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.
Hemolytic anemia occurred in a 70-year-old female after a five-day course of intravenous cefamandole. The patient's serum contained an IgG antibody which was reactive with red blood cells which had been coated in vitro with cefamandole but not with uncoated cells. An in vitro assay of allogeneic mononuclear phagocytosis of cefamandole-coated red cells sensitized with the patient's anti-cefamandole indicated that the anti-cefamandole could induce significant phagocytosis. The anti-cefamandole was easily inhibited in vitro by cefamandole as well as by a variety of related cephalosporins indicating broad cross-reactivity, with the antigenic site primarily the 7-amino-cephalosporanic acid nucleus. Penicillins could inhibit the anti-cefamandole but only when using concentrations 3-10 X those of cephalosporins. Eleven examples of anti-penicillin tested failed to react with cefamandole-coated red cells. Screening of 344 random sera from hospitalized patients found only five (1.5%) reactive with cefamandole-coated red cells; three of these sera were also reactive with penicillin-coated red cells. The patient's hemolysis subsided following cessation of the drug. This is the first report of anti-cefamandole-induced hemolytic anemia.
Intravascular hemolysis due to passive transfer of anti-A or anti-B has been a frequently reported transfusion complication. In most reported cases, passive anti-A has been implicated. However, cases of hemolysis due to anti-B have also been reported following administration of intravenous immunoglobulin (IVIG) and during platelet transfusions. In our case, a 6-day-old infant with E. coli sepsis underwent double-volume exchange transfusion for hyperbilirubinemia. Modified whole blood used during the exchange consisted first of one unit of group B, D+, AS-1 packed red blood cells (RBCs), resuspended in group AB fresh frozen plasma (FFP). followed by one unit of group O, D–, CPDA-1 RJBCs resuspended in group AB FFP. During the second infusion, the infant displayed an increase in temperature and hemoglobinuria, characteristics consistent with an acute intravascular hemolytic transfusion reaction. Clerical errors and hemolysis due to polyagglutinable infant RBCs were ruled out. Further laboratory investigation revealed the presence of an anti-B antibody coating the infant’s RBCs. Follow-up testing of the O, D– donor serum revealed an anti-B titer of 16,384 (saline) and >64,000 with monospecific anti-lgG. A second uneventful double exchange was performed using washed group O, D– RBCs resuspended in 5 percent albumin. Immunohematology 1995; 11:43–45.
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