Function and Ultrastructure of Transfused, Surviving, Human Platelets in Patients with Thrombocytopenic Complicating Disease

Platelet concentrates prepared from freshly drawn blood were infused into patients with thrombocytopenic complicating disease. All exhibited a prolonged bleeding time, no clot retraction of a whole blood clot, platelet counts between 20,000 to 100,000 per cu. mm., usually, abnormal platelet ultrastructure and prothrombin consumption times under 15 seconds. Detection of platelet antibodies was attempted and the ultrastructure with a differential platelet count under the electron microscope of the patient's own platelets was documented. The platelet concentrates were given and it was possible to follow the fate of the donor's platelets by ultrastructural changes. Parallel studies of the coagulation mechanisms of the patients were followed serially. We found that some platelets survived up to seven days, although in some patients, platelets circulated but did not survive. Therefore immediate circulation of platelets cannot be equated with survival. In one patient with hypersplenism and a positive platelet agglutinin test no transfused platelets appeared to circulate. The ultrastructure of transfused platelets is greatly altered in bleeding patients. In the two patients with aplastic anemia and one with leukemia surviving platelets circulated which did not enter into the mechanisms of prothrombin activation, but which continued to circulate for some days with no improvement in the prothrombin consumption time over the pretransfusion level. Ultra‐structural studies of these platelets showed that the circulating platelets possessed their granules which contain platelet factor 3 activity. The differential platelet count under the electron miscroscope becomes abnormal as the donor platelets are stored. Our work suggests that the ultrastructure and differential platelet count of a platelet concentrate must be essentially normal for survival to be achieved.