Summary Haemorrhage is often responsible for the lethal course of acute myeloid leukaemia (AML). Previously, multiple platelet function defects were identified by flow cytometric analysis of platelet activation markers in AML. The role of flow cytometric analysis of platelet function in characterization of prognostic markers of haemorrhage in AML patients has not been well elucidated. The objective of this prospective study was to analyse platelet function in 50 AML patients at diagnosis and to compare results with clinical bleeding score, graded by common toxicity criteria. Platelet activation markers CD62P, CD42b, CD63 and PAC‐1 were analysed following in vitro activation by thrombin receptor activating peptide. The following plasma haemostasis parameters were measured: soluble P‐selectin, activated partial thromboplastin time, thrombin time, prothrombin time, d‐dimer, fibrinogen, and von Willebrand factor antigen. In a multivariate analysis, P‐selectin (CD62P) <36 molecules of equivalent soluble fluorochrome × 103 (P < 0·0015) and platelet count <40 × 109/l (P = 0·01) were significant predictors of haemorrhage at diagnosis. Haemorrhage at diagnosis predicted grade 3–4 haemorrhage in the first 28 d following diagnosis (P = 0·018). The presented results indicate that low P‐selectin is a prognostic marker of haemorrhage in AML.

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SummaryPrevious findings of megakaryocytic hypogranulation and dysmegakaryocytopoietic features in acute myeloid leukaemia (AML) strongly indicate defects in platelet production. The bleeding tendency of these patients may result from dysregulated platelet production, resulting in thrombocytopenia as well as qualitative platelet defects. The present study examined platelet function at diagnosis in 50 AML patients by whole blood flow cytometry. Following in vitro platelet agonist stimulation, platelet activation markers were analysed and compared with 20 healthy individuals. To detect recent in vivo platelet activation, plasma soluble P-selectin (sP-selectin) was measured. Flow cytometric analysis of platelet activation markers demonstrated reduced CD62P [35AE6 vs. 118AE5 · 10 3 molecules of equivalent soluble fluorochrome (MESF); P < 0AE0001], CD63 (11AE3 vs. 50AE7 · 10 3 MESF; P < 0AE0001), and PAC-1 (41AE5 vs. 90AE5%; P ¼ 0AE0001) while reductions in CD42b were abnormal (45AE6 vs. 70%; P < 0AE0001). sP-selectin levels were similar in patients and healthy controls (0AE04 vs. 0AE27 fg/platelet; P ¼ 0AE84). The presented data indicate that AML pathogenesis may result in multiple platelet defects, involving adhesion, aggregation, and secretion and demonstrate that flow cytometry is a feasible method for platelet function analysis in patients with thrombocytopenia.