The Kidd-null phenotype, Jk(a-b-), is rare, and a patient with this phenotype may develop anti-Jk3, a red blood cell (RBC) antibody reactive with a domain common to both Jka and Jkb. Like other antibodies to high-prevalence antigens, the presence of this antibody poses challenges in the immunohematologic evaluation of these patients. Thoughtful laboratory testing is necessary to resolve the antibody specificity and to reveal other underlying antibodies. Moreover, the rarity of the Kidd-null phenotype makes finding blood donors difficult for those who need transfusion and have developed anti-Jk3. This review describes methods used in identifying anti-Jk3 in four pregnant patients. Blood bank records were retrospectively reviewed to illustrate the common approach in anti-Jk3 identification. In all cases, pertinent blood bank history was gathered, and extended RBC phenotyping was performed, followed by adsorption studies and testing of selected RBCs. Underlying antibodies were found in two of the cases. This review also reiterates some common challenges encountered with Kidd antibody analysis and highlights the importance of patient ethnic ancestry and obtaining accurate patient transfusion history.
The Kidd-null phenotype, Jk(a–b–), is rare, and a patient with this phenotype may develop anti-Jk3, a red blood cell (RBC) antibody reactive with a domain common to both Jka and Jkb. Like other antibodies to high-prevalence antigens, the presence of this antibody poses challenges in the immunohematologic evaluation of these patients. Thoughtful laboratory testing is necessary to resolve the antibody specificity and to reveal other underlying antibodies. Moreover, the rarity of the Kidd-null phenotype makes finding blood donors difficult for those who need transfusion and have developed anti-Jk3. This review describes methods used in identifying anti-Jk3 in four pregnant patients. Blood bank records were retrospectively reviewed to illustrate the common approach in anti-Jk3 identification. In all cases, pertinent blood bank history was gathered, and extended RBC phenotyping was performed, followed by adsorption studies and testing of selected RBCs. Underlying antibodies were found in two of the cases. This review also reiterates some common challenges encountered with Kidd antibody analysis and highlights the importance of patient ethnic ancestry and obtaining accurate patient transfusion history.
Para-Bombay is a rare phenotype with a homozygous nonfunctional FUT1 gene and a normal FUT2 gene leading to H-deficient red blood cells (RBCs) with or without ABH substances, depending on inheritance of the ABO gene. This case is about a 5-day-old male baby suffering from sepsis who required a 45-mL packed RBC transfusion. The baby's sample tested as A1B, D+ and mother's sample tested as group O, D+ with group 4 discrepancy due to ABO isoagglutinins. Further workup of the mother's sample with anti-H lectin was negative, which suggested the mother to be group Oh, D+. Antibody screening was panreactive with negative autocontrol, suggestive of anti-H. The titer of immunoglobulin (Ig)M anti-H was 64, IgG titer using dithiothreitol was 8, and anti-IH was absent. A negative adsorption and elution test suggested that RBCs were devoid of A and B antigens. The father's sample tested clearly as group A1, D+; hence, the cis-AB blood group was ruled out in the baby. The secretor study of the mother's saliva revealed the presence of B and H substances that neutralized polyclonal B and H antisera. Therefore, we concluded that the mother was of the para-Bombay (Bh) phenotype. This case highlights the importance of reverse grouping and resolving blood grouping discrepancies between mother and child-in this case because of an incongruous ABO blood type of the baby and the mother who was previously tested as group O, D+.
Para-Bombay is a rare phenotype with a homozygous nonfunctional FUT1 gene and a normal FUT2 gene leading to H-deficient red blood cells (RBCs) with or without ABH substances, depending on inheritance of the ABO gene. This case is about a 5-day-old male baby suffering from sepsis who required a 45-mL packed RBC transfusion. The baby’s sample tested as A1B, D+ and mother’s sample tested as group O, D+ with group 4 discrepancy due to ABO isoagglutinins. Further workup of the mother’s sample with anti-H lectin was negative, which suggested the mother to be group Oh, D+. Antibody screening was panreactive with negative autocontrol, suggestive of anti-H. The titer of immunoglobulin (Ig)M anti-H was 64, IgG titer using dithiothreitol was 8, and anti-IH was absent. A negative adsorption and elution test suggested that RBCs were devoid of A and B antigens. The father’s sample tested clearly as group A1, D+; hence, the cis-AB blood group was ruled out in the baby. The secretor study of the mother’s saliva revealed the presence of B and H substances that neutralized polyclonal B and H antisera. Therefore, we concluded that the mother was of the para-Bombay (Bh) phenotype. This case highlights the importance of reverse grouping and resolving blood grouping discrepancies between mother and child―in this case because of an incongruous ABO blood type of the baby and the mother who was previously tested as
Units of red blood cell (RBC) concentrates with rare phenotypes are typically not included in method validation studies for cryopreservation processes; rather, they are reserved for patients with rare blood needs. Some rare RBC phenotypes may demonstrate membrane abnormalities, like acanthocytosis as observed for RBCs with the McLeod phenotype, and are specifically banked for these rare attributes; however, the impact that rare RBC phenotypes have on post-thaw quality has not been well studied. To evaluate how a rare RBC phenotype is affected by the cryopreservation process, 4 RBC units, cryopreserved in 1993 using manual methods, were selected for evaluation. These RBCs included one with the McLeod phenotype and three with phenotypes not known to cause significant membrane changes. Post-thaw, an altered deglycerolization protocol, implemented to reduce supernatant glycerol after cryopreservation, was used before processing RBCs on an automated closed system (ACP 215; Haemonetics, Boston, MA) to accommodate the use of a closed system cell processor not available when the RBC units were previously cryopreserved. RBC quality was tested at 24 hours, 7 days, and 14 days post-deglycerolization. Before deglycerolization, an extracted sample from the thawed glycerolized RBC unit was used to obtain genetic material for phenotype confirmation. Genotyping confirmed the McLeod phenotype. When comparing McLeod with non-McLeod units, RBCs from the McLeod donor exhibited acanthocytosis, higher rigidity, and lower morphology scores than RBCs from the non-McLeod units post-deglycerolization. Hemolysis, however, was comparable across all 4 units, meeting regulatory standards. Therefore, McLeod RBCs can withstand cryopreservation, suggesting that units from these donors, glycerolized using older methods, can be deglycerolized using the ACP 215 and stored hypothermically for 14 days. It was also determined that genotyping can be performed on non-leukocyte-reduced cryopreserved RBCs, allowing for confirmation of genetic profiles of donor units banked before the implementation of molecular methods.
