Rh Factor
Rh Factor
Karl Landsteiner, an Austrian—later American—physician discovered ABO blood groups in 1900. In 1940, 10 years after receiving the Nobel Prize, he made still another famous discovery. This was a blood group called the Rh factor, named after rhesus monkeys, in which it was first found. Approximately 85% of white individuals in the United States have the factor (positive) and the other 15% do not (negative). The Rh factor is encoded by a dominant allele at a single gene. Rh-positive and Rh-negative bloods are incompatible; shock and even death may follow their mixing when Rh-positive blood is introduced into an Rh-negative person who has been sensitized by an earlier transfusion of Rh-positive blood. Rh incompatibility accounts for a peculiar and often fatal hemolytic disease of the newborn (erythroblastosis fetalis). If an Rhnegative mother has an Rh-positive baby (father is Rh-positive) she can become immunized by fetal blood during the birth process. Anti-Rh antibodies are predominately IgG and can cross the placenta during a subsequent pregnancy and agglutinate fetal blood. Erythroblastosis fetalis normally is not a problem in cases of ABO incompatibility between mother and fetus because antibodies to ABO antigens are primarily IgM and cannot cross the placenta.
The genetics of the Rh factor are very much more complicated than it was believed when the factor was first discovered. Some authorities think that three genes located close together on the same chromosome are involved,whereas others adhere to a system of one gene with many alleles. In 1968 a revision of the single gene concept listed 37 alleles necessary to account for the phenotypes then known.Furthermore, the frequency of the various alleles varies greatly between whites, Asians, and blacks.
Erythroblastosis fetalis can now be prevented by giving an Rh-negative mother anti-Rh antibodies just after the birth of her first child. These antibodies remain long enough to neutralize any Rh-positive fetal blood cells that may have entered her circulation, thus preventing her own antibody machinery from being stimulated to produce the Rh-positive antibodies. Active, permanent immunity is blocked.The mother must be treated after every subsequent pregnancy (assuming the father is Rh+). If the mother has already developed an immunity, however, the baby may be saved by an immediate, massive transfusion of blood free of antibodies.
Karl Landsteiner, an Austrian—later American—physician discovered ABO blood groups in 1900. In 1940, 10 years after receiving the Nobel Prize, he made still another famous discovery. This was a blood group called the Rh factor, named after rhesus monkeys, in which it was first found. Approximately 85% of white individuals in the United States have the factor (positive) and the other 15% do not (negative). The Rh factor is encoded by a dominant allele at a single gene. Rh-positive and Rh-negative bloods are incompatible; shock and even death may follow their mixing when Rh-positive blood is introduced into an Rh-negative person who has been sensitized by an earlier transfusion of Rh-positive blood. Rh incompatibility accounts for a peculiar and often fatal hemolytic disease of the newborn (erythroblastosis fetalis). If an Rhnegative mother has an Rh-positive baby (father is Rh-positive) she can become immunized by fetal blood during the birth process. Anti-Rh antibodies are predominately IgG and can cross the placenta during a subsequent pregnancy and agglutinate fetal blood. Erythroblastosis fetalis normally is not a problem in cases of ABO incompatibility between mother and fetus because antibodies to ABO antigens are primarily IgM and cannot cross the placenta.
The genetics of the Rh factor are very much more complicated than it was believed when the factor was first discovered. Some authorities think that three genes located close together on the same chromosome are involved,whereas others adhere to a system of one gene with many alleles. In 1968 a revision of the single gene concept listed 37 alleles necessary to account for the phenotypes then known.Furthermore, the frequency of the various alleles varies greatly between whites, Asians, and blacks.
Erythroblastosis fetalis can now be prevented by giving an Rh-negative mother anti-Rh antibodies just after the birth of her first child. These antibodies remain long enough to neutralize any Rh-positive fetal blood cells that may have entered her circulation, thus preventing her own antibody machinery from being stimulated to produce the Rh-positive antibodies. Active, permanent immunity is blocked.The mother must be treated after every subsequent pregnancy (assuming the father is Rh+). If the mother has already developed an immunity, however, the baby may be saved by an immediate, massive transfusion of blood free of antibodies.
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