparisons. But there was no statistically significant difference in platelet aggregation between patients on nilotinib either first- or second-line therapy (P=0.073). Conclusion Platelet aggregation response to collagen and ADP was normal in all CML-CP patients, but it had an impaired response to AA<AQ: Pls check whether the change is appropriate>. Further studies are needed to establish the particular mechanism of this inhibition.