Units of red blood cell (RBC) concentrates with rare phenotypes are typically not included in method validation studies for cryopreservation processes; rather, they are reserved for patients with rare blood needs. Some rare RBC phenotypes may demonstrate membrane abnormalities, like acanthocytosis as observed for RBCs with the McLeod phenotype, and are specifically banked for these rare attributes; however, the impact that rare RBC phenotypes have on post-thaw quality has not been well studied. To evaluate how a rare RBC phenotype is affected by the cryopreservation process, 4 RBC units, cryopreserved in 1993 using manual methods, were selected for evaluation. These RBCs included one with the McLeod phenotype and three with phenotypes not known to cause significant membrane changes. Post-thaw, an altered deglycerolization protocol, implemented to reduce supe
Maternal antibody-mediated fetal red blood cell destruction secondary to non-D Rh system antibodies is a significant cause of hemolytic disease of the fetus and newborn. Here, we report a rare case of severe perinatal hemolytic disease associated with maternal antibody to the e antigen. In addition to severe anemia, the infant developed hyperbilirubinemia. Resolution of the infant's anemia and hyperbilirubinemia occurred after treatment with phototherapy, intravenous immunoglobulin, and transfusion.
Maternal antibody-mediated fetal red blood cell destruction secondary to non-D Rh system antibodies is a significant cause of hemolytic disease of the fetus and newborn. Here, we report a rare case of severe perinatal hemolytic disease associated with maternal antibody to the e antigen. In addition to severe anemia, the infant developed hyperbilirubinemia. Resolution of the infant’s anemia and hyperbilirubinemia occurred after treatment with phototherapy, intravenous immunoglobulin, and transfusion.
The ABO blood group system includes phenotypes, or subgroups, that differ in the amount of A and B antigens present on the red blood cells (RBCs). These subgroups also differ in the A, B, or H substances present in secretions (for individuals who have the secretor phenotype). B subgroups are very rare and are less frequently reported than A subgroups. Usually, B subgroups are discovered during serologic testing when there is a discrepancy between RBC and serum grouping results. Subgroups of B are usually identified by a reference laboratory using molecular and adsorption-elution methods. This report details a case of a young, healthy, pregnant woman with a B subgroup detected by a small transfusion service using adsorption-elution methods. Serology and genotyping of the ABO gene was performed at a reference laboratory where the serology was consistent with a B subgroup, but no changes were identified in ABO gene sequencing. It is important to correctly identify B subgroups in donors and recipients to help resolve ABO discrepancies and potentially prevent ABO incompatibility in blood transfusion, thus minimizing transfusion reactions.
The ABO blood group system includes phenotypes, or subgroups, that differ in the amount of A and B antigens present on the red blood cells (RBCs). These subgroups also differ in the A, B, or H substances present in secretions (for individuals who have the secretor phenotype). B subgroups are very rare and are less frequently reported than A subgroups. Usually, B subgroups are discovered during serologic testing when there is a discrepancy between RBC and serum grouping results. Subgroups of B are usually identified by a reference laboratory using molecular and adsorption-elution methods. This report details a case of a young, healthy, pregnant woman with a B subgroup detected by a small transfusion service using adsorption-elution methods. Serology and genotyping of the ABO gene was performed at a reference laboratory where the serology was consistent with a B subgroup, but no changes were identified in ABO gene sequencing. It is important to correctly identify B subgroups in donors and recipients to help resolve ABO discrepancies and potentially prevent ABO incompatibility in blood transfusion, thus minimizing transfusion reactions.
The Lewis blood group system is unique because antigens are neither alleles of the same gene nor are they synthesized by red blood cells (RBCs); rather, they are adsorbed onto the RBC membrane from plasma as glycolipids. Antibodies against Lewis antigens are predominantly naturally occurring immunoglobulin (Ig)M type that sometimes react at 37°C and the antihuman globulin phase. Lewis compound antigens, ALeb and BLeb, have been described that were confirmed because of the presence of antibodies against them. These compound antigens are the result of an interaction between ABO, H, SE, and LE genes.
The Lewis blood group system is unique because antigens are neither alleles of the same gene nor are they synthesized by red blood cells (RBCs); rather, they are adsorbed onto the RBC membrane from plasma as glycolipids. Antibodies against Lewis antigens are predominantly naturally occurring immunoglobulin (Ig)M type that sometimes react at 37°C and the antihuman globulin phase. Lewis compound antigens, ALeb and BLeb, have been described that were confirmed because of the presence of antibodies against them. These compound antigens are the result of an interaction between ABO, H, SE, and LE genes.
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