Rh Factor
Rh factor describes blood type compatibility issues involving Rh blood groups. These play a critical role in transfusions and in obstetrics.
Rh blood groups were first discovered in 1940 by Karl Landsteiner and Alexander Wiener in their experiments with Rhesus monkeys, hence the name. Forty years earlier, Landsteiner had identified blood types A, B, AB and O, a discovery that made blood transfusions safe.
Landsteiner and Wiener noted that unexplained accidents in transfusions were attributed to this Rh blood group. The Rh blood group is also a correlary in hemolytic disease of the newborn, which is characterized by the breaking apart of red blood cells.
People with the Rh (rhesus) protein on the surface of their red blood cells are called Rh-positive (about 85 % of the population). Those who lack the protein are Rh-negative (about 15 %). The immune system of an Rh-negative person destroys Rh-positive blood, as it does any foreign antigen.
Specifically, Rh factor is a non-glycosylated, hydrophobic red blood cell surface protein with a size of 32 kDa and a structure similar to transporter glycoproteins. The Rh gene locus in humans consists of two structural genes, RHD and RHCE, and lies on chromosome 1.
When blood from an Rh-positive donor is used for transfusion into an Rh- negative recipient, the latter will develop specific antibodies which may produce a hemolytic reaction if Rh-positive cells are again introduced in a transfusion. When an Rh-negative patient receives Rh-positive blood, the recipient produces anti-Rh antibodies to destroy the foreign cells by making them agglutinate, or clump together. This reaction in the body can cause serious injury or death to the patient.
Rh factor is also a critical to the blood compatibility of parents.If an Rh-negative woman gives birth to an Rh-positive child fathered by an Rh- positive man, there is a risk that she will become sensitized to the Rh factor in her baby's blood and begin to produce anti-Rh antibodies. Her first baby will not usually be affected, but in subsequent pregnancies, the mother may send enough damaging antibodies into the child's bloodstream to threaten its life.
Usually trophoblast cell layers in the placenta separate fetal cells from the mother's blood, however, some cells may still escape into the mother's circulation during late pregnancy or childbirth.
Anti-Rh antibodies, or IgG white blood cells, are not naturally present in the body, and the mother's initial antibody response is too late and too dilute to affect the fetus of the first pregnancy. In the second pregnancy, however, the mother's IgG cells are already present and have the ability to penetrate the trophoblast and to agglutinate the red blood cells of the fetus.
This condition is erythroblastosis fetalis, or hemolytic disease of the newborn (HDN), and consists of severe anemia, brain damage or even death. About one in 20 births conceived of Rh-positive mothers and Rh-negative fathers results in death. Before Rh factor was identified, it was a common cause of stillbirth pregnancies.
Parents with different ABO blood types have no Rh incompatibility problems because cells that enter the mother from the fetus are destroyed by antibodies, called IgM white blood cells, which already exist in the mother's blood.
IgM antibodies rarely cause agglutination in the fetus because they are unable to cross the trophoblast, and they are able to destroy the foreign red blood cells before they can trigger an IgG immune response.
To resolve general Rh-incompatibility, mothers receive anti-Rh antibodies after the first birth to destroy any Rh-positive fetal red blood cells that have entered the mother's circulation. This process of sensitization prevents the mother's immune system from producing IgG antibodies against the Rh factor.
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