A total of 362 patients transfused one to 48 units of Australia (Au) antigen negative blood in an average of 8.9 units (1 unit=200ml) in the Department of Surgery, Sendai National Hospital from December '70 to October '72 were submitted in the present study.
Blood for transfusion was screened by SGOT level and immunoelectrosyneresis (IES) method for Au antigen. Au antigen or antibody by IES and passive hemagglutination test (PHA), together with routine liver function, were followed up in recepients for consecutive 3 months after transfusion at intervals of one or two weeks. The recepients with elevation over 50 Karmen units of SGPT for more than two weeks were suspected of posttransfusion hepatitis, among which the cases with 200 Karmen units were defined as authentic hepatitis and the cases with impaired laboratory findings for more than 6 months from onset were as protracted hepatitis, respectively.
The results were as follows.
1) During the present survey, posttransfusion hepatitis was developed in 36 (9.9%) of 362 recepients. Twenty two (61.1%) of this 36 cases was suspicious of hepatitis and the remaining 14 (38.9%) including 5 jaundiced, was judged authentic hepatitis. Seven (19.4%) among them were protracted.
2) Since the screening test by IES for Au antigen carrier was introduced, incidence of posttransfusion hepatitis was decreased to 10% from the past annual incidence of 20% in author's clinic.
3) No case with Au antigenemia was found among the Au negative recepients after the Au antigen carrier screening. Antibody response to Au antigen, however, was positive in 75 (20.7%) out of 362 by IES method and in 123 (45.9%) out of 268 by PHA method.
4) Au antibody responder was devided into 2 groups in the aspects of the time of antibody appearance and elevation of titer. In the first group, antibody was appeared between one week and two months after transfusion and its titer was rapidly elevated. The second group was that antibody undetectable during admission was found 4 to 12 months after transfusion and persisted at a low titer.
5) Out of 36 with posttransfusion hepatitis, 21 cases were revealed to have antibody response to Au antigen. Comparing the cases of positive Au antibody with the cases of negative Au antigen or antibody, no difference was observed from the points of protraction and becoming severe. So far as in the cases with positive Au antibody concerned, such matters as protraction and becoming severe were seemed to be influenced by the time of appearance and pattern in PHA titer.
6) In the cases with no blood transfusion, Au antibody detection rate of 20% on admission was increased up to 30% at their discharge.

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1) Human sera were fractionated with dextran-gel (Sephadex G-200) into three peaks of different protein components. The first contained high molecular 19S globulins, the second had 7S globulins and some albumin with 4S sedimentation constant. Complete anti-A or anti-B had the agglutinating activity in the first fraction and incomplete antibodies were detected in the second fraction.
2) Sephadex G-200 fractionation of anti-A or B in cases with various histories revealed that the severe hemolytic disease of the newborn was associated with the strong 7S antibody activity in the maternal serum. On the other hand, 19S antibody was shown not to correlate with the infant's findings.
3) 19S and 7S fractions were treated with heat, salivary neutralization, or 2-mercaptoethanol; 19S antibodies lost the activity by these treatments but 7S antibodies retained the antiglobulin activity though the titer was reduced.

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Passive agglutinations using latex particles or formol-alcohol-treated tanned sheep cells were compared with the conventional tests of leukocyte agglutination, complement fixation, and anti-globulin consumption, and were found to excel these tests in simplicity and specificity. Application of passive agglutinations will prove quite useful for the detection of leukocyte antibodies in routine screening.
The patient's serum which contained leukocyte antibodies was fractionated with DEAE cellulose into IgG, IgA, and IgM. Passive agglutination activities were found in the IgG and IgM, while no activity was detected in the IgA fraction.

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1) Fractionation of human sera with DEAE ion-exchange cellulose column gave three fractions: the first containing most of the IgG, the second in which IgA is eluted, and the third with IgM. Sera were selected from about 300 mothers, which possessed anti-A or anti-B antibodies with similar titers in the three fractions, IgG, IgA and IgM.
2) Agglutination tests using various methods revealed that IgG antibodies showed the peculiarities of the incomplete antibody, while IgA and IgM were complete agglutinins.
3) The thermal optimum was tested for IgG, IgA and IgM antibodies, but no significant difference was observed in the range from 4°C to 37°C.
4) Treatments which are usually used for the detection of so-called immune anti-A or B were applied to each fraction. Soluble blood group substances readily neutralized IgA and IgM, but only reduced IgG antibody activities. By the heating test, IgM was most sensitive, IgG was unexpectedly weak, and IgA was most resistent. Mercaptoethanol-treatment left IgG unaffected, moderately weakened IgA, and completely deprived IgM of the activity.
5) Presence of hemolytic activity in each fraction differred from case to case and was not well related to the agglutinating activity.

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1) Passive agglutination of the latex particles sensitized with leukocyte antigen was applied for the detection of anti-leukocyte antibodies. The suitable latex particles had the diameter of ca. 0.81μ. The sensitized latex particles were stable for 2 days. The dilution medium fitted for the agglutination was borate buffer of pH 8.2-9.2.
2) Leukocyte antibodies were screened by the latex particle agglutination on the patients' sera with various history of blood transfusion. Proportion of the leukocyte antibodies with titers above 1:16 was 77% in the hematological diseases group, 66% in the febrile transfusion reaction group, 50% in the frequent transfusion group, and 20% in the massive transfusion group. 98% of the cases had leukocyte antibodies in the group of bone marrow transfusion.

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