Its time to phase in RHD genotyping for patients with a serologic weak D phenotype

I n 2014, the College of American Pathologists (CAP) Transfusion Medicine Resource Committee (TMRC) reported the results of a survey of more than 3100 laboratories concerning their policies and procedures for testing serologic weak D phenotypes and administration of Rh immune globulin (RhIG). Among the findings of this survey is the observation that there is a lack of standard practice in the United States for interpreting the RhD type when a serologic weak D phenotype is detected. In some laboratories, an individual with a serologic weak D phenotype, especially if a blood donor, is interpreted to be RhD-positive. In the same or other laboratories, especially if a serologic weak D phenotype is detected in a female of childbearing potential, the individual is likely to be managed as RhD-negative for transfusions and, if pregnant, considered a candidate for RhIG. Also, the performance characteristics of serologic typing methods for RhD vary. For patients, including pregnant women, the majority of laboratories have policies and procedures that do not use the indirect antiglobulin (weak D) test, thereby avoiding detection of a serologic weak D phenotype so that the RhD type will be interpreted to be RhDnegative. Other laboratories typically perform a weak D test for the same category of patients. For blood donors and newborns, it is standard practice for laboratories to have policies and procedures for RhD typing to ensure that serologic weak D phenotypes are detected and interpreted as RhD-positive. The goal of these RhD typing practices is to protect RhD-negative persons from inadvertent alloimmunization to the D antigen by exposure to RhD-positive red blood cells (RBCs), including RBCs expressing a serologic weak D phenotype. Although there has not been a recent prospective study in the United States, it is estimated that current RhD typing practice, together with contemporary obstetric practices for administration of antepartum and postpartum RhIG, is 98.4% to 99% successful in preventing RhD alloimmunization and RhD hemolytic disease of the fetus or newborn. However, there are unwarranted consequences associated with the practice of not determining the RHD genotype of persons with a serologic weak D phenotype, including unnecessary injections of RhIG and transfusion of RhD-negative RBCs—always in short supply—when RhD-positive RBCs could be transfused safely. CAP’s TMRC reviewed the current status of RHD genotyping and proposed that selective integration of ABBREVIATIONS: ACOG = American College of Obstetricians and Gynecologists; CAP = College of American Pathologists; TMRC = Transfusion Medicine Resource Committee.