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Delayed hemolytic transfusion reactions occur via an anamnestic immune response in patients previously alloimmunized by certain RBC antigens. Conventional pretransfusion antibody screening tests and crossmatches are unable to detect certain antibodies that potentially can cause these reactions because they may be present in low concentrations or have low affinity for their respective antigen or their indicator antigen may be absent from test RBCs. We report the second case of a delayed hemolytic transfusion reaction caused by an undetectable (by routine methods) anti-Js(a) in a patient with a sickle cell syndrome (hemoglobin SC disease) and multiple alloantibodies, in whom retrospective indirect antiglobulin tests enhanced by polyethylene glycol revealed the presence of weakly reactive anti-Js(a).

Null types of 12 human erythrocyte blood groups are reviewed. They have helped in identifying new antigens and defining the various genetically-distinct systems. They are very valuable in identifying the antibodies in alloimmunized people and in transfusion therapy of some of these people. Fy(a-b-) erythrocytes resist invasion by malarial parasites. At least two (Rh null and the McLeod type) are responsible for congenital hemolytic disorders. Testing for K15(Kx) on neutrophils appears to be diagnostic for chronic granulomatous disease of the sex-linked recessive type.

Low-ionic-strength solution (LISS) reagents and methodologies have become popular in recent years in hospital transfusion service laboratories for alloantibody detection and compatibility testing of blood recipients. It has been the experience with all other hemagglutination technics that some examples of alloantibodies unpredictably fail to react. Such is the case with this patient's alloantibody with respect to LISS. The patient had a significant hemolytic transfusion reaction due to Kell incompatibility of one unit of packed human erythrocytes. Using various LISS reagents and methodologies, the anti-Kell was undetectable in pretransfusion and posttransfusion samples through the fifth day. The anti-Kell was of immunoglobulin class IgG, and it was detected in saline solution or albumin at room temperature, at 37 C and by the antiglobulin technic.

Kell null red blood cell samples can be prepared using 2-aminoethylisothiouronium bromide (AET). This article describes a modification whereby only three drops of a 5% red blood cell suspension may be AET treated. This procedure has been used routinely in the authors' laboratory for more than a year. One patient's serum contained anti-Kpb plus anti-C and anti-D. Tests with panel cells pretreated with AET made it possible to identify underlying Rh antibodies without using a panel of genetic Kpb negative red blood cells. Of 24 red blood cell eluates from patient sample with warm autoantibodies, one had specificity within the Kell blood group system. This small volume AET-treatment method is a quick screen for the differentiation of a Kell-related specificity from a non-Kell specificity of both warm autoantibodies and alloantibodies to high-incidence antigens.

When the ionic strength of blood samples is reduced, blood group antibodies bind to red blood cells that lack the corresponding antigen. Upon normalization of the ionic strength, the antibodies elute into the supernatant fluid. We compared, in semiquantitative terms, this nonspecific and reversible binding of various blood group antibodies. Studies with anti-CD antibodies showed that the nonspecific binding increased when the ionic strength was progressively lowered. In 1/10 normal ionic strength, practically all of a high-titer anti-CD antibody bound to Rh(D)-negative RBC (phenotype ce). The majority of the other antibodies studied (anti-C, -c, -Fya, -Fyb, and -S) behaved similarly in 1/10 normal ionic strength, but the binding of some (anti-E, -s, and -Jka) was, at times, less complete. Most examples of anti-K antibodies, however, demonstrated very poor nonspecific binding to K-negative RBC in low ionic strength (LIS). The authors propose that the augmentation of specific blood group antibody reactions in LIS is the direct result of this nonspecific binding, and that the failure of these conditions to support the nonspecific binding of anti-K antibodies might explain the lack of augmentation (and, at times, even the impairment) of the reactions of anti-K with its antigen.

Blood groups (ABO, Rh, MNSs, Kell, Duffy, and Kidd) and HLA markers were tested in cases involving 563 children of disputed parentage. In 149 (26.5%) cases, the accused men were excluded as the biologic fathers of the children in question. One hundred forty of the 149 exclusions were direct exclusions. Five exclusions were based on red blood cell data alone, i.e., HLA was non-exclusionary. Of the remaining 414 cases in which the alleged father could not be excluded as the biologic father, in 361 (87.2%) instances, the plausibility of paternity ws 95% or greater, and in 385 (93.0%) instances the comparison of men value was 20 or greater. Caucasians, blacks, and men of other races were involved in 367 (65.1%), 185 (33%), and 11 (1.9%) cases, respectively. No significant difference among races was observed in the rate of exclusion of accused men. However, of the non-excluded men, in a significantly greater proportion of black men than white men, the plausibility of paternity was below 95%. The difference was probably due to lower polymorphism of the markers tested in blacks than in whites. It is suggested that tests for additional polymorphic genes be directed towards the 12-15% of the nonexclusionary cases with plausibility of paternity values below 95%.