A second example of anti-Esa, an antibody to a high-incidence Cromer antigen.

A blood sample contained an antibody to a high-incidence antigen that reacted with all red blood cells (RBCs) tested by the indirect antiglobulin test (IAT). The antibody reacted with papain-, ficin-, and trypsin-treated RBCs, but not with a-chymotrypsin-treated RBCs. This pattern of reactivity suggested the possibility that the antibody was recognizing an antigen in the Cromer blood group system. Tests against RBCs deficient in decay-accelerating factor (which carries the Cromer antigens) were weakly positive. Tests with antibodies to high-incidence Cromer antigens and with RBCs lacking high-incidence Cromer antigens led to identification of the second example of anti-Esa in an Es(a-) person. The antibody was IgG1 and reacted by the IAT to a titer of 64. The monocyte monolayer assay indicated potential clinical significance of this antibody in relation to transfusion.

An acute hemolytic transfusion reaction caused by an anti-P1 that reacted at 37 degrees C.

BACKGROUND: Hemolytic transfusion reactions (HTRs) due to anti-P1 have rarely been reported. There is only one report (from 1945) of an acute HTR due to anti-P1. CASE REPORT: A 74-year-old woman with anti-P1 was given blood that had been found to be compatible by the use of prewarmed serum and saline-suspended red cells (RBCs) and of an antiglobulin test with anti-IgG. The test mixtures were not centrifuged or inspected for agglutination after the 37 degrees C incubation phase. After transfusion of 50 mL of P1 + blood, the patient had an acute HTR (hemoglobinemia, hemoglobinuria, and increased blood pressure, temperature, and respiration). RESULTS: When studied by a reference laboratory, the anti-P1 was shown to be easily detectable (3+ agglutination) by a prewarming technique (saline or low-ionic-strength saline [LISS]), which included centrifugation at 37 degrees C, but only weak reactions were observed when centrifugation after 37 degrees C incubation was omitted. The indirect antiglobulin test was weakly positive (1+) with anti-IgG, but polyspecific anti-human globulin reacted 2+. The anti-P1 agglutinin was IgM, and its titer was 16 at 37 degrees C (prewarmed) and 256 at 23 degrees C; it caused hemolysis of RBCs at 37 degrees C under conditions known to enhance hemolysis. An indirect monocyte monolayer assay gave results of 11.2 and 22 percent in testing of P1 + RBCs incubated with the patient's serum alone and with patient's serum plus fresh normal serum (as a source of complement), respectively (normal < or = 3%). CONCLUSION: An acute HTR was caused by a hemolytic anti-P1 that reacted at 37 degrees C. This antibody was not detected by the hospital in a prewarmed crossmatch that omitted 1) the addition of LISS, 2) the reading for agglutination after the 37 degrees C incubation, and 3) the use of antiglobulin sera containing anti-complement.