Neonatal platelet function

UMMS Affiliation

Department of Pediatrics

Publication Date


Document Type



Blood Platelet Disorders; Blood Platelets; Humans; Infant, Newborn; Platelet Activation; Platelet Function Tests; Signal Transduction


Hematology | Oncology | Pediatrics


Healthy newborns maintain normal circulating platelet counts, with a platelet ultrastructure that does not differ from adults. In vitro assessments of intrinsic platelet function, however, have demonstrated transient hyporesponsiveness that is most marked in platelets from preterm infants. Decreased responses were originally considered to be the result of platelet activation and degranulation during labor and delivery, but more recent studies of platelet activation markers have not supported this theory. Decreased activation responses are due to relative deficiencies of phospholipid metabolism, calcium mobilization, granule secretion, and aggregation. These result in turn from differences in intrinsic signal transduction in the neonatal platelet compared with the adult. In contrast, there is enhanced platelet adhesion due to the presence in neonatal plasma of larger, more functionally potent von Willebrand factor multimers. These ultralarge multimers may result from decreased activity of von Willebrand factor-cleaving protease in neonatal plasma and are associated with shorter bleeding times and Platelet Function Analyser-100 closure times in neonates. In the immediate newborn period, this enhanced platelet adhesion may compensate for the decreased intrinsic platelet activation in healthy neonates, but may leave sick neonates at increased risk of bleeding.

DOI of Published Version



Semin Thromb Hemost. 2003 Aug;29(4):363-72. doi 10.1055/s-2003-42587

Journal/Book/Conference Title

Seminars in thrombosis and hemostasis

Related Resources

Link to article in PubMed

PubMed ID