Platelet rich plasma was obtained using mainly Haemonetics V50, and occasionally Hitachi SMS 10. The procedures were performed 565 times on 54 male and 28 female voluntary donors ranging in age from 18 to 60. The criteria followed was to draw 200ml whole blood per donor. The plasma obtained was 10-12% of the donor's circulating blood volume.
Donors were divided into two groups. Group A donated once a week for four consecutive weeks, rested 4 weeks, then repeated this routine totalling 12 plasmaphereses over the course of five months. Group B was plasmapheresed at two week intervals totalling 12 plasmaphereses over a six month period.
In Group A, nine of the fifty-four donors completed the program of 12 plasmaphereses, with the remainder ranging from 4 to 11 completed plasmaphereses. In Group B, five of twenty four donors completed the 12 plasmaphereses program, the remaining members completing from 4 to 11 plasmaphereses.
At each plasmaphereses, the parameters of red cell, hematocrit, hemoglobin, platelet, white cell, total serum protein, albumin, α₁-, α₂-, β-, γ-globulin, IgG, IgA, IgM, S-GPT, alkaline phosphatase, blood urea nitrogen, cholesterol, prothrombin time and partial thromboplastin time were determined before and immediately after the procedure, and three and seven days following.
Immediately after plasmapheresis, total serum protein, albumin, α₁-, α₂-, β-, γ-globulin, immunoglobulins and platelet counts showed a decrease of 85-90% of the pre-apheresis values. In all donors, these returned to pre-apheresis values within 3 to 7 days after aphereses.
During the half year course of consecutive plasmaphereses in both A and B groups, it was observed that no change was noticed in all determinations except IgG and IgM which showed declining tendency although it was not statistically significant.

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A male infant was born to a 20-year old, primipara healthy mother, after a 38-week umcomplicated gestation. He showed generalized purpura at 2 hours of age, but no hepatosplenomegaly. His platelet count was 1.7×10⁴/μl and had no response to platelet transfusion from random donors, but gradually increased to 32.5×10⁴/μl on 24 days of age. Mixed passive Haemagglutination test revealed that his platelets were destructed by maternal platelet specific antibody, passively come through placenta. After analyzing specificity of the mother's serum, it was not identical with any of the known platelet specific antisera. So, we diagnosed this case as a neonatal alloimmune thrombocytopenia due to a new platelet specific antigen (Yuk^a). It might be possible that other same cases will be found in Japan.

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We have experienced a case of neonatal allo-immune thrombocytopenia. The mother developed a platelet-specific antibody against a new platelet antigen (Yuk^a). In the study of Yuk^a family, Yuka antigen is found to be inherited as a autosomal dominant trait.

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