23/06/2022
Hemolithic Disease of the newborn
Newborn hemolytic disease occurs when maternal-specific IgG antibodies for fetal blood group antigens cross the placenta and destroy the fetus' erythrocytes. The consequences of that transfer can be minor, serious, or deadly. Severe hemolytic disease of the newborn, called fetal erythroblastosis, appears most commonly when the mother and fetus express different alleles of the Rhesus antigen (Rh). Although there are actually five alleleos of the Rh antigen, the expression of allele D triggers the stronger immune response; therefore, individuals carrying the Rh antigen D allele are called Rh+.
A Rh respuesta woman fertilized by a Rh+ father is in danger of presenting a Rh antigen response, and rejecting a Rh+ fetus. During pregnancy, fetal erythrocytes are separated from the mother’s circulation by a layer of cells in the placenta called trophoblast. During the first pregnancy with a Rh+ fetus, a Rh primer woman generally is not exposed to enough fetal erythrocytes to activate her Rh-specific B cells. Still, at the time of childbirth, the separation between the placenta and the uterus wall allows larger amounts of fetal blood from the umbilical cord to enter the maternal circulation. These fetal erythrocytes stimulate Rh-specific cells to assemble an immune response, resulting in the production of plasma cells and Rh-specific memory B cells in the mother. The secret IgM antibody removes fetal Rh+ erythrocytes from the mother’s circulation, but memory cells remain—a threat to any subsequent pregnancy with a Rh+ fetus. Important that since IgM antibodies do not cross the placenta, Rh IgM anti-antigen is not a threat to the fetus.
The activation of IgG secret memory cells in a subsequent pregnancy results in the formation of anti-Rh IgG antibodies that can either way cross the placenta and damage fetal erythrocytes.
