Fig. 4.

A-F. Spontaneous and collagen-induced healthy donor platelet aggregation triggered by the acute (A, B) versus follow-up phase plasma (C, D) and serum (E, F) from patient 3. (A) Spiking with control plasma without agonist and in collagen-induced aggregation: spontaneous aggregation did not occur (no agonist) and collagen-induced aggregation was vivid. (B) Spiking with patient plasma at acute phase induced immediate spontaneous aggregation (no agonist), enhanced by collagen. Collagen-induced platelet aggregation was modestly inhibited by intravenous immunoglobin (IVIG) (5 mg/mL) when spiked with control plasma (A) or on patient plasma (B), while Glycoprotein (GP) IIb/IIIa inhibitor (eptifibatide) (2 μg/mL) abolished aggregation. The five-week follow-up patient plasma did not trigger spontaneous aggregation (D), but patient serum depicted delayed spontaneous aggregation (F). Compared with plasma (C) or serum controls (E), collagen-induced aggregation in the presence of patient plasma (D) or serum (F) was nearly normal, despite ticagrelor and fondaparinux medication. Adding platelet factor 4 (PF4) (5 μg/mL) did not markedly enhance aggregation (C-F), but IVIG 10 mg/mL abolished aggregation in the presence of PF4 (C-F).