PB0629 - Platelet functional activity in pediatrics patients with acute myeloid and lymphocytic leukemia

Background: Acute myeloid (AML) and lymphocytic (ALL) leukemia are malignant diseases caused by an abnormal proliferation of different hematopoietic cell subtypes. It is well documented, that acute leukemia can cause severe impairments in platelet functions which can cause complications such as bleeding. Flow cytometry is a promising tool to study of platelet status in AL patients, especially children. However, the platelet flow cytometry data for pediatric patients with AL is lacking, and it can be helpful in determining the mechanisms of AL progression and response to treatment.

Aims: A pilot study to investigate the functional activity of platelets in pediatric patients with ALL and AML, and to assess its relationship with platelet aggregation.

Methods: 19 AL patients: 8 - AML, 11 - ALL and 17 clinically healthy children were involved in the study. Platelet functional activity was measured by whole blood flow cytometry using antibodies against CD42b, CD41, PAC1, CD63, CD62P, as well as Annexin V. Platelet aggregation activity was assessed by impedance aggregometry. All experiments were performed in accordance with Helsinki Declaration.

Results: Agonist-induced aggregation was significantly lower in both study groups compared to control. AL patients had enhanced basal GPIIb/IIIa activation (% of PAC1+ platelets), whereas the levels of GPIIb/IIIa and its active form (PAC-1) were significantly reduced after activation. Agonist-induced degranulation of both α- and δ-granules was lower in both AL groups compared to control, and AML patients had a tendency for lower granule secretion. A strong inverse correlation between % of PAC1+ and AnnexinV+ platelets was observed in control and ALL groups, whereas AML group had no significant correlation.

Conclusion(s): This study investigated the functional activity of platelets in pediatric patients with ALL and AML on the onset of the disease. Obtained results might be helpful in deepening our understanding of AL progression and its relationship with hemostasis.