Abstract
BLEEDING tendencies secondary to thrombopenia are of increasing frequency in medical, surgical and obstetric disorders. This has been attributed to diverse causes: chemotherapeutic agents1 , 2; insecticides3; increased incidence of leukemia4; radioisotopes; cytotoxic agents in industry5; complete blood replacement by transfusion during pulmonary or cardiovascular surgery6; and the alarm reaction secondary to surgery and anesthesia.7 The clinical management of such thrombopenia necessitates a clear understanding of the etiologic mechanisms that produce a decrease in circulating platelets. Within recent years, it has become clear that many cases of purpura, especially idiopathic thrombocytopenic purpura and hypersplenism, are due to . . .

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