HBsAg was determined quantitatively by radioimmunoassay and by Laurell electrophoresis in sera of 90 patients with acute hepatitis B, 57 patients with chronic hepatitis B, and 154 HBsAg positive blood donors. Of 55 patients with clearance of HBsAg from the circulation within six months, 54 (98%) showed an at least 50% reduction in concentration within 16 days. All 55 patients had such a decrease within 20 days. No such decrease was found in seven patients with acute hepatitis B who became HBsAg carriers. Therefore, quantitative HBsAg concentration in paired sera seems to be a reliable and early prognostic marker in acute hepatitis B. In patients with clearance of HBsAg most of the antigen is already present in the circulation at hospitalization and is eliminated with a mean half-life of 8.8 days. Patients with chronic hepatitis exhibit on average nearly the same HBsAg concentration (about 40,000 ng/ml) as patients with acute hepatitis B at hospitalization (about 39,000 ng/ml) and HBsAg positive blood donors on average a lower HBsAg concentration (about 8,000 ng/ml).

This case seems to be of interest because it is the first report of severe CA-induced hemolysis after rubella infection, it is the first description of an IgG lambda-monotypic CA, and, along with previous case reports (three established and three suspected cases), it indicates a relationship between rubella infection and the CA specificity anti-PR:

The donor history is not adequate for identifying potential donors with risk factors. Deliberately false statements concerning risk factors are a clear breach of trust between the blood bank and potential donors. These unreliable donors represent an incalculable risk for the transfusion recipient. Therefore, it is appropriate to validate donor statements about drug consumption by random hair and urine analyses and to exclude from the donor pool all persons revealed as drug users.

A solid-phase radioimmunoassay using anti-HBe-coated polysterence beads and iodine-125-labeled anti-HBe of human origin was developed for the detection of HBeAg. Anti-HBe could be determined by a blocking test. Both assays were about 500-fold more sensitive than immunodiffusion. Few nonspecific positive results for HBeAg could be recognized in the anti-HBe test by increase in cpm over that of the negative control. HBeAg was not found in acute hepatitis A and non A-non B hepatitis or in a control group of accident patients. On admission to the hospital 12 of 48 (25%) acute hepatitis B patients from Greece and 17 of 20 (85%) acute hepatitis B patients from Germany were HBeAg-positive. All 39 initially HBeAg negative sera were already anti-HBe positive. Tests of the acute stage and follow-up sera of the 20 German patients indicated that HBeAg is regularly present in the incubation period and early acute phase of hepatitis B. After onset of disease the antigen is cleared from the serum very rapidly in uncomplicated cases and is usually followed by the appearance of anti-HBe. Like anti-HBc, anti-HBe can serve as a tool for the diagnosis of hepatitis B after the disappearance of HBsAg.