Table II.

Typical lumi-aggregometry findings in the commonly encountered platelet defects within the HMB cohort.

Platelet defect	Aggregation results	Secretion results
Secretion defects	Absence of secondary wave aggregation to most agonists used in low concentrations, and epinephrine at all concentrations	Significantly reduced levels of ATP secretion (when normalized for platelet count)
Thromboxane pathway defects	Absence/severe reduction of aggregation in response to arachidonic acid while response to thromboxane mimetics is preserved (for cyclooxygenase defects) or absence of aggregation response to both arachidonic acid and thromboxane mimetics (for thromboxane receptor defects) Commonly, absence of secondary wave aggregation to most agonists used in low concentrations, and epinephrine at all concentrations	Normal
Gi-coupled receptor defects	Reduced aggregation to ADP with notable deaggregation even at high concentrations of agonist Reduced primary wave response to epinephrine and absence of secondary wave	Normal