Studies on the blood of a Co (a-b-) proposita and her family.

The serum of a pregnant woman whose red cells typed as Co(a-b-) contained an alloantibody that, at the time of the infants delivery, was hemolytic in vitro and had a titer of 32,000 by the antiglobulin test. This antibody, which reacted with cells of all Colton-phenotypes except the proposita's own cells, showed very weak reactions with other Co(a-b-) cells and therefore cannot be called anti-Co3. The red cells of the proposita may carry a very weak Co3 antigen. No other persons of the Co(a-b-) phenotype were found in her members, among three of the four generations tested, suggested that an inhibitor gene may be responsible for the unusual Colton phenotypes in this family. The proposita's infant required one exchange transfusion with red cells obtained from the proposita. Red cells from 40,000 donors reacted with the serum of the proposita.

Anti-Tcb, an antibody that defines a red cell antigen antithetical to Tca.

A patient's serum, used as a source of anti-Goa typing serum, was found to contain a second antibody that detected a 'new' red cell antigen present in approximately 5 percent of blacks, but not yet found in Caucasians. Among blacks, the 'new' antigen shows an antithetical relationship to the high frequency antigen Tca, as evidenced by tests on eight unrelated Tc(a-) black women and the families of two of these propositi. The antigen, designated Tcb, has not been found on the red cells of Tc(a-) persons whose racial origins differ from the propositi of this report, which suggests that more than one genetic mechanism can produce the Tc(a-) phenotype. The presence of both anti-Goa and anti-Tcb in the same serum appears to be a coincidental and unrelated finding.

Anti-Rh32 causing severe hemolytic disease of the newborn.

A case of severe hemolytic disease of the newborn due to anti-Rh32 (R = N) is described. The infant recovered without any evidence of neurologic defects, following one exchange transfusion and phototherapy. Using commercial antisera, very weak reactions with anti-Rh2(C) and apparently normal reactions with anti-Rh5(e) were found in the family members carrying the R = N gene complex. However titrations with individual antisera revealed a weakened expression of the Rh5(e) antigen, albeit to a lesser extent than the Rh2(C). It is felt that the serologic findings are due to the fact that the R = N haplotype was paired with an Rh gene carrying normal amounts of Rh4(c) and Rh5(e) antigens. In addition, the maternal anti-Rh32 appears to be pure.

Fatal hemolytic disease of a newborn due to anti-D in an Rh-positive Du variant mother.

This report presents an account of fatal hemolytic disease of the newborn (HDN) due to anti-D in a mother whose red cells showed the phenotypic characteristics of Rh positive Du variant. The proposita's third pregnancy was uneventful until the eighth month, when she presented with an unusually large abdomen. A sonogram showed fetal hydrops, and amniocentesis yielded a delta OD450 reading in Zone 3. Anti-D with a titer of 4096 was identified in the mother's serum. Following delivery by cesarean section, the premature infant did not respond to resuscitation. The autopsy findings were consistent with Rh erythroblastosis fetalis. The proposita has been classified as a Category VI Du variant with anti-D in her serum.