Asunto(s)
Tipificación y Pruebas Cruzadas Sanguíneas/métodos , Hemaglutininas/sangre , Aglutininas/sangre , Incompatibilidad de Grupos Sanguíneos/prevención & control , Tipificación y Pruebas Cruzadas Sanguíneas/economía , Prueba de Coombs , Crioglobulinas , Pruebas Diagnósticas de Rutina/economía , Pruebas de Hemaglutinación , Humanos , Soluciones Hipotónicas/farmacología , Temperatura , Reacción a la TransfusiónRESUMEN
The formation of erythrocyte autoantibodies following transfusion therapy has been described in case reports and small series. To determine the frequency, serological characteristics, and clinical significance of this phenomenon in paediatric patients with sickle cell disease, we analysed the patient database at the Duke University Pediatric Hematology Clinic. We identified children who received multiple erythrocyte transfusions, then reviewed clinical records to identify children who developed erythrocyte autoantibodies in association with transfusions. Among 184 paediatric patients who received multiple erythrocyte transfusions, 14 children (7.6%) developed warm (IgG) erythrocyte autoantibodies. Median transfusion exposure at the time of autoantibody formation was 24 erythrocyte units, range 3-341 units. The autoantibody reacted as a panagglutinin in 11 cases but had anti-e specificity in three patients. Surface complement also was detected in five patients. Clinically significant haemolysis was documented in four patients, each of whom had both surface IgG and C3 detected. The development of erythrocyte autoantibodies was associated with the presence of erythrocyte alloantibodies. Formation of warm erythrocyte autoantibodies in association with transfusions is not rare in paediatric patients with sickle cell disease. Clinicians should be aware of this complication and recognize that the presence of surface C3 is often associated with significant haemolysis.
Asunto(s)
Anemia de Células Falciformes/inmunología , Autoanticuerpos/análisis , Transfusión de Eritrocitos/efectos adversos , Eritrocitos/inmunología , Adolescente , Adulto , Anemia de Células Falciformes/sangre , Anemia de Células Falciformes/terapia , Niño , Femenino , Hemólisis , Humanos , Inmunoglobulina G/análisis , Isoanticuerpos/análisis , Masculino , Resultado del TratamientoRESUMEN
BACKGROUND AND OBJECTIVES: The Rh phenotypes hrB- and VS+ are both rare in Whites but more common in Blacks. The high-incidence antigen hrB is present on most red cells that are e+. The presence of VS on red cells is associated with an aberrant expression of e, often called eS. MATERIALS AND METHODS: Using conventional serologic methods, including a monoclonal anti-hrB-like antibody, we studied 65 e+ samples that were apparently hrB-. RESULTS: Of the 65, we found that 59 (91%) were VS+. Recent findings have indicated that in VS+ persons a change from leucine to valine occurs at amino acid 245 of the RHCE-encoded polypeptide. While this residue is predicted to lie within the red cell membrane bilayer, the change presumably affects alanine 226 (that is present when e is expressed) in such a way that eS is seen. CONCLUSIONS: Our findings suggest that the change from e to eS may result in nonexpression or marked depression of expression of hrB that is, perhaps, an epitope of e. While the molecular basis of the hrB-phenotype is not known, it is unlikely that the leucine-to-valine change at residue 245, resulting in the aberrant from of e, explains all hrB-samples. First, hrB-VS+ and hrB- VS- samples must differ. Second, some hrB- VS+ samples are C+, some are C-. Presumably diverse molecular bases are involved in hrB-phenotypes.
