Very few studies have investigated dose response of aspirin and agreement of different platelet function assays in children. One hundred five children were studied at baseline and after interventional cardiac catheterization during aspirin treatment and, in cases of aspirin resistance (AR), after dose increase. Results from arachidonate-induced aggregation (AA) were compared with aggregation induced by ADP, PFA-100 closure times (CTs), urinary 11-dehydro-thromboxane B2 (urinary 11-dhTxB2) levels, and Impact-R % surface coverage. Aspirin at 2-5 mg/kg/day inhibited platelet function in a large majority. While 19 % showed bruising and mild epistaxis, no thrombotic complications were recorded. AR was detected by AA in seven children (6.7 %). After dose increase, the majority showed inhibition by aspirin. Infants had higher urinary 11-dhTxB2 baseline levels; this assay showed some correlation with AA. Both assays manifested high sensitivity and specificity for aspirin while inferior results were found for the other assays. With the PFA-100, 15.2 % of patients were found to have AR, but this corresponded to AR by AA in only one of seven children.
CONCLUSION: While there was poor agreement among assays, AA and urinary 11-dhTxB2 show good specificity for the monitoring of aspirin therapy in children. Aspirin at 2-5 mg/kg inhibits platelet function; AR in children is rare and can be overcome by dose increase.