ReferencesMarks MR. Reid ME. Ellisor SS. Adsorption of unwanted cold autoagglutinins by formaldehyde treated rabbit red blood cells (abstract). Transfusion I980;20:629. Waligora SK. Edwards JM. Use of rabbit red cells for adsorption of cold autoagglutinins. Transfusion 1983:23:328.
A D variant, DtI?To the Editor:We noticed that some D-negative red cells, though they were negative in a D" test after exposure to anti-D, could bind anti-D and yield it o n elution.We temporarily call these red cells D,I. As shown in Table I , most phenotypes with D,I had C. c, and e antigens, but no cells of an EEhomozygote have yet adsorbed anti-D. We used a commercial anti-D (Ortho Diagnostics. Raritan. NJ). a purified anti-D (kindly sent from Mr. Moulds. Gamma Biologicals. Houston. TX) and a monoclonal anti-D (kindly distributed by Prof. Ono. Nihon University) for absorption-elution studies. but the purified and monoclonal anti-D reagents were not available for use with all the Rhnegative cells tested. Eluates were made by the chloroformt richloroet hylene method. '
By the use of sucrose gelatin veronal buffer (SGVB), a simple screening test was developed by us to detect sera with low complement activity, including C9-deficient sera. Using this screening test, we were able to identify sera with low complement activity including C9-deficient sera among a large number of samples. Further examinations, estimation of the protein concentration of C9, C4, C3, etc., enabled classification of serum with low complement activity into C9-deficient serum, serum deficient in the other components, and serum with low complement activity caused by non-specific activation of complement through the classical pathway by low temperature in vitro. Among 145,640 sera from Osaka donors, 138 sera were found to be deficient in C9 by these methods. The whole complement activity (CH50) of the 138 sera was 13.1 +/- 3.0 U/ml. The C9 protein in these sera was undetectable, not only by the single radial immunodiffusion method, but also by the sensitive ELISA method. C9 activities in these sera were less than 0.1% of the level in pooled normal human serum. These findings and the family studies revealed that 138 blood donors unquestionably had a hereditary C9 deficiency. The incidence of C9 deficiency among Osaka donors was calculated to be 0.095%.
The risk of neonatal alloimmune thrombocytopenia and refractoriness to platelet transfusion induced by the antigens of the HPA-1, HPA-7W, and HPA-8W systems was extremely rare in Japanese. However, attention must be paid to the involvement of the HPA-4 and HPA-6W systems in these clinical disorders.
We developed an allele-specific polymerase chain reaction (ASPCR) method using
originally designed primers to determine the genotype of the human platelet
antigens (HPAs) 2, 3 and 4 in parallel. The results were compared with those
obtained by PCR restriction fragment length polymorphism and the mixed
passive hemagglutination test. Seventy-three individuals were tested and the
ASPCR results were in good agreement with those determined by the other two
methods. This method enables the genotyping of HPA-2, -3 and -4 in parallel
without the use of platelets, platelet-specific alloantibodies or restriction enzymes.
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