Asunto(s)
Sistema del Grupo Sanguíneo Rh-Hr/genética , Población Negra/genética , Genoma Humano , Haplotipos , Humanos , Población Blanca/genéticaRESUMEN
BACKGROUND: It is known that some "warm"-reactive autoantibodies are directed against epitopes on the red cell anion exchanger, protein band 3. Some such antibodies (but not all) recognize Wrb. It is also known that Dia and Dib represent an amino acid polymorphism of band 3. STUDY DESIGN AND METHODS: Autoantibodies from 119 patients were tested against Di(b-) red cells. Seventy-four of these autoantibodies were subsequently absorbed with Di(b-) red cells. RESULTS: All 119 autoantibodies initially reacted with the Di(b-) red cells, which showed that none contained only anti-Dib. Among the 74 adsorbed with Di(b-) red cells, two were found to contain an unadsorbed anti-Dib component. CONCLUSION: No example of autoanti-Dib as the only autoantibody present was found among the 119 samples tested. However, 2 (2.7%) of 74 autoantibodies subjected to adsorption with Di(b-) red cells were seen to contain an anti-Dib component. This low incidence of autoanti-Dib is in marked contrast to the high incidence of autoanti-Wrb, although both antibodies define epitopes associated with the red cell anion exchanger, band 3.
Asunto(s)
Proteína 1 de Intercambio de Anión de Eritrocito/inmunología , Autoanticuerpos/análisis , Antígenos de Grupos Sanguíneos/inmunología , Eritrocitos/inmunología , Anemia Hemolítica/inmunología , HumanosRESUMEN
BACKGROUND: In patients in whom autoantibodies of broad specificity (panagglutinins) are present in the serum, adsorption studies are often necessary to identify alloantibodies that are simultaneously present. STUDY DESIGN AND METHODS: Samples from 138 patients in whom the direct antiglobulin test was positive and antibody was present in the serum were studied. When antibody identification studies before or after initial adsorption suggested the presence of an alloantibody, additional alloadsorptions were performed. RESULTS: Among the samples from 138 patients, 71 contained only panagglutinating autoantibody, and another 19 contained either autoantibodies or alloantibodies that were not accompanied by panagglutinins. The remaining 48 samples contained both panagglutinins and a total of 62 antibodies that appeared to be alloimmune in nature. Alloadsorption with antigen-negative red cells showed that 29 (47%) of the apparent alloantibodies were in fact partially adsorbed autoantibodies that mimicked alloantibodies by their reactions. CONCLUSION: Initial autoadsorption often left unadsorbed alloantibodies and autoantibodies with mimicking specificities. Initial alloadsorption more often left only true alloantibodies unadsorbed. From the screening tests, it appeared that 43 percent of the 138 patients were alloimmunized. Recognition of the mimicking nature of the partially adsorbed autoantibodies found that the real incidence of alloimmunization in the patients was 23 percent. Recognition of this phenomenon considerably simplifies the selection of blood for transfusion to these patients.
Asunto(s)
Autoanticuerpos/sangre , Antígenos de Grupos Sanguíneos/inmunología , Eritrocitos/inmunología , Isoanticuerpos/sangre , Prueba de Coombs , Humanos , Técnicas de InmunoadsorciónRESUMEN
BACKGROUND: JMH is a high-frequency red cell blood group antigen that resides on a 76- to 80-kDa glycosylphosphatidylinositol-linked protein also known as CDw108. Antibodies with JMH specificity are often autoimmune and are usually, if not always, clinically benign. Some individuals with JMH-variant antigen produce alloantibodies to JMH, but little evidence concerning their clinical significance is available. This article reports on two patients who express a JMH-variant antigen and produced alloanti-JMH. STUDY DESIGN AND METHODS: Murine monoclonal antibodies and human antibodies to JMH were used in hemagglutination, radioimmunoassay, and Western blot testing of red cells from two JMH-variant patients; antiserum from one of these patients was also used in biochemical studies. In addition, in vivo survival of JMH-positive red cells was studied in the same patient. RESULTS: Biochemically, both examples of red cells with the JMH-variant phenotype expressed a JMH protein with a molecular weight similar to that of the normal JMH protein. For both patients, family studies suggested an autosomal recessive pattern of inheritance. Survival study demonstrated reduced in vivo red cell survival in one patient. CONCLUSION: JMH-variant phenotypes express a protein of normal molecular weight and are inherited in an autosomal recessive pattern. Furthermore, individuals with this phenotype can produce clinically significant antibodies.
