[ABO incompatibility and complications in hematopoietic stem cell transplantation]. / Incompatibilidad ABO en el trasplante de células progenitoras hematopoyéticas y sus complicaciones.

Background: Hematopoietic stem cell transplants (HSCT) can be performed regardless of the ABO group compatibility between donor and recipient. ABO incompatibility in HSCT is related to pure red cell aplasia (PRCA), or passenger lymphocyte syndrome. The impact of ABO incompatibility on graft-versus-host disease and transplant-related mortality is controversial due to the heterogeneity of procedures carried out in different transplant centers. Objective: To determine the prevalence of ABO incompatibility and its complications in a hematopoietic stem transplant unit. Material and methods: An observational, retrospective study was carried out in patients undergoing HSCT from January 2014 to January 2020. All trasplant patients were included. Qualitative variables were analyzed using chi-squared test, and Wilcoxon and Student's t tests were used for quantitative variables. A p < 0.05 was considered significant. Results: 124 patients undergoing HSCT were analyzed, out of which 31 had ABO incompatibility, with a punctual prevalence of 24.4%; among them, 54% presented with major incompatibility, 32% minor incompatibility and 13% bidirectional incompatibility. Three cases of PRCA were reported. There were no differences in survival at one year in both groups. Conclusions: The ABO incompatibility ant its complications were not related to the increase in mortality. Randomized prospective studies are required to define the role of ABO incompatibility in HSCT prognosis.

Introducción: los trasplantes de células progenitoras hematopoyéticas (TCPH) se pueden hacer independientemente de la compatibilidad de grupo sanguíneo ABO entre donador y receptor. La incompatibilidad ABO (IABO) en los TCPH puede presentar complicaciones, como aplasia pura de serie roja (APSR), o síndrome de linfocito pasajero. El impacto de la IABO en la enfermedad del injerto en contra del huésped y la mortalidad relacionada al trasplante es controversial por la heterogeneidad de procedimientos que se hacen en los distintos centros de trasplante. Objetivo: determinar la prevalencia de la IABO y sus complicaciones en los pacientes trasplantados en una unidad de trasplante de progenitores hematopoyéticos. Material y métodos: se hizo un estudio tipo observacional, descriptivo, en pacientes sometidos a TCPH de enero de 2014 a enero de 2020. Se incluyeron todos los pacientes trasplantados. Las variables cualitativas se analizaron con chi cuadrada y para las variables cuantitativas se usó la prueba de Wilcoxon y t de Student. Una p < 0.05 fue significativa. Resultados: se analizaron 124 pacientes sometidos a TCPH y 31 de ellos presentaron IABO, con una prevalencia puntual de 24.4%; entre ellos, 54% presentaron incompatibilidad mayor, 32% incompatibilidad menor y 13% incompatibilidad bidireccional. Se reportaron tres casos de APSR. No hubo diferencias en la supervivencia global a un año en ambos grupos. Conclusiones: la IABO y sus complicaciones no se relacionaron con aumento en la mortalidad. Se requieren estudios prospectivos aleatorizados para definir el papel de la IABO con el pronóstico del trasplante.

Antibodies to human neutrophil antigen HNA-3b implicated in cases of neonatal alloimmune neutropenia.

BACKGROUND: Neonatal alloimmune neutropenia results from maternal alloimmunization to human neutrophil antigens. The alloantibodies involved in neonatal alloimmune neutropenia are against human neutrophil antigens HNA-1a, HNA-1b, HNA-1c, HNA-1d, HNA-2, HNA-3a, HNA-4a, HNA-4b, and HNA-5a; however, to date, antibodies specific to HNA-3b have not been reported. STUDY DESIGN AND METHODS: Blood samples from 10,000 unselected neonates were analyzed, resulting in the selection of 88 neutropenic newborns (neutrophil count <1.5 × 109 /L) from 83 mothers (three pairs of twins and one triplet). HNA-3 genotyping was performed by polymerase chain reaction-restriction fragment length polymorphism to identify the cases of maternal-fetal HNA-3 incompatibility. Serologic studies for detecting maternal HNA-3 alloantibodies were performed with the granulocyte agglutination test, the white blood cell immunofluorescence test, and a LABScreen Multi-HNA Kit. RESULTS: Genotyping studies identified 13 of 88 (14.8%) instances of maternal-fetal HNA-3 incompatibility, with all mothers typed as HNA-3a/a and neonates typed as HNA-3a/b. Serologic studies revealed that five of 13 (38.5%) mothers carried anti-HNA-3b plus human leukocyte antigen antibodies and that three of 13 (23.1%) mothers had anti-HNA-3b without human leukocyte antigen antibodies. CONCLUSION: Here, we report the first three cases of neonatal alloimmune neutropenia associated with HNA-3b antibodies resulting in a neonatal alloimmune neutropenia incidence of one in 3333 live births.

Transfusion therapy for sickle cell disease: a balancing act.

