Detection of circulating T-activating enzyme in the serum of a patient having hemolytic-uremic syndrome and disseminated intravascular coagulation.

A three-and-a-half-year old boy suffering from streptococcal pneumonia developed hemolytic-uremic syndrome and disseminated intravascular coagulation (DIC). His red blood cells (RBC) were shown to be T- and Tk-activated; serial testing showed his mature RBCs as well as neocytes remained T-activated at 40 days. Anti-T was detected in his serum, with only one of two T-activated RBC samples. T-activating enzyme was shown to be present in his serum.

A case report: anti-Pr as a cause of blond typing discrepancies:.

Anti-Pr in the blood of an 83-year-old male patient caused discrepant ABO and Rh typing results. The antibody had a titer of 32,000 with adult red cells and 16,000 with cord red cells at room temperature; there was a prozone in teh first two tubes of the titration. The patient's hemogloblin level dropped from 12.2 g/dl to 9.4 g/dl during his eight-day course of hospitalization.

Control of the antigen-antibody ratio in antibody detection/compatibility tests.

An evaluation was made of the variation and importance of dropper volume delivery on pretransfusion testing in ten hospital transfusion services which annually perform a combined total of 225,000 compatibility tests on the serum of approximately 70,000 patients. The pretransfusion testing by these institutions typifies practices throughout the United States in that serum and red blood cells are used with little awareness of actual volumes used and the resultant proportion of one reactant to the other. Tests of the hospitals' dropper pipettes showed a range of serum delivery per test of 0.0465 to 0.1155 ml. Commercial reagent red blood cell vial droppers delivered (according to cell concentration) from 0.00166 to 0.00294 ml packed red blood cells (pcv). From these findings, it could be shown that the serum to cell ratio in the tests done in two transfusion services was as low as 19 to 1 and that the highest ratio of 70 to 1 was used in only one institution. In none was the serum-cell ratio the optimum of 80 to 1.

A Ge-like autoantibody in the serum of a patient receiving gold therapy for rheumatoid arthritis.

A 61-year-old nulliparous woman who had never been transfused was admitted to the hospital because of severe anemia. She had been treated with gold salts for 4.5 years for rheumatoid arthritis. Because she had a negative direct antiglobulin test, an anti-Ge found in her serum was believed to be an alloantibody. Subsequent testing of her initial serum sample with autologous red cells drawn 12 months later showed them to be strongly agglutinated, indicating that she had had a transient depression of her Ge antigen and that the anti-Ge was an autoantibody. It was postulated that these transient effects may have been related to the gold therapy.

Broadening the base of a rare donor program by targeting minority populations.

Some red cell phenotypes are found exclusively in one race and may be of low frequency. Finding compatible blood for patients needing one of these rare types has been extremely difficult. A program was implemented to screen large numbers of donors for blood types found solely in their racial group. Implementation steps included obtaining broad community endorsement of the concept, educating blood service personnel, developing educational materials, enlisting the support of a knowledgeable physician from a minority group, developing a computer program to facilitate selection of donors to be tested, beginning the program and making the necessary adjustments, doing the laboratory testing to identify rare bloods, notifying the rare donors, and maintaining the enthusiasm of the entire blood service for the rare donor screening program. After 7706 black donors were typed, 1 Cr-, 5 Hy-, 24 U-, and 20 Js(b-) persons were found; one U- donor was also Js(b-).

A case report of a hemolytic transfusion reaction caused by anti-Holley.

Clinical and laboratory investigation of a black male patient, who received emergency transfusion of blood incompatible for a high incidence antigen, provided evidence for the pathogenetic importance of high titer anti-Holley antibodies with poor avidity. The red blood cells of the patient and two siblings were remarkable in being negative for two high incidence antigens, Hy and hrS, and weak for a third, Gy.

rG. Potential pitfall in parentage testing.

Extensive studies were done on the family of an infant investigated for possible hemolytic disease of the newborn (HDN). Fourteen members in four generations were shown to carry the rG gene with r, R1 or R2. If testing had not included anti-CD(G) serum, three false exclusions of paternity and four of maternity might have resulted in this large Caucasian family. The findings also demonstrated that titration of Rh antisera against the red cells of family members could not be relied upon to assess zygosity or dosage.

Frequency of alloantibodies accompanying autoantibodies.