Asunto(s)
Antígenos de Grupos Sanguíneos/análisis , Eritrocitos/inmunología , Anciano , Animales , Western Blotting , Femenino , Humanos , Isoantígenos , Masculino , Ratones , Peso MolecularRESUMEN
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.
RESUMEN
The red cells of a white male blood donor typed as Rh:-1, -2, -3,w4,w5,6,-17,w19,-31,-32,-34, and -46. Although the donor has no history of transfusion, his serum contains an alloantibody that is weakly reactive with most red blood cells (RBCs) tested. Only Rhnull and D-- RBCs are nonreactive. Reactivity is enhanced with ficin- or papain-treated RBCs and is unaffected by AET or DTT treatment of the RBCs. Previously described Rh:-46 RBCs have been of deletion types D--, D, and Rhnull, or Rh:32. In three multitransfused patients, the Rh46 antigen was temporarily suppressed and the phenotype eventually reverted to normal. This is the first report of RBCs of the Rh:-32,-46 phenotype that are not of a rare Rh deletion or Rhnull type. In addition, the Rh:w5,w19,-31,-34 phenotype is rarely found in whites.
RESUMEN
Some years ago differences in red cell blood group phenotypes among individuals of different ethnic backgrounds were of little moment to blood transfusion services. This was because in many instances the ethnic group of the majority of patients closely matched that of the donor pool. The dramatic population movements of the last 20-30 years have changed this situation. Now it is not uncommon for a transfusion service whose donors are primarily European Caucasian in ancestry to be required to supply blood for patients, a substantial proportion of whom are of Black or Oriental extraction. This problem affects the donor service in terms of supply and demand, and both the donor service and hospital transfusion service in terms of antibody identification. In this paper some aspects of this problem are explored and illustrations are given of how knowledge of an antibody-maker's ethnic background can sometimes be used to accelerate identification of an antibody, particularly one directed against a very common antigen. The effects of differences in antigen frequency are also considered in terms of long-term transfusion support of some patients.
Asunto(s)
Antígenos de Grupos Sanguíneos/genética , Incompatibilidad de Grupos Sanguíneos/genética , Tipificación y Pruebas Cruzadas Sanguíneas/métodos , Isoanticuerpos/sangre , Grupos Raciales , Sistema del Grupo Sanguíneo ABO/genética , Anemia de Células Falciformes/terapia , Transfusión Sanguínea , Sistema del Grupo Sanguíneo Duffy/genética , Humanos , Antígenos del Grupo Sanguíneo de Lewis/genética , Sistema del Grupo Sanguíneo Rh-Hr/genéticaRESUMEN
In a retrospective study on samples from 10,000 recently transfused patients, 35 samples were found to contain an antibody that reacted with ficin-treated red cells but was not demonstrable by low-ionic-strength saline solution and indirect antiglobulin test (LISS-IAT). In those 35 patients, the specificity of the antibody was such that each patient would have been transfused with antigen-negative blood had the antibody reacted in LISS-IAT. Tests on red cells from the units already transfused showed that 19 patients had among them received, by chance, 32 antigen-positive and 74 antigen-negative units. The remaining 16 patients had among them received 57 units that were, again by chance, all antigen negative. One patient given antigen-positive blood suffered a delayed transfusion reaction; in two others the antibodies became LISS-IAT active after transfusion. However, similar changes to the LISS-IAT-active state were seen with two antibodies of patients given only antigen-negative blood. Also found in the 10,000 patients were 28 clinically insignificant antibodies, 77 sera in which the antibody was too weak to identify, and 216 autoantibodies that reacted only with ficin-treated red cells. These data support a belief, generally held in the United States but not necessarily elsewhere, that the use of protease-treated red cells for routine pretransfusion tests creates far more work than the accrued benefits justify.