Nearly one fifth of patients transfused with blood containing Australia antigen(Au(1)‐positive blood) produced antibodies against the Au(1) antigen. The antibodies were also found in recipients of Au(1)‐netagive blood, although less frequently. A plasma product, heat‐treated (60°C, 10 h) plasma protein solution, may also be an antigenic stimulus for antibody production. After transfusion the Au antigen became demonstrable in the serum of 18 of 55 recipients of Au(1)‐positive blood and in the serum of 10 of 99 recipients of Au(1)‐negative blood. Almost all of them developed hepatitis. In some patients, the antigen appeared before the elevation of SGPT level. The prevalence of post‐transfusion hepatitis in the recipients of Au(1)‐positive blood was higher than in the recipients of Au(1)‐negative blood, and the difference was most significant between the groups who received less than five units of blood. The recipients who produced antibodies against the Au(1) antigen seemed less susceptible to the development of post‐transfusion hepatitis. Since the majority of recipients of Au(1)‐positive blood developed post‐transfusion hepatitis, the transfusion of Au(1)‐positive blood should be avoided. However, eliminating Au(1)‐positive blood evidently will not completely prevent the occurrence of post‐transfusion hepatitis. The need to develop more sensitive techniques than double diffusion in agar for detecting the antigen and to investigate other agents than the Au(1) antigen is discussed in order to establish a screening procedure of carriers of hepatitis virus.
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Okochi et al. (1970) studied this question.
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