Blood samples of 109 patients with warm autoantibodies were evaluated for the presence of accompanying alloantibody. Clinically significant alloantibodies were present in 41, or 38 percent, of the cases.

Erb, an allele to Era, and evidence for a third allele, Er.

An antibody against a low-incidence antigen was detected in the serum of a woman whose newborn infant was found to have a positive direct antiglobulin test. The antibody failed to agglutinate 79 examples of red cells having low-incidence antigens and 16 examples of high-incidence antigen-negative red cells. The woman's serum reacted strongly with her husband's red cells in the antiglobulin test and with 5 of 6 Er(a-) cell samples from unrelated donors, suggesting that the antigen has an antithetical relationship to Era. The failure of the serum to react with one Er(a-) cell sample and with cells from the Er(a+) daughter of an Er(a-b+) mother gives evidence for a silent allele, Er. Four Er(b+) bloods were found among 605 random white donors, indicating a gene frequency for Erb of 0.0033.

Transient reduction in erythrocyte membrane sialoglycoprotein beta associated with the presence of elliptocytes.

Erythrocyte membranes from an anaemic patient receiving gold therapy for rheumatoid arthritis had reduced beta-sialoglycoprotein (beta-SGP) content but normal expression of sialoglycoproteins alpha, delta and gamma. Elliptocytes were present in the peripheral blood. The serum of the patient contained anti-beta-SGP which did not appear to bind to her own cells. It reacted with all erythrocytes apart from beta-SGP deficient Leach phenotype cells. The antibody was inhibited by purified beta-SGP from normal red cells, bound to beta-SGP on immunoblots and also reacted with the abnormal beta-related-SGP in erythrocyte membranes of both the Gerbich type and Yus type of Gerbich negative. Two years later the patient was no longer anaemic, no elliptocytes were seen in her peripheral blood film and her erythrocyte membranes had normal beta-SGP content. Antibody was no longer present in her serum and antibody from the earlier sample now reacted with the patient's erythrocytes. Erythrocyte membrane beta-SGP is known to be important in the maintenance of normal cell shape. It is likely that the transient occurrence of elliptocytes in the patient resulted from the concurrent temporary reduction in beta-SGP content of her erythrocyte membranes.

Chloramphenicol antibody causing interference in antibody detection and identification tests.

Investigation of the serum of three patients with positive antibody detection tests demonstrated the cause in each to be an antibody against chloramphenicol, a bacteriostatic agent used in commercial red blood cell reagents. Washing of these red cells prior to use prevented agglutination. All three examples of anti-chloramphenicol antibody were IgM and were in low titer when tested at room temperature and 37 C in saline. Two of the antibodies bound complement. The possibility of an antibody to an ingredient of the commercial preservative solution should be considered if problems are encountered in tests with unwashed commercial red blood cell reagents.

Variant of type B blood in an El Salvador family. Expression of a variant B gene enhanced by the presence of an A2 gene.

A variant of type B blood was found in three members of a family from El Salvador. In two members, both genotype BO, the blood and saliva had the characteristics of the phenotype Be1 . In the third member, genotype A2B, the red cell B antigen was stronger than in his BO genotype relatives. Thus, in this family, the presence of the A2 gene appeared to enhance the expression of the B gene.

The Kmod blood group phenotype in a healthy individual.

This report describes a healthy blood donor whose red cells have weakened expression of Kell blood group antigens. Kell antigen activity could not be detected by flow cytometric analysis and was demonstrable only by sensitive serologic techniques. As with normal-strength Kell antigens, reactivity could be abolished by treatment with 2-aminoethylisothiouronium bromide (AET). The donor's red cells have Kx antigen activity. Other commonly tested blood group antigens (MNSs, Rh, P1, Lewis, Duffy, and Kidd systems) appear normal. Clinical and serologic examination showed that this case is different from previously described examples of modified Kell expression. The propositus's phenotype has remained unchanged for 19 months, which suggests that it is not a transient condition. However, family studies provide no evidence that it is inherited. A 93-kD protein, which reacted weakly by Western blot with rabbit antibody to Kell protein, was isolated from the propositus's red cells by immunoprecipitation. This finding was not reproduced in subsequent studies, which suggests that the quantity of Kell protein recovered was at the threshold level detectable by the technique used. The red cell phenotype is categorized as Kmod, of which this is the first example reported in a healthy individual.