Dealing with serious blood loss in an injured person has long been a difficult challenge for medical scientists. One solution has been to treat the patient with blood transfused from another person or an animal. In some instances, this approach worked and the patient recovered. In other cases in the past, however, the blood transfusion actually worsened the patient's condition and hastened death. Until the early 1900s, no one could predict which type of reaction would occur as the result of any one blood transfusion. As a result, most European nations had outlawed the practice of blood transfusion by the beginning of the nineteenth century.
An explanation for the phenomenon of blood rejection was developed around 1900 by Austrian-American physician Karl Landsteiner. Landsteiner found that human blood serum (the cell-free portion of blood) could be divided into four categories depending on its ability to cause clotting of red blood cells. He called these four groups A, B, AB, and O. In 1927, Landsteiner found a second set of blood factors, which he named M, N, and MN, and in 1940, he discovered yet a third class of blood factors, known as Rh positive and Rh negative. The last of these discoveries, made with colleagues Philip Levine and Alexander Wiener, resulted from studies with Rhesus monkeys.
Landsteiner, Levine, and Wiener found that blood from monkeys injected into rabbits and guinea pigs clotted because of the presence of an antigen, which they designated as the Rh (Rhesus) factor. They went on to show that the factor also occurs among some humans, but not others. Individuals who carry the factor are designated as Rh positive and those who do not as Rh negative.
Researchers also found that the Rh factor is inherited according to Gregor Mendel's laws of genetics. This discovery had practical importance, because it explained a relatively common medical disorder known as erythroblastosis fetalis. In this condition, an Rh negative woman who becomes pregnant with an Rh positive fetus may develop antibodies against the Rh factor in the fetus. This development usually causes no problem during the woman's first pregnancy, since the number of antibodies produced tends to be small. But by the time a second pregnancy occurs, the situation has changed. The number of Rh antibodies produced by the mother's body has become large enough to cause destruction of red blood cells in the fetus, with consequent complication such as anemia, jaundice, and premature birth. Today, this reaction can usually be controlled by immunizing susceptible women with a drug known as RhoGam. Unfortunately, not all women who need the treatment get it, and a small number of women don't benefit from it. Nevertheless, by 1995, Rh problems in the newborn had declined from 20,000 babies a year in the United States to 4,000 babies a year.
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