Transfusion therapy is a key intervention in decreasing morbidity and mortality in patients with sickle cell disease (SCD). Current indications for acute and chronic transfusion therapy have significantly increased the number of RBC units transfused to patients with SCD worldwide. This review summarizes transfusion management for the treatment or prevention of neurologic and perioperative complications, acute chest syndrome, and acute anemia associated with SCD. Despite the recognized benefits of transfusion therapy, it is not without the risks of iron overload, alloimmunization, and delayed hemolytic transfusion reactions. Transfusional iron overload management includes automated RBC exchange, noninvasive imaging to monitor iron burden, and iron chelation with parenteral or oral agents. Although limited and extended RBC antigen matching reduces antibody formation, the prevalence of RBC alloimmunization in patients with SCD remains high. Recent studies demonstrate that RH genetic diversity in patients with SCD contributes to Rh alloimmunization, suggesting that even more refined RBC matching strategies are needed. Advances in molecular blood group typing offer new opportunities to improve RBC matching of donors and recipients and can be of particular benefit to patients with SCD.

Estudio de la variante aint del antígeno A / Study of a antigen aint variant

Se definen como A intermedio (Aint) los hematíes que comparten caracteres con A1 y A2. Existen diferencias cualitativas y cuantitativas en los epitopes A. Los hematíes A1 son aglutinados por la lectina de Ulex Europaeus (anti-H), en tanto los hematíes Aint son débilmente aglutinados por ambas de manera inesperada. Se realizó una búsqueda de individuos Aint en una población hospitalaria de acuerdo con la reacción con las lectinas mencionadas. Se evaluó el proceso de aglutinación producida mediante una técnica cinética. Se estudiaron 557 muestras, resultando 285 O (51,1 por ciento), 216 A (38,8 por ciento), 45 B (8,1 por ciento), 8 A1B (1,4 por ciento) y 3 A2B (0,6 por ciento). Las muestras A se subdividieron en 173 A1, (80,2 por ciento), 31 A2 (14,3 por ciento) y 12 Aint (5,5 por ciento). Se observó, en las curvas de cinética, diferencia de reacción entre los hematíes de grupo A1 Aint y A2. Nuestros resultados concuerdan con observaciones previas sobre la marcada heterogeneidad de los hematíes Aint. El reconocimiento de de variantes débiles del grupo A reviste importancia cuando se presentan reacciones transfusionales hemolíticas y en la práctica forense. Importa señalar que el valor de este estudio es relevante, en Inmunogenética Poblacional, por su contribución al conocimiento del mestizaje con poblaciones negras (AU)

Estudio de la variante aint del antígeno A / Study of a antigen aint variant

Se definen como A intermedio (Aint) los hematíes que comparten caracteres con A1 y A2. Existen diferencias cualitativas y cuantitativas en los epitopes A. Los hematíes A1 son aglutinados por la lectina de Ulex Europaeus (anti-H), en tanto los hematíes Aint son débilmente aglutinados por ambas de manera inesperada. Se realizó una búsqueda de individuos Aint en una población hospitalaria de acuerdo con la reacción con las lectinas mencionadas. Se evaluó el proceso de aglutinación producida mediante una técnica cinética. Se estudiaron 557 muestras, resultando 285 O (51,1 por ciento), 216 A (38,8 por ciento), 45 B (8,1 por ciento), 8 A1B (1,4 por ciento) y 3 A2B (0,6 por ciento). Las muestras A se subdividieron en 173 A1, (80,2 por ciento), 31 A2 (14,3 por ciento) y 12 Aint (5,5 por ciento). Se observó, en las curvas de cinética, diferencia de reacción entre los hematíes de grupo A1 Aint y A2. Nuestros resultados concuerdan con observaciones previas sobre la marcada heterogeneidad de los hematíes Aint. El reconocimiento de de variantes débiles del grupo A reviste importancia cuando se presentan reacciones transfusionales hemolíticas y en la práctica forense. Importa señalar que el valor de este estudio es relevante, en Inmunogenética Poblacional, por su contribución al conocimiento del mestizaje con poblaciones negras

Maternal immunization to Gov system alloantigens on human platelets.

BACKGROUND: Immunization to platelet alloantigens can occur during pregnancy or after the transfusion of blood components. Platelet alloantibodies can cause neonatal alloimmune thrombocytopenia and posttransfusion purpura. Transfusion-induced alloimmunization to a novel platelet alloantigen system, Gov, expressed on the 175-kDa glycosyl phosphatidylinositol-anchored platelet glycoprotein, CD109, was previously described. This report describes three unrelated patients who were alloimmunized to Gov(a) or Gov(b) during pregnancy. STUDY DESIGN AND METHODS: Platelets were typed by using radioimmunoprecipitation for HPA-1a, -3a, -5a, -5b, Gov(a), and Gov(b) and by polymerase chain reaction-restriction fragment length polymorphism for HPA-1a, -1b, -3a, and -3b. Maternal sera were screened for platelet antibodies by using radioimmunoprecipitation and the antigen capture assay. RESULTS: Patients 1 and 2 were investigated after the diagnosis of neonatal alloimmune thrombocytopenia in their children, and alloantibodies specific for Gov(b) and Gov(a), respectively, were detected in maternal serum. Serum from patient 3, who had mild idiopathic thrombocytopenia purpura with no detectable autoantibody, was found to contain alloantibodies to Gov(b) and to HPA-5b, presumably as a result of immunization during pregnancy. Platelet typings confirmed that the patients were at risk for alloimmunization to the respective antigen. CONCLUSION: This report of three cases of maternal alloimmunization to antigens in the Gov system indicates that immunization can occur via placental transfer of antigen and that Gov system alloantibodies may be associated with neonatal alloimmune thrombocytopenia.