1. Direct transfusions of platelet-rich polycythemic blood, using the multiple syringe technic and siliconized apparatus, were performed in 14 cases of "idiopathic" ("megakaryocytic") and 8 of "secondary" ("amegakaryocytic") thrombocytopenia. Effects on platelet number and function, and on hemorrhagic manifestations were studied.

2. Platelets disappeared very rapidly from the circulation (one-half to twelve hours) in the 12 patients with acute idiopathic thrombocytopenia and in 1 patient with chronic thrombocytopenia with a low platelet count. They disappeared more slowly (twenty-four hours) in the other case of chronic idiopathic thrombocytopenia in which there was a higher platelet count. Essentially similar platelet disappearance curves were obtained in 2 patients, before and after unsuccessful splenectomy. In the patients with secondary thrombocytopenia, the survival of platelets in the circulation was much longer (average forty-eight to ninety-six hours).

3. Behavior of clot retraction and prothrombin activity of serum paralleled closely that of the platelet count. The bleeding time and capillary fragility usually remained improved for twenty-four to forty-eight hours after the platelet count had fallen to the initial level. Likewise, the hemorrhagic manifestations were improved in every case for many hours after the platelet level had returned to its original value. Similar, but less marked beneficial effects on the hemorrhagic manifestations were also obtained with transfusions of fresh blood from donors with normal platelet counts, provided fresh blood was used and precautions taken to prevent excessive loss of platelets.

4. Remissions were observed in 2 patients with idiopathic thrombocytopenia following direct transfusion of polycythemic blood. In both cases, the injected platelets disappeared promptly from the circulation but within twenty-four hours the platelet count began to rise and a long-sustained remission became established. This finding suggests the possibility that polycythemic blood may contain a stimulatory principle which can determine or accelerate a spontaneous remission.

5. Conclusions. The prompt disappearance of injected platelets from the circulation of patients with "idiopathic" thrombocytopenia suggests a humoral destructive mechanism, which is not present in the "secondary" or "amegakaryocytic" cases. This destructive mechanism does not appear to originate in the spleen. Our observations do not exclude an inhibitory effect upon platelet production from the megakaryocytes of the bone marrow. Polycythemic blood may contain a platelet stimulatory factor.

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