There are several genetic variants in the DNA sequence of the ABO gene that give rise to ABO subgroups. The most important of these are the A1 and A2 subgroups, which differ in the activity of their transferase enzyme gene products. The transferase activity in A2 individuals is less efficient in catalyzing the formation of the A antigen from the H antigen compared with those in the A1 subgroup, resulting in lower expression of A antigen. Type A2 individuals have relatively fewer Type I, Type III and Type IV carrier chains than Type A1 individuals. The difference in carbohydrate sequence is thought to explain why a small percentage of A2 and A2B individuals produce anti-A1 antibody, which can cause discrepancies in determining their blood type.
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For example, type A1 individuals can become type B if they have an infection with certain types of bacteria. These bacteria produce deacetylase, which can remove acetyl groups from N-acetylgalactosamine residues on the A antigen, forming galactosamine. Since galactose is the terminal chain sugar in group B individuals, this chemical modification will cause the patient’s cells to react with both anti-A and anti-B reagents when ABO typing is done. The Acquired B syndrome will reverse when the infection has been eradicated, but the patient should not be transfused with type AB or B products, due to the presence of anti-B. Other illnesses that modify sugar chains in the ABO antigens include hematologic disorders, including leukemia, myelodysplasia and other myeloproliferative disorders. Old age and other illnesses such as thalassemia can decrease the expression of ABO antigens, leading to discrepancies in blood type …show more content…
An Rh-negative woman may be exposed to the D antigen in her first pregnancy, through bleeding during delivery, medical procedures such as chorionic villus sampling, through a previous miscarriage or by receiving D-positive RBCs via transfusion. The initial exposure produces mainly IgM antibodies, which do not cross the placenta, but a second exposure will cause rapid production of IgG anti-D, causing future pregnancies with Rh-positive fetuses to be at risk. During prenatal testing, D-negative mothers are checked for sensitization with an indirect Coombs test, which will identify anti-D in the serum. To prevent sensitization, D-negative mothers receive an injection of Rhoimmune globulin, which attaches to and removes any fetal RBCs that are present in the maternal circulation. The injections are given at 28 weeks gestation, when fetal production of the D antigen begins, at 34 weeks, when hemorrhage is most likely to occur, and after
For example, type A1 individuals can become type B if they have an infection with certain types of bacteria. These bacteria produce deacetylase, which can remove acetyl groups from N-acetylgalactosamine residues on the A antigen, forming galactosamine. Since galactose is the terminal chain sugar in group B individuals, this chemical modification will cause the patient’s cells to react with both anti-A and anti-B reagents when ABO typing is done. The Acquired B syndrome will reverse when the infection has been eradicated, but the patient should not be transfused with type AB or B products, due to the presence of anti-B. Other illnesses that modify sugar chains in the ABO antigens include hematologic disorders, including leukemia, myelodysplasia and other myeloproliferative disorders. Old age and other illnesses such as thalassemia can decrease the expression of ABO antigens, leading to discrepancies in blood type …show more content…
An Rh-negative woman may be exposed to the D antigen in her first pregnancy, through bleeding during delivery, medical procedures such as chorionic villus sampling, through a previous miscarriage or by receiving D-positive RBCs via transfusion. The initial exposure produces mainly IgM antibodies, which do not cross the placenta, but a second exposure will cause rapid production of IgG anti-D, causing future pregnancies with Rh-positive fetuses to be at risk. During prenatal testing, D-negative mothers are checked for sensitization with an indirect Coombs test, which will identify anti-D in the serum. To prevent sensitization, D-negative mothers receive an injection of Rhoimmune globulin, which attaches to and removes any fetal RBCs that are present in the maternal circulation. The injections are given at 28 weeks gestation, when fetal production of the D antigen begins, at 34 weeks, when hemorrhage is most likely to occur, and after