Lactate production by thrombin-activated platelets of patients with primary thrombocythemia

Platelet activation needs a high energy demand which is supplied by the degradation of glucose into lactate. Platelet response to agonists in patients with primary thrombocythemia is defective. We studied the production of lactate by the platelets of patients with this disease and defective platelet aggregation. Ten patients suffering from primary thrombocythemia and ten controls were included in this study. The lactate generation was measured in resting and thrombin activated platelets in absence or presence of glucose. Resting platelets incubated for 30 min in phosphate-buffered saline (PBS) generated the same amount of lactate in patients (44.6 ± 21.6 μmol/10 11 cells) and controls (41.0 ± 17.3 μmol/10 11 cells). Addition of glucose led to similar increases in lactate formation by platelets in patients (82.2 ± 26.4 μmol/10 11 cells) and controls (88.1 ± 34.5 μmol/10 11 cells). The addition of thrombin in absence of glucose did not modify the lactate formation respective to PBS. Finally, the incubation of platelets with both glucose and thrombin caused further increases in the generation of lactate in both groups, patients (236.9 ± 83.9 μmol/10 11 cells) and controls (228.6 ± 63.5 μmol/10 11 cells) without differences between them. The production of lactate in both groups was also similar when platelets were incubated for 10 min or 20 min with both thrombin and glucose. However at 5 min, platelets of patients generated more lactate (97.8 ± 23.7 μmol/10 11 cells) than controls (66.5 ± 38.7 μmol/10 11 cells, p < 0.05). These results suggest that thrombin is able to induce an initial hyperactivity of those pathways involved in the platelet energy production of patients with primary thrombocythemia.