Investigating anti-D in an individual with the weak D type 2 genotype.

Anti-D in individuals with a weak D phenotype is an unexpected finding that may require additional investigation to determine whether the anti-D is an autoantibody or alloantibody. Further investigation may also include assessment of the patient's RHD genotype and exclusion of anti-G. We present a case of an 84-year-old man with the weak D type 2 genotype who developed an unexpected anti-D along with anti-C. Individuals with the weak D type 2 genotype are thought not to be at risk for developing alloanti-D, although the distinction between alloanti-D and autoanti-D may be difficult to ascertain. Furthermore, investigations may affect transfusion recommendations. This patient was restricted to crossmatch-compatible, D-C- red blood cells even though the clinical significance of the anti-D was uncertain. This report is one of a few reported cases of an individual with the weak D type 2 genotype with demonstrable anti-D but without evidence for alloanti-D.

Four examples of anti-TSEN and three of TSEN-positive erythrocytes.

BACKGROUND: TSEN (MNS33) is a low-incidence antigen in the MNS blood group system encoded by hybrid glycophorin genes. TSEN is expressed by a unique amino acid sequence that results from the junction of GPA(58) to GPB(27), if the GPB carries S antigen. Until this study, only one example of anti-TSEN had been found. Antibody screening red blood cells (RBCs) positive for both S and s (ref. No. C873) reacted with four patient sera. Initially, the RBCs had been typed as S+s+, but later were typed as S-s+ in another laboratory. Two other RBC samples, one from a volunteer blood donor (D.L.), the other from a patient whose serum contained anti-En(a)FR (J.S.), also gave anomalous results when tested with anti-S. We suspected the presence of TSEN-positive hybrids on all three RBC samples. MATERIALS AND METHODS: Reactive sera (O.B., E.C., S.K., R.F.) were tested against RBCs with normal MNS phenotypes and with TSEN-positive RBCs. The RBCs of D.L., J.S. and C873 were tested with anti-S whose reactivity with S+s+ TSEN+ RBCs had been established previously, and with the original example of anti-TSEN. Immunoblotting was performed on the C873, D.L. and J.S. RBC membranes using a monoclonal antibody to an epitope common to both glycophorin A and glycophorin B. RESULTS: The sera from O.B., E.C., S.K. and R.F. were strongly reactive on the indirect antiglobulin test with TSEN+ RBCs. The RBCs of C873, D.L. and J.S. were typed as TSEN+. Immunoblotting pattern of D.L. and C873 were consistent with TSEN heterozygotes, while that of J.S. was consistent with a TSEN homozygote. CONCLUSIONS: Based on the estimated number of screening events with C873 RBCs, the incidence of anti-TSEN is approximately 1 in 20,000 sera. The antibody is found in patients with and without documented exposure to allogeneic RBCs. All known examples of anti-TSEN are IgG, but their clinical significance is not known.

Fatal hemolytic transfusion reaction resulting from ABO mistyping of a patient with acquired B antigen detectable only by some monoclonal anti-B reagents.

BACKGROUND: Some monoclonal anti-B reagents are prepared exclusively from an anti-B clone, ES4, that is known to detect acquired B antigens that are not detectable by other anti-B clones or polyclonal anti-B reagents. CASE REPORT: A 92-year-old group A, Rh-negative man with diverticulitis was mistyped as group AB with the use of a monoclonal anti-B. The hospital did not detect anti-B in the patient's serum. After a negative antibody screen, blood was issued through an abbreviated crossmatch (i.e., immediate-spin crossmatch). The patient was given 3 units of group AB blood and 1 unit of group A blood, and no problems were reported. After the transfusion of a ¿fourth unit of AB blood the patient had a severe hemolytic transfusion reaction which resulted in kidney failure and death 10 days later. After the transfusion reaction, the patient's pretransfusion red cells were found to be group A with an acquired B antigen. The monoclonal anti-B used the hospital was formulated from the ES4 clone. A sample of the patient's serum taken before the transfusion was later found to contain a weak anti-B, detectable most obviously by the antiglobulin test, which was not performed at the crossmatch stage. The manufacturers of monoclonal anti-B reagents prepared from ES4 have since modified their reagents (i.e., lowered the pH) so that they now detect only the strongest examples of acquired B antigen. CONCLUSION: A fatal hemolytic transfusion reaction resulted because a monoclonal anti-B that detected acquired B antigen was used to type red cells from an elderly man whose serum had weak anti-B that was not detected by abbreviated compatibility testing.