ABSTRACT
BACKGROUND: Although uncommon, acute hemolytic transfusion reactions (AHTRs) have been reported after transfusion of group O single-donor apheresis platelets (SDPs) to group A, B, and AB recipients. Current methods for identifying "high-titer" SDPs include tube and gel methods. The risk of a high-titer unit is considered low with group O, poststorage, pooled platelet concentrates (PPLTs); however, data regarding anti-A and anti-B titers in PPLTs are lacking. STUDY DESIGN AND METHODS: Anti-A and anti-B titers were determined in 185 PPLTs by direct agglutination using manual gel and tube methods. PPLTs tested included 124 group O PPLTs, 25 group A PPLTs, 26 group B PPLTs, and 10 PPLTs containing a mix of either groups O plus A or groups O plus B (mixed PPLTs). The reciprocal of the highest dilution giving macroscopic agglutination was considered the agglutinin titer. RESULTS: Mean anti-A and anti-B titers in group O PPLTs were, respectively, 16 and 8 by tube and 64 and 32 by gel (p < 0.0001). Gel titers were one to two dilutions higher than tube and sensitive to reagent red cell lots. With the use of at least 64 as a critical titer, 60 percent of group O PPLTs tested by gel would be considered high-titer. In mixed PPLTs, the addition of one non-group O PLT significantly decreased or neutralized the corresponding anti-A or anti-B (p < 0.0001). CONCLUSION: Anti-A and anti-B titers in group O PPLTs are comparable to those reported in group O SDPs and significantly lower than titers reported in AHTR. A critical direct agglutinin titer of 64 for identifying high-titer units by gel is too low and should be increased to 128 or higher.
Subject(s)
ABO Blood-Group System/immunology , Antigens, Human Platelet/immunology , Blood Component Removal , Blood Group Incompatibility/immunology , Isoantigens/immunology , Platelet Transfusion/adverse effects , Acute Disease , Agglutination Tests/methods , Blood Group Incompatibility/epidemiology , Blood Platelets/immunology , Humans , Isoantigens/blood , Platelet Transfusion/statistics & numerical data , Retrospective Studies , Risk FactorsSubject(s)
Cytomegalovirus Infections/prevention & control , Hematopoietic Stem Cell Transplantation , Leukocyte Reduction Procedures , Adult , Antibodies, Viral/biosynthesis , Antibodies, Viral/blood , Child , Cytomegalovirus/immunology , Cytomegalovirus Infections/diagnosis , Cytomegalovirus Infections/epidemiology , Cytomegalovirus Infections/transmission , Female , Follow-Up Studies , Hematologic Neoplasms/complications , Hematologic Neoplasms/surgery , Hematopoietic Stem Cell Transplantation/adverse effects , Hematopoietic Stem Cell Transplantation/standards , Hematopoietic Stem Cells/virology , Humans , Leukocytes/virology , Male , Nucleic Acid Amplification Techniques , Retrospective Studies , Transfusion Reaction , Transplantation, Homologous , Unnecessary ProceduresABSTRACT
OBJECTIVE: Prenatal noninvasive determination of fetal Rh status is an important aid to the management of hemolytic disease of the fetus and newborn. We performed real-time polymerase chain reaction on fetal DNA derived from maternal plasma to determine fetal Rh status. STUDY DESIGN: Cell-free plasma DNA from 98 D-negative pregnant women was tested for the presence of exons 4, 5, and 10 of RHD. The presence of fetal DNA was confirmed by detection of SRY or biallelic insertion/deletion polymorphisms in the maternal plasma and buffy coat. RESULTS: Seventy-two D-positive infants and 26 D-negative infants were determined by serologic studies. All 3 RHD exon sequences were detected in 68 of 72 mothers of D-positive infants. The presence of fetal DNA in mothers of D-negative infants was confirmed in all 10 boys and in 14 of 16 girls. CONCLUSION: Fetal RHD genotyping in this study correctly predicted fetal Rh status in 92 of 98 (94%) cases.