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W J Judd

Publications and source records attributed to W J Judd.

90 records · Page 5Linked to original sources

Chloroquine dissociation of antigen-antibody complexes. A new technique for typing red blood cells with a positive direct antiglobulin test.

We have investigated a method using the quinoline derivative chloroquine diphosphate (200 mg/ml, pH 5.0) to dissociate antibody without denaturing red blood cell antigens. All samples treated with chloroquine diphosphate demonstrated some dissociation of the coating immunoglobulin, and in most cases, the ability to dissociate the coating immunoglobulin was related to the strength of the direct antiglobulin test (DAT). Complete dissociation of antibody was observed in 22 of 40 strongly in vitro sensitized samples and 47 of 56 in vivo sensitized specimens, with no apparent loss of ABH, Rh, MNSs, P1, Lewis, Kell, Duffy, or Kidd antigens. We have found the chloroquine dissociation technique to be of value in the examination of red blood cells with a positive DAT, either for the qualitative or quantitative expression of antigens.

ABO Blood-Group System↗

Autoagglutinins with apparent anti-P specificity reactive only by low-ionic-strength salt techniques.

Two blood samples containing autoagglutinins reactive in room temperature tests using low-ionic strength salt (LISS) reagents, but not by conventional saline-albumin or enzyme tests, are reported. The anti-P specificity of both sera, when tested near or diluted in group AB serum, was evident by their failure to agglutinate LISS-suspended Tj(a-),(p), and P1 red blood cells. However, one of the two samples displayed no anti-P specificity when diluted in LISS solution as opposed to group AB serum. Some urine samples inhibited this latter serum. Inhibition did not correlate with urinary Sda antigen content, nor with pH, Na+, K+, C1-, or osmolality levels. However, there was some correlation between inhibition and urinary conductivity levels. Moreover, partial inhibition was observed in tests with globoside. While there are no data to indicate that these LISS-dependent autoagglutinins are of clinical consequence in vivo, it is likely that they represent low-affinity autoantibodies reacting only in a low-ionic environment. They establish a further cause of anomalous serologic reactions associated with LISS techniques.

Adolescent↗

A 'new' high frequency antigen Era.

Three examples of an antibody defining a 'new' high frequency red blood cell antigen, Era, are described. Family studies show Era to be inherited, but the mode of inheritance may not be straightforward.

Blood Group Antigens↗

Studies on the blood of an MiV/Mk proposita and her family.

An individual (J-1) was shown to be heterozygous for the MiV and Mk genes. Her red cells typed as M+(weak), N-, S-, s+(strong), U+, Hil+, Wr(a-b-), En(a+weak). Polyacrylamide gel electrophoresis analysis of her red cell membranes revealed absence of PAS-staining bands corresponding to normal MN and Ss sialoglycoprotein (SGP), and presence of a hybrid MNSs SGP [(alpha-delta)MiV] similar but not identical to that reported for an MiV homozygote. However, J-1 cannot be homozygous for MiV since the red cells of two of her children are Hil- and s-, carry only a single dose of M antigen, and have a sialic acid content that is consistent with the presumption that they are Mk heterozygotes. J-1's hybrid MNSs SGP is considered to be gene-fusion product resulting from unequal crossover between a normal alpha M and delta gene, and her red cells lack that portion of the Ena antigen that is resistant to ficin. Her hybrid MNSs SGP differs, therefore, from that reported for the MiV homozygote, which probably arose from unequal crossover between alpha N and delta genes. Further, the red cells of the MiV homozygote carry the ficin-resistant Ena determinant.

Aged↗

Is a room-temperature crossmatch necessary for the detection of ABO errors?

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.

ABO Blood-Group System↗

Studies on the blood of an MsHe/MSu proposita and her family. Serological evidence that Henshaw-producing genes do not code for the 'N' antigen.

The serum of a black woman has been found to contain a potent alloanti-N that reacted in direct agglutination tests with the 'N' antigen carried on Ss-active sialoglycoprotein. Thus far, such antibodies have been observed only in the sera of MSu/MSu individuals. However, our proposita had red cells that lacked 'N'. Her blood type was M+, N-, S-, s+, U+, He+. Results of family studies indicate that she is of the genotype MsHe/MSu. Our findings are consistent with recently reported data on the structure of the Henshaw antigen, which is located on a Ss-active sialoglycoprotein that does not carry 'N'.

Blood Group Incompatibility↗

The evaluation of a positive direct antiglobulin test (autocontrol) in pretransfusion testing revisited.

