Key Points
- To examine platelet function and factor VIII parameters in chronic myeloid leukemia to elucidate mechanisms underlying abnormal bleeding tendencies.
- Evaluated bleeding time, platelet retention, and agonist-induced platelet aggregation (using ADP, collagen, epinephrine, ristocetin, and arachidonic acid) in 17 patients with chronic myeloid leukemia.
- Measured intracellular ATP and ADP concentrations, ATP secretion using a Lumi-aggregometer, and factor VIII components (FVIIIR:Ag, FVIIIR:CoF, and FVIII:C), testing for circulating factor VIII inhibitors.
- Platelet retention was reduced in 13 of 17 patients, while aggregation was impaired in response to epinephrine (41%), ADP (24%), and collagen (24%), alongside abnormal ristocetin aggregation in 9 of 17 patients.
- Intracellular ATP and ADP stores and ATP release were significantly decreased, accompanied by concurrent reductions in FVIIIR:Ag, FVIIIR:CoF, and FVIII:C in patients with defective ristocetin response without evidence of plasma inhibitor activity.
Structured PICO
PPopulation17 patients with Chronic Myeloid Leukemia (CML)
OOutcomePlatelet function and factor VIII levelssurrogate
Patients with CML may develop acquired von Willebrand's disease, contributing to platelet dysfunction and potential bleeding tendencies.