Investigation of two cases that died from fulminant hepatitis B and acute hepatitis B (severe type) following transfusion with HBsAg-negative blood by R-PHA.

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We experienced two cases that died from fulminant hepatitis B and acute hepatitis B (severe type) following transfusion with HBsAg-negative blood examined by R-PHA. The results of R-PHA examination of the donor blood retrospectively showed that all of the containers of preserved blood were HBsAg-negative, but that one container for patient transfusion used in case 1 was HBsAg- positive, having a cut-off index of 5.58 as examined by RIA, and that that of the other used to transfuse case 2 had a cut-off index of 2.93 in HBsAg value. Both donor bloods had a high titer of anti-HBc as examined by IAHA and had a negative HBeAg and positive anti-HBe as revealed by RIA. Therefore, both of these bloods were considered to have caused the resulting type-B post-transfusion hepatitis. Furthermore, HBeAg was not recognized through the clinical course in both cases following post- transfusion hepatitis. Thus, the sequence of the precore region on HBV-DNA was analyzed for the transfused bloods causing the type-B post-transfusion hepatitis and for the patients' sera of both cases. As a result, all of the obtained HBV are HBV mutants that were found to be defective in the precore region of the HBV genome and to be incapable of encoding HBe antigen. Moreover, it was clear in one case that the sequence of the precore region on HBV-DNA from this patient corresponded well with that from the blood donor. Specifically revealed was a point mutation from guanine to adenine at nucleotide 83 in the precore region of HBV-DNA, converting codon 28 for tryptophan (TGG) to a stop codon (TAG).

Investigation of two cases that died from fulminant hepatitis B and acute hepatitis B (severe type) following transfusion with HBsAg-negative blood by R-PHA.

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