Direct antiglobulin tests (DATs) using anti-IgG were performed on 65,049 blood samples from prospective transfusion recipients; 3570 tests (5.49%) were positive. Using criteria published previously (primarily excluding patients not transfused within the preceding 14 days), 778 samples from other than neonatal patients were selected for further evaluation. Eluates that did not react were obtained on 518 (66.6%) of these samples. Warm-reactive autoantibodies were apparent in 192 eluates, while 16 contained drug-related antibodies, anti-A or anti-B from prior transfusion with ABO mismatched blood components, or anti-D passively acquired from immune serum globulin. Fifty-two eluates contained alloantibodies; however, in only six of these cases did the corresponding serum lack unexpected alloantibodies, as determined by routine pretransfusion studies. Three additional weakly reactive clinically significant alloantibodies were detected solely through additional serum tests performed on DAT-positive samples. On the basis of these findings, the DAT had a low predictive value when used to detect the early manifestations of an immune response to recently transfused red cells. Elimination of the autocontrol from routine pretransfusion testing, therefore, carries minimal risk to patients yet will undoubtedly contribute to the containment of health care costs. Moreover, the risk is lower than that associated with the elimination of the antiglobulin crossmatch.

Antibody Specificity↗

Donath-Landsteiner hemolytic anemia due to an anti-Pr-like biphasic hemolysin.

Anemia, hyperbilirubinemia, and reticulocytosis subsequent to viral infection were present in a 32-year-old woman. The direct antiglobulin test was negative, and no unexpected antibodies were detected in pretransfusion tests. Rosettes of red cells (RBCs) around neutrophils were observed in peripheral blood smears, and a Donath-Landsteiner (D-L) test was positive. However, the patient did not show the classic features of paroxysmal cold hemoglobinuria (PCH). There was no hemoglobinuria, and in vivo hemolysis was not precipitated by cold. The D-L antibody was IgG, but classic anti-P specificity was not apparent. Rather, protease- or neuraminidase-treated RBCs, as well as certain sialic acid deficient RBCs of uncommon MN phenotypes, were not hemolyzed in D-L tests. Further, D-L antibody activity could be inhibited by MN sialoglycoprotein. These data support a diagnosis of chronic D-L hemolytic anemia, caused by an anti-Pr-like biphasic hemolysin.

Adult↗

Discrepancies in reverse ABO typing due to prozone. How safe is the immediate-spin crossmatch?

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)

ABO Blood-Group System↗

False-positive results with chemically modified anti-D do not indicate a need to use a separate, immunologically inert Rh control reagent.

Thirteen of 1450 (0.9%) Rh-negative samples submitted for pretransfusion or prenatal testing gave weak false-positive reactions in immediate-spin (IS) tests with chemically modified anti-D (CM-D). Only seven reacted in control tests with anti-A and/or -B. The other six samples could have been considered Rh positive; however, such a conclusion is inappropriate, since stronger (greater than or equal to 3+) reactions are expected in IS tests with CM-D and the vast majority of true Rh-positive blood samples. Moreover, three of the six false-positive CM-D reactions associated with negative control tests were from patients previously found to be Rh negative. The other three samples gave 1+ to 2+ reactions with CM-D and did not react with anti-A and/or -B; these erroneous CM-D reactions were recognized by confirmatory tests with high-protein anti-D and Rh control reagents that were performed because previous typing results were not on file. Such confirmation, as well as careful grading and proper interpretation of serologic reactions, serves to prevent erroneous Rh typing without the use of a separate, immunologically inert Rh control reagent.

Blood Grouping and Crossmatching↗

Anti-i causing acute hemolysis following a negative immediate-spin crossmatch.

A unique case of acute hemolysis following transfusion of red cells (RBCs) that were found compatible by immediate-spin (IS) crossmatch technique is reported. Screening tests for unexpected antibodies, using low-ionic-strength saline (LISS), 10 minutes' incubation at 37 degrees C, and anti-IgG, were nonreactive; however, 1 transfused unit was found crossmatch incompatible by indirect antiglobulin technique (IAT). An anti-i (titer 512 at 4 degrees C) that was not an autoantibody was identified in the patient's serum. Unlike the incriminated donor RBCs, most I+ RBCs did not react by LISS-IAT. Variable reactivity was seen with ficin-treated I+ RBCs, and there was marked hemolysis of iadult and icord RBCs. In marked contrast, dominant Lu(a-b-) RBCs, with reduced expression of i, did not react by any test method; nor did autologous I+, Lu(b+) RBCs. The in vivo clinical significance of this anti-i was confirmed by monocyte monolayer assay and RBC survival studies. The patient's i antigen may have been altered, by either chemotherapy or disease, and lacked part of the i antigen-mosaic. Her antibody was directed at epitopes of i that were absent from her RBCs. Those i epitopes missing from her RBCs are also absent on dominant Lu(a-b-) RBCs. This anti-i represents a unique cause of an acute hemolytic transfusion reaction. It also represents a case of acute immune-mediated hemolysis following transfusion of IS crossmatch-compatible blood when screening tests for unexpected antibodies are nonreactive. Because of the rarity of such cases (less than 1/200,000 RBC units transfused), modifications to pretransfusion testing protocols are not proposed.

Blood Grouping and Crossmatching↗