Search

Three patients with acquired-B antigens are reported whose red blood cells also manifested T- and Tk-activation. The results of tests using purified Arachis hypogaea and Bandeiraea simplicifolia (BS II) lectins, and red blood cells either T, Tk or both T and Tk-activated by bacterial enzymes in vitro, suggest that the acquired-B phenomenon, T-activation and Tk-activation result from the action of different bacterial enzymes.

Three group O sera manifesting prozone in reverse ABO tests are reported. All were implicated in erroneous blood typing results. One sample failed to react with A1 red cells (RBCs) in immediate-spin (IS) tests, had anti-A and -B titers of 8192 and 2048, respectively, by indirect antiglobulin technique (IAT), and was from a diabetic patient; the parenteral administration of A substance present in porcine insulin is a possible cause of hyperimmunity in this case. The second sample was from the recipient of a single unit of group B fresh-frozen plasma; the serum anti-A and -B titers were 10,240 by IAT, but only weak reactions with A1 and B RBCs were noted in routine IS reverse typing tests; the hyperimmunity in the patient concerned was likely due to crossreacting anti-A, B stimulated by B-active glycoproteins and/or glycolipids in the transfused plasma. The third serum also had anti-A and anti-B IAT titers of 10,240 but did not react with A1 and B RBCs by IS; the hyperimmunity in this case may be related to sepsis from intestinal flora carrying A- and/or B-like antigens. These antibodies lysed A1 and/or B RBCs in tests incubated at room temperature (RT) and strongly agglutinated those RBCs by IS when diluted 10-fold with saline. The absence of the prozone phenomenon in tests with RBCs suspended in diluents containing EDTA is consistent with the previously published mechanism for anti-A prozone: namely, the steric hindrance of agglutination by the C1 component of human complement.(ABSTRACT TRUNCATED AT 250 WORDS)

The detection of anti-A and anti-B isohemagglutinins by low-ionic-strength saline tests at 37 degrees C and by the indirect antiglobulin technique, without an "immediate'spin" or room-temperature phase, has been studied. Using such a procedure, all but one of 2746 patient blood samples reacted in accordance with ABO type when tested against A2 and B red cells. However, the discrepant sample also was nonreactive when tested by "immediate-spin" technique against saline-suspended A2 red cells. Our findings indicate that compatibility tests performed at 37 degrees C in low-ionic-strength saline are as sensitive as "immediate-spin" tests with saline-suspended red cells for the detection of ABO errors. Performing serologic tests for unexpected alloantibodies and donor-recipient compatibility without an "immediate-spin" or room-temperature phase abbreviates pretransfusion testing and reduces the detection of clinically insignificant alloantibodies solely reactive at room temperature.