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Each blood component must have its ABO and D antigen status tested as a primary mechanism of preventing ABO-incompatible blood transfusions and D antigen sensitization. Additionally, components must be tested for the presence of unexpected, clinically significant antibodies to prevent potential recipient hemolysis. Red blood cell (RBC) products often undergo further RBC antigen characterization to supply blood products for patients with alloantibodies or patients with chronic anemia (e.g., sickle cell disease [SCD]) who require phenotype-matched RBC components. Most blood centers use serologic methods to perform these tests, but the use of molecular testing is growing. Serologic methods include tube testing, gel method (also known as column agglutination), or solid phase. These tests, and the various methods, are discussed in more detail in the chapter on pretransfusion testing ( Chapter 21 ).
ABO blood group phenotypes include A, B, AB, and O. Reciprocal antibodies are consistently present in the majority of individuals’ sera without previous RBC exposure (e.g., anti-B antibodies in blood group A patients), and these antibodies may result in severe intravascular hemolysis after transfusion of ABO-incompatible blood components. Prevention of ABO-incompatible transfusion is the primary objective of pretransfusion testing.
ABO is determined by testing donor RBCs with anti-A and anti-B (known as “forward” or “front” type) and donor plasma with group A 1 and group B RBCs (known as “reverse” or “back” type). Discrepancies between front and back type must be resolved before labeling a blood component ( Chapter 25 ). RBC genotyping can be used to resolve typing discrepancies.
The D antigen (also termed Rh or Rh(D)) is the most immunogenic RBC antigen and therefore the D antigen is second to the ABO blood group in importance in transfusion medicine. D-negative products must be appropriately labeled, such that a recipient of a D-negative product does not form anti-D. Currently, donor centers use typing reagents to detect the D antigen, and these reagents must be sensitive enough to detect the presence of weak D. Weak D testing can either be performed by including the antihuman globulin phase, which takes additional time, reagents, and controls, or through the use of certain automated techniques, which are sensitive enough for “weak D” detection such that a separate “weak D” test is not required. D-negative donors in Germany and Austria were RHD tested by molecular methods, and about 1 in 1000 have the RHD gene and express the D antigen but at levels that are not detected by routine serologic tests (e.g., D el ). In addition, transfusion of these products with low levels of D antigen can result in sensitization of the D-negative recipient. Therefore, these donors were removed from the D-negative donor pool ( Chapter 26 ).
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