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Twenty-four thrombocytopenic patients refractory to random-donor platelet support were given 106 platelet transfusions obtained from 57 different HLA-typed single donors. For critical evaluation of the transfusion responses, “fullhouse” HLA typing of donors and a precise measurement of the number of infused platelets were performed. Posttransfusion platelet increments were related to the HLA matching of donor-recipient pairs and to leukocyte crossmatch tests in vitro. The transfusion response displayed a striking difference depending on the absence (type-0 match) or presence (type-1 or-2 match) of donor HLA antigens differing from the recipient. Whereas 95% of transfusions from type-0 match donors resulted in a compatible platelet increment, only 20% successful transfusion responses could be achieved with type-1 or -2 match donors. In 77% of type-1 or -2 match transfusions with poor posttransfusion platelet increments, the lymphocyte cytotoxicity test (incubation time 180 min at room temperature) was positive. This test therefore seems to be a useful tool in predicting the outcome of transfusion responses in type-1 and -2 match pairs. In contrast, the lymphocyte cytotoxicity tests were of no predictive value in type-0 match pairs. The influence of specific antigranulocyte antibodies on type-0 match platelet transfusions was assessed in four recipients. Although severe transfusion reactions were observed, no detrimental influence on platelet increments could be observed, at least following the initial transfusion.

A randomized study was performed in 54 thrombocytopenic patients with acute leukemia. Alloimmunization of recipients of random multiple-donor platelet concentrates (MD group) was compared to that of patients receiving random single-donor platelets (SD group). In the SD patients, formation of alloantibodies (mostly anti-HLA) occurred less frequently (p less than 0.002), after a longer time period (p less than 0.002), and after a higher number of transfusions (p less than 0.005) as compared to MD patients. SD patients also became refractory to random platelets less frequently (p less than 0.005), after a longer time period, and after a higher number of transfusions (p less than 0.02). In SD patients, the increments after the first and the last transfusion were in the same range, whereas in MD patients, the 1-hr (p less than 0.001) and the 24-hr (p less than 0.025) increments decreased from the first to the last transfusion. Thus, the use of random SD platelet transfusions postponed alloimmunization.

1. A hemophilia-like disease acquired during the first pregnancy of a young woman, is described. 2. The clotting abnormality was caused by a circulating anticoagulant which, in all probability, inhibited the antihemophilic globulin. 3. The anticoagulant was demonstrated in the patient's second child during his first two and one-half months of life. 4. The transplacental transfer of the anticoagulant and the analogy of this condition to hemophilia (resistant to therapy) following iso-immunization against antihemophilic globulin, strongly suggest that an immunologic mechanism accounts for the development of this abnormality. 5. The patient recovered eighteen months after her second delivery and sixteen months after x-ray sterilization. The possible relation between endocrine factors and recovery is discussed.

1. A circulating anticoagulant was demonstrated in three patients with "collagen disease." In all cases it was associated with a false positive blood serology and a four plus cephalin cholesterol flocculation. 2. In one instance, the anticoagulant was transferred to a newborn infant where it persisted for seven weeks. The infant also demonstrated the abnormal serologic and turbidimetric tests during the first six months of life. 3. The anticoagulant probably acted as anti-thromboplastin. 4. The occurrence of a clotting inhibitor in association with other manifestations of hypersensitivity and its transplacental transfer strongly suggest that the mechanism of development is immunologic in type. 5. This study included a total of thirty patients with lupus erythematosus disseminatus and associated conditions conventionally grouped under the term "collagen disease." The incidence of circulating anticoagulants was 10 per cent.

A new abnormal hemoglobin was observed in 15 members over four generations of a large Swiss family and has been termed "Hemoglobin Zürich." The discovery of this hemoglobin was prompted by a severe hemolytic crisis in two members of the family after sulfonamide therapy. During this episode, virtually all erythrocytes and reticulocytes contained a single large inclusion body which was visible with Giemsa and brilliant cresyl blue stains. Outside the hemolytic episode, the erythrocytes revealed no morphologic abnormalities. The results of enzyme studies were all within normal limits. The association of a hemoglobinopathy with a drug-induced inclusion body anemia without any demonstrable enzyme defect is a new entity. The anomalous hemoglobin is inherited as a dominant character and affects both sexes. Thus far, only the heterozygous form has been observed.

A randomized study was performed in 54 thrombocytopenic patients with acute leukemia. Alloimmunization of recipients of random multiple-donor platelet concentrates (MD group) was compared to that of patients receiving random single-donor platelets (SD group). In the SD patients, formation of alloantibodies (mostly anti-HLA) occurred less frequently (p less than 0.002), after a longer time period (p less than 0.002), and after a higher number of transfusions (p less than 0.005) as compared to MD patients. SD patients also became refractory to random platelets less frequently (p less than 0.005), after a longer time period, and after a higher number of transfusions (p less than 0.02). In SD patients, the increments after the first and the last transfusion were in the same range, whereas in MD patients, the 1-hr (p less than 0.001) and the 24-hr (p less than 0.025) increments decreased from the first to the last transfusion. Thus, the use of random SD platelet transfusions postponed alloimmunization.

Two patients with polycythemia vera received intravenously an accidental tenfold overdosage of radiophosphorus therapy (60 and 50 mCi 32P, respectively). In both patients, the occurrence of hemorrhagic complications 3 wk after the 32P medication led to detection of the error and referral to our hospital. Upon admission they showed an agranulocytosis, severe thrombocytopenia, and bone marrow aplasia. In both cases, spontaneous recovery of the hematopoiesis was observed from day 40 posttreatment onward. In one patient, a slow but ultimately complete normalization of blood counts and marrow morphology took place, whereas in the other, a mild thrombocytopenia persists. Nearly 5 yr after the accidental overdosage, both patients are clinically well. Symptoms of polycythemia vera have not reappeared up to now. Attempts were made to evaluate the radiation dose absorbed by the bone marrow. In the first patient, the daily 32P excretion was determined from day 22 to day 60, whereas in the other patient a whole body count was performed on day 78 after administration. From these results, an approximate cumulative bone marrow dose of 10 Sv (1000 rem) could be calculated.