Rh incompatibility may induce a hemolytic transfusion reaction and in newborns causes the hemolytic disease erythroblastosis fetalis. Erythroblastosis fetalis occurs in Rh(D) newborns delivered by Rh(D ) mothers and results from an immune reaction of anti-D immunoglobulins passed across the placenta from the mother. The anti-D antibodies are produced by the mother in response to the D antigen expressed on the fetal erythrocytes that leak into her circulation during pregnancy. Administration of anti-D antibodies (RhoGAM) to the mother during pregnancy and after parturition destroys any circulating Rh(D) fetal erythrocytes that persist in the mother’s blood, thus preventing Rh-incompatibility reactions in future pregnancies.
Blood Type Erythrocyte Surface Antigen Serum Antibody Can Give Blood to Can Receive Blood From A A antigen Anti-B A and AB A and O B B antigen Anti-A B and AB B and O AB A and B antigens No antibodies Only AB A, B, AB, and O (universal blood recipient) O O antigen (no A or B antigens) Anti-A and anti-B A, B, AB, and O (universal blood donor) Only O TABLE ABO Blood Group System F10.1.1
Hemoglobin consists of four polypeptide chains of globin ,  , ,and , each complexed to an iron-containing heme group (Fig. 10.4). The structure of the polypeptide chains varies. Depending on the particular polypeptides present, the following types of hemoglobin can be distinguished:  Hemoglobin HbA is most prevalent in adults, accounting for about 96% of total hemoglobin. It is a tetramer with two  and two  chains (2 2).
 Hemoglobin HbA2 accounts for 1.5% to 3% of total hemoglobin in adults. It consists of two  and two  chains (22).
 Hemoglobin HbF accounts for less than 1% of total hemoglobin in adults. It contains two  and two  chains (22) and is the principal form of hemoglobin in the fetus.
HbF production falls dramatically after birth; however, in some individuals HbF is produced throughout their entire lives. Although HbF persists in slightly higher percentages than normal in those with sickle cell disease and thalassemia, it does not appear to have a pathologic role.
Mutations in the genes encoding the globin chains can cause disorders in hemoglobin production. An example of a mutation in the gene encoding hemoglobin  is discussed in the Folder 10.3. Interestingly, more than 550 types of abnormal hemoglobin molecules have been identified, but the majority of them have no clinical significance.
 FOLDER 10.2 Clinical Correlation: Hemoglobin in Patients with Diabetes