This study was undertaken to document the incidence of immediate, nonhemolytic transfusion reactions and to identify a technique or set of techniques that would best identify the different causes of these reactions. A variety of tests were employed to detect lymphocyte, granulocyte, platelet and anti-IgA antibodies. During this study 26,318 units of blood components were transfused on 5,030 occasions. 191 immediate, nonhemolytic reactions were experienced giving an incidence per unit of 0.73%. Blood specimens from 101 of these patients were investigated along with serum from 57 patients who showed no reaction to transfusion as controls. We show that standard B cell lymphocytotoxicity testing is the technique with which most antibodies can be detected (64% of reactors positive vs. 30% of controls, p< 0.001). Additional tests did not significantly increase the level of antibody detection.

To enable the detection of IgG class, anti-IgA antibodies (IgG-aIgA) and to investigate the possible occurrence of IgE class, anti-IgA antibodies (IgE-aIgA), we developed a solid phase immunoradiometric assay (IRA), which uses purified IgA coupled covalently to microcrystalline cellulose as an immunosorbent. Radiolabeled, Fc specific anti-IgG and anti-IgE antibodies were used to detect specific aIgA after incubation of test sera or controls with the immunosorbent. IgG-aIgA were detected by the IRA in 100 and 67 per cent of control sera with class specific and limited specificity aIgA. The IRA was sensitive to approximately two ng of class specific IgG-aIgA. IgG-aIgA also were detected by IRA in 7.9 per cent of sera from patients with urticarial transfusion reactions and 73 per cent of sera from patients with ataxia telangiectasia and IgA deficiency. Sera from 50 normal blood donors did not have detectable IgG-aIgA. Tests for IgE-aIgA were negative in all cases, including control sera with class specific IgG-aIgA. We conclude that the IRA is a sensitive and reproducible method for detection of class specific and limited specificity IgG-aIgA, and that IgE-aIgA do not mediate urticarial transfusion reactions.

Monitoring of donors with selective IgA deficiency, i.e., with less than 0.5 mg IgA/l, led to the observation that serum IgA levels wer not constant. Small but significant fluctuations in IgA levels were noted (coefficient of variance: 143%) which were greater than the variability inherent in the testing methodology (coefficient of variance: 10%). These fluctuations created difficulties in terms of defining IgA-deficient blood products and had implications with respect to the mechanisms involved in IgA deficiency. With respect to supplying IgA-deficient blood products, in our experience a cutoff level of 0.5 mg/l should be the maximum permissible IgA concentration in order to ensure that no adverse reactions occur in individuals with class-specific anti-IgA.

This study was undertaken to document the incidence of immediate, nonhemolytic transfusion reactions and to identify a technique or set of techniques that would best identify the different causes of these reactions. A variety of tests were employed to detect lymphocyte, granulocyte, platelet and anti-IgA antibodies. During this study 26,318 units of blood components were transfused on 5,030 occasions. 191 immediate, nonhemolytic reactions were experienced giving an incidence per unit of 0.73%. Blood specimens from 101 of these patients were investigated along with serum from 57 patients who showed no reaction to transfusion as controls. We show that standard B cell lymphocytotoxicity testing is the technique with which most antibodies can be detected (64% of reactors positive vs. 30% of controls, p less than 0.001). Additional tests did not significantly increase the level of antibody detection.