Coexistent IgG2 and IgA deficiencies in blood donors.

BACKGROUND: To meet the transfusion requirements of IgA-deficient patients with anti-IgA, blood services screen random donors to identify potential donors of IgA-deficient blood components. New information reveals that some IgA-deficient persons may also be deficient in IgG2 and may be at increased risk for bacterial infections. STUDY DESIGN AND METHODS: Serum samples from IgA-deficient blood donors and patients were tested for IgG2 concentration by radial immunodiffusion using monospecific anti-IgG2. RESULTS: Four (9.0%) of 44 IgA-deficient blood donors and 14 (31.5%) of 44 IgA-deficient patients had coexistent IgG2 and IgA deficiencies. Follow-up interviews with the 4 donors who had coexistent IgG2 and IgA deficiencies revealed that 3 had recurrent respiratory infections and had been hospitalized at least once for pneumonia. The fourth donor did not report a history suggestive of recurrent infections. CONCLUSION: Some blood donors, recruited specifically because they are IgA deficient, may also be deficient in IgG2. Persons identified by donor screening programs as being IgA deficient should be tested for IgG2. If deficient in IgG2, they should be evaluated for a history of recurrent bacterial infections and counseled accordingly.

The r' gene is overrepresented in hrB-negative individuals.

A screening program was implemented to identify hrB- donors. D- C+, D-C-, and D+C- samples from African-American donors were typed with multiple examples of anti-hrB and anti-hrB-like, and one example each of anti-V and anti-VS. Of 75 D-C+ donors, 4 (5%) typed as hrB-, and 14 others had weak or variable expression of hrB. Of these 18 individuals, 15 were V-VS+, and 3 were V+VS+. No hrB- sample was found in 90 C- donors, 26 of whom were V+VS+, and 1 was V-VS+. A review of our records of 44 hrB- patients and donors studied earlier revealed that at least 12, and possibly as many as 30, carried r or rs. All hrB- donors found in our screening program had D-C+VS+ RBCs, indicating an overrepresentation of r. Our record review also showed that the presence of r and rs more often results in hrB- RBCs, and that the most effective way to screen for hrB- donors is to type African Americans who have D-C+ RBCs.

Correlation of monocyte monolayer assays and posttransfusion survival of Yt(a+) red cells in patients with anti-Yta.

Anti-Yta is an antibody to a high-frequency (99.8%) antigen and has been reported to have variable clinical significance. A retrospective review of monocyte monolayer assay (MMA) results on sera from 79 patients with anti-Yta was conducted to determine the reliability of this assay to predict the clinical significance of anti-Yta. Results of the MMA, other serological tests, and patient transfusion histories were analyzed. The MMA was found to be a reliable predictor of the clinical significance of anti-Yta when samples for analysis were collected at least six weeks after initial detection of the antibody. Only 18.2 percent of those examples of anti-Yta tested appeared to be clinically significant.

Laboratory tests to exclude IgA deficiency in the investigation of suspected anti-IgA transfusion reactions.

Four methods were compared as to their suitability for excluding IgA deficiency in the investigation of suspected anti-IgA transfusion reactions. The methods were radial immunodiffusion, passive hemagglutination inhibition, sandwich enzyme-linked immunosorbent assay, and membrane enzyme immunoassay. Parallel testing was performed on sera from 40 patients or blood donors previously found to have anti-IgA and low or undetectable levels of IgA. All test methods identified the 40 sera as having abnormally low IgA levels. The membrane enzyme immunoassay required 10 minutes or less for testing, as compared to 3 hours for passive hemagglutination inhibition, 4 hours for sandwich enzyme-linked immunosorbent assay, and 48 hours for radial immunodiffusion. The membrane enzyme immunoassay offers the potential for a rapid, instrument-free screen of IgA levels and therefore may be useful in identifying those patients with suspected anti-IgA anaphylactic transfusion reactions who are not IgA deficient and do not require IgA-deficient blood components for additional transfusions.

A weak B antigen with serologic reactivity between B1 and B2 red blood cells found in a Chinese family.

During a serologic study on red cell samples from individuals representing three generations of a Chinese family, an unusual pattern of reactivity was noted in a sample from a daughter of an A1B2 individual. The results of direct ABO grouping, titration, and adsorption studies demonstrated that the red blood cells (RBCs) from the proposita and two of the proposita's uncles (1) expressed more B antigen than group B2 RBCs but less than group B1 RBCs; (2) expressed the B1 antigen but at a lower level than group B1 RBCs; and (3) expressed more H antigen than B1 RBCs but slightly less than B2 RBCs. The saliva from the proposita contained soluble B and H antigens, and her serum contained a weak B-gene-specified transferase. Serologic reactivity of her RBCs was intermediate between that of B1 and B2, RBCs. That is similar to reactivity of Aint RBCs, which is intermediate between A, and A2 RBCs. The proposita may represent a Bint phenotype.

Absence of autoanti-Jk3 as a component of anti-dl.

Thirty-five examples of anti-dl, autoantibodies initially reacting with all red blood cells against which they were tested, were examined prior to, and following adsorption with Jk(a-b-) red blood cells. None of them was found to contain autoanti-Jk3. One example of autoanti-Jka was identified in an adsorbed eluate. The antibody had been produced by a pregnant Caucasian, in whom laboratory and clinical evaluation showed that the auto-antibody was benign in vivo.

The Redelberger antigen Rba.

A new low frequency antigen, Rba, has been found in three blood donors. Studies on their families show that the antigen is inherited as a Mendelian autosomal dominant character. Rba segregates independently from ABO, MNSs P1, Rh, Kell, Duffy, Kidd, ACP1 and PGM1. Anti-Rba is not common in sera containing multiple antibodies ot low frequency antigens.