The Rh Group

The Rh blood group is named for the rhesus monkey, in which the Rh antigens were discovered in 1940. This group is determined by three genes called C, D, and E, each of which has two alleles: C, c, D, d, E, e. Whatever other alleles a person may have, anyone with genotype DD or Dd has D antigens on his or her RBCs and is classified as Rh-positive (Rh+). In Rh-negative (Rh~) people, the D antigen is lacking. The Rh blood type is tested by using an anti-D reagent. The Rh type is usually combined with the ABO type in a single expression such as O+ for type O, Rh-positive, or AB~ for type AB, Rh-negative. About 85% of white Americans are Rh+ and 15% are Rh~. ABO blood type has no influence on Rh type, or vice versa. If the frequency of type O whites in the United States is 45%, and 85% of these are also Rh+, then the frequency of O+ individuals is the product of these separate frequencies: 0.45 X 0.85 = 0.38, or 38%. Rh frequencies vary among ethnic groups just as ABO frequencies do. About 99% of Asians are Rh+, for example.

_Think About It_

Predict what percentage of Japanese Americans have type B~ blood.

In contrast to the ABO group, anti-D antibodies are not normally present in the blood. They form only in Rh~ individuals who are exposed to Rh+ blood. If an Rh~ person receives an Rh+ transfusion, the recipient produces anti-D. Since anti-D does not appear instantaneously, this presents little danger in the first mismatched transfusion. But if that person should later receive another Rh+ transfusion, his or her anti-D could agglutinate the donor's RBCs.

A related condition sometimes occurs when an Rh~ woman carries an Rh+ fetus. The first pregnancy is likely to be uneventful because the placenta normally prevents maternal and fetal blood from mixing. However, at the time of birth, or if a miscarriage occurs, placental tearing exposes the mother to Rh+ fetal blood. She then begins to produce anti-D antibodies (fig. 18.18). If she becomes pregnant again with an Rh+ fetus, her anti-D antibodies may pass through the placenta and agglutinate the fetal eryth-rocytes. Agglutinated RBCs hemolyze, and the baby is born with a severe anemia called hemolytic disease of the newborn (HDN), or erythroblastosis fetalis. Not all HDN is due to Rh incompatibility, however. About 2% of cases

Saladin: Anatomy & I 18. The Circulatory System: I Text I © The McGraw-Hill

Physiology: The Unity of Blood Companies, 2003 Form and Function, Third Edition

698 Part Four Regulation and Maintenance

698 Part Four Regulation and Maintenance

Hemolytic Disease The Newborn Saladin

Figure 18.18 Hemolytic Disease of the Newborn (HDN). (a) When an Rh~ woman is pregnant with an Rh+ fetus, she is exposed to D (Rh) antigens, especially during childbirth. (b) Following that pregnancy, her immune system produces anti-D antibodies. (c) If she later becomes pregnant with another Rh fetus, her anti-D antibodies can cross the placenta and agglutinate the blood of that fetus, causing that child to be born with HDN.

Figure 18.18 Hemolytic Disease of the Newborn (HDN). (a) When an Rh~ woman is pregnant with an Rh+ fetus, she is exposed to D (Rh) antigens, especially during childbirth. (b) Following that pregnancy, her immune system produces anti-D antibodies. (c) If she later becomes pregnant with another Rh fetus, her anti-D antibodies can cross the placenta and agglutinate the blood of that fetus, causing that child to be born with HDN.

result from incompatibility of ABO and other blood types. About 1 out of 10 cases of ABO incompatibility between mother and fetus results in HDN.

HDN, like so many other disorders, is easier to prevent than to treat. If an Rh~ woman gives birth to (or miscarries) an Rh+ child, she can be given an Rh immune globulin (sold under trade names such as RhoGAM and Gamulin). The immune globulin binds fetal RBC antigens so they cannot stimulate her immune system to produce anti-D. It is now common to give immune globulin at 28 to 32 weeks' gestation and at birth in any pregnancy in which the mother is Rh~ and the father is Rh+.

If an Rh~ woman has had one or more previous Rh+ pregnancies, her subsequent Rh+ children have about a 17% probability of being born with HDN. Infants with HDN are usually severely anemic. As the fetal hemopoi-etic tissues respond to the need for more RBCs, erythro-blasts (immature RBCs) enter the circulation prematurely— hence the name erythroblastosis fetalis. Hemolyzed RBCs release hemoglobin, which is converted to bilirubin. High bilirubin levels can cause kernicterus, a syndrome of toxic brain damage that may kill the infant or leave it with motor, sensory, and mental deficiencies. HDN can be treated with phototherapy—exposing the infant to ultraviolet light, which degrades bilirubin as blood passes through the capillaries of the skin. In more severe cases, an exchange transfusion may be given to completely replace the infant's Rh+ blood with Rh~. In time, the infant's hemopoietic tissues will replace the donor's RBCs with Rh+ cells, and by then the mother's antibody will have disappeared from the infant's blood.

_Think About It_

A baby with HDN typically has jaundice and an enlarged spleen. Explain these effects.

How To Bolster Your Immune System

How To Bolster Your Immune System

All Natural Immune Boosters Proven To Fight Infection, Disease And More. Discover A Natural, Safe Effective Way To Boost Your Immune System Using Ingredients From Your Kitchen Cupboard. The only common sense, no holds barred guide to hit the market today no gimmicks, no pills, just old fashioned common sense remedies to cure colds, influenza, viral infections and more.

Get My Free Audio Book


Post a comment