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Rh factor,protein substance present in the red blood cells of most people, capable of inducing intense antigenic reactions. The Rh, or rhesus, factor was discovered in 1940 by K. Landsteiner and A. S. Wiener, when they observed that an injection of blood from a rhesus monkey into rabbits caused an antigenic reaction in the serum component of rabbit blood (see immunityimmunity,
ability of an organism to resist disease by identifying and destroying foreign substances or organisms. Although all animals have some immune capabilities, little is known about nonmammalian immunity.
..... Click the link for more information. ). When blood from humans was tested with the rabbit serum, the red blood cells of 85% of the humans tested agglutinated (clumped together). The red blood cells of the 85% (later found to be 85% of the white population and a larger percentage of blacks and Asians) contained the same factor present in rhesus monkey blood; such blood was typed Rh positive. The blood of the remaining 15% lacked the factor and was typed Rh negative. Under ordinary circumstances, the presence or lack of the Rh factor has no bearing on life or health. It is only when the two blood types are mingled in an Rh-negative individual that the difficulty arises, since the Rh factor acts as an antigen in Rh-negative persons, causing the production of antibodies. Besides the Rh factor, human red blood cells contain a large number of additional antigenic substances that have been classified into many blood group systems (see blood groupsblood groups,
differentiation of blood by type, classified according to immunological (antigenic) properties, which are determined by specific substances on the surface of red blood cells.
..... Click the link for more information. ); however, the Rh system is the only one, aside from the ABO system, that is of major importance in blood transfusions. If Rh-positive blood is transfused into an Rh-negative person, the latter will gradually develop antibodies called anti-Rh agglutinins, that attach to the Rh-positive red blood cells, causing them to agglutinate. Destruction of the cells (hemolysis) eventually results. If the Rh-negative recipient is given additional transfusions of Rh-positive blood, the concentration of anti-Rh agglutinins may become high enough to cause a serious or fatal reaction. The same type of immune reaction occurs in the blood of an Rh-negative mother who is carrying an Rh-positive fetus. (The probability of this situation occurring is high if the father is Rh positive.) Some of the infant's blood may enter the maternal circulation, causing the formation of agglutinins against the fetal red blood cells. The first baby is usually not harmed. But, if the mother's agglutinins pass into the circulation of subsequent fetuses, they may destroy the fetal red blood cells, causing the severe hemolytic disease of newborns known as erythroblastosis fetaliserythroblastosis fetalis
, hemolytic disease of a newborn infant caused by blood group incompatibility between mother and child. Although the Rh factor is responsible for the most severe cases of erythroblastosis fetalis, the disease may be produced by any of the other blood
..... Click the link for more information. .
(also rhesus factor), an antigen contained in the red blood cells of 85 percent of all persons and in the red blood cells of rhesus monkeys (Macacus rhesus). The Rh factor was discovered in 1940 by the Austrian scientists K. Landsteiner and A. Wiener. The blood of persons whose red blood cells contain the Rh factor is called Rh-positive. There are several different antigens in the Rh-factor system, including the Hr group, which together with Rh makes up the total Rh-Hr system. This system includes three varieties of Rh agglutinogen (D, C, and E), three varieties of Hr agglutinogen (c, d, and e), and other less common variants. Hr agglutinogen is contained in the red blood cells of 83 percent of all human beings. The Rh factor is transmitted by heredity as a dominant character and does not change throughout life (seeHEREDITY).
Determination of the Rh-factor and the blood group is obligatory for blood transfusion. When a person is injected parenterally with any agglutinogen of the Rh-Hr system that is absent from his blood, specific antibodies are elaborated. With repeated injection of that antigen, an “antigen-antibody” reaction occurs that produces functional bodily disturbances. Thus, if Rh-positive blood is transfused to an Rh-negative recipient who already has an antibody to Rh, such reactions as chills, fever, and short-term pains in the loin may occur. Severe cases may involve massive hemolysis with renal insufficiency. A distinctive feature of Rh transfusion reactions is their late manifestation—one or two hours after the transfusion. Treatment of these reactions involves venesection, followed by infusion of Rh-negative blood.
When an Rh-negative woman is pregnant with an Rh-positive fetus, she may become isoimmunized. Antibodies formed with repeated pregnancies may lead to an undeveloped pregnancy or intrauterine death of the fetus with subsequent involuntary abortion. If the infant is born alive, it may suffer from erythroblastosis fatalis.
Rh incompatibility develops no earlier than the seventh or eighth week of pregnancy, when hematopoiesis occurs in the embryo. Prophylaxis against Rh incompatibility is injection of anti-Rh gamma globulin.
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Kassirskii, I. A., and G. A. Akleseev. Klinicheskaia gematologiia, 4th ed. Moscow, 1970.
Grishchenko, I. I., and V. A. Shileiko. Izoimmunizatsiia k rezus-faktoru u beremennykh. Kiev, 1971.
Persianinov, L. S. “Nesovmestimost’ krovi materi i ploda.” In his book Akusherskii seminar, 2nd ed., vol. 2. Tashkent, 1973.
V. A. FROLOV