Hemolytic Disease of the Newborn Is Caused by Type II Reactions

Hemolytic disease of the newborn develops when maternal IgG antibodies specific for fetal blood-group antigens cross the placenta and destroy fetal red blood cells. The consequences of such transfer can be minor, serious, or lethal. Severe hemolytic disease of the newborn, called erythroblastosis fetalis, most commonly develops when an Rh+ fetus expresses an Rh antigen on its blood cells that the Rh- mother does not express.

During pregnancy, fetal red blood cells are separated from the mother's circulation by a layer of cells in the placenta called the trophoblast. During her first pregnancy with an Rh+ fetus, an Rh- woman is usually not exposed to enough fetal red blood cells to activate her Rh-specific B cells. At the time of delivery, however, separation of the placenta from the uterine wall allows larger amounts of fetal umbilical-cord blood to enter the mother's circulation. These fetal red blood cells activate Rh-specific B cells, resulting in production of Rh-specific plasma cells and memory B cells in the mother. The secreted IgM antibody clears the Rh+ fetal red cells from the mother's circulation, but the memory cells remain, a threat to any subsequent pregnancy with an Rh+ fetus. Activation of these memory cells in a subsequent pregnancy results in the formation of IgG anti-Rh antibodies, which cross the placenta and damage the fetal red blood cells (Figure 16-14). Mild to severe anemia can develop in the fetus, sometimes with fatal consequences. In addition, conversion of hemoglobin to bilirubin can present an additional threat to the newborn because the lipid-soluble bilirubin may accumulate in the brain and cause brain damage.

Hemolytic disease of the newborn caused by Rh incompatibility in a subsequent pregnancy can be almost entirely prevented by administering antibodies against the Rh antigen to the mother within 24-48 h after the first delivery. These antibodies, called Rhogam, bind to any fetal red blood cells that enter the mother's circulation at the time of delivery and facilitate their clearance before B-cell activation and ensuing memory-cell production can take place. In a subsequent pregnancy with an Rh+ fetus, a mother who has been treated with Rhogam is unlikely to produce IgG anti-Rh antibodies; thus, the fetus is protected from the damage that would occur when these antibodies crossed the placenta.

The development of hemolytic disease of the newborn caused by Rh incompatibility can be detected by testing maternal serum at intervals during pregnancy for antibodies to the Rh antigen. A rise in the titer of these antibodies as pregnancy progresses indicates that the mother has been exposed to Rh antigens and is producing increasing amounts of antibody. The presence of maternal IgG on the surface of fetal red blood cells can be detected by a Coombs test. Isolated fetal red blood cells are incubated with the Coombs reagent, goat antibody to human IgG antibody. If maternal IgG is bound to the fetal red blood cells, the cells agglutinate with the Coombs reagent.

If hemolytic disease caused by Rh incompatibility is detected during pregnancy, the treatment depends on the severity of the reaction. For a severe reaction, the fetus can be given an intrauterine blood-exchange transfusion to replace fetal Rh+ red blood cells with Rh- cells. These transfusions are given every 10-21 days until delivery. In less severe cases, a blood-exchange transfusion is not given until after birth, primarily to remove bilirubin; the infant is also exposed to low levels of UV light to break down the bilirubin and prevent cerebral damage. The mother can also be treated during the pregnancy by plasmapheresis. In this procedure, a cellseparation machine is used to separate the mother's blood into two fractions, cells and plasma. The plasma containing the anti-Rh antibody is discarded, and the cells are reinfused into the mother in an albumin or fresh-plasma solution.

The majority of cases (65%) of hemolytic disease of the newborn have minor consequences and are caused by ABO

DEVELOPMENT OF ERYTHROBLASTOSIS FETALIS (WITHOUT RHOGAM)

RBCs with Rh antigen

Placenta

Mother

DEVELOPMENT OF ERYTHROBLASTOSIS FETALIS (WITHOUT RHOGAM)

Placenta

Mother

RBCs with Rh antigen

Haemolytic Diseases New Born
Plasma cells
Hemolytic Disease The Newborn

1st Pregnancy

Delivery

Rh-specific B cell Memory cell

1st Pregnancy

Delivery

Rh-specific B cell Memory cell

Effect Rhogam Maternal Antibodies

2nd Pregnancy

IgG anti-Rh Ab crosses placenta and attacks fetal RBCs causing erythroblastosis fetalis

2nd Pregnancy

IgG anti-Rh Ab crosses placenta and attacks fetal RBCs causing erythroblastosis fetalis

PREVENTION (WITH RHOGAM)

Mother

(treated with Rhogam)

B cell

Mother

(treated with Rhogam)

B cell

Rhogam

Prevents B-cell activation and memory cell formation

Rhogam

Prevents B-cell activation and memory cell formation

FIGURE 16-14

Development of erythroblastosis fetalis (hemolytic disease of the newborn) caused when an Rh- mother carries an Rh+

fetus (left), and effect of treatment with anti-Rh antibody, or Rhogam (right).

blood-group incompatibility between the mother and fetus. Type A or B fetuses carried by type O mothers most commonly develop these reactions. A type O mother is most likely to develop IgG antibody to the A or B blood-group antigens either through natural exposure or through exposure to fetal blood-group A or B antigens in successive pregnancies. Usually the fetal anemia resulting from this incompatibility is mild; the major clinical manifestation is a slight elevation of bilirubin, with jaundice. Depending on the severity of the anemia and jaundice, a blood-exchange transfusion may be required in these infants. In general the reaction is mild, however, and exposure of the infant to low levels of UV light is enough to break down the bilirubin and avoid cerebral damage.

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Responses

  • Christian
    How does igg antibodies cross placenta during hemolytic disease of the newborn?
    8 years ago
  • yonas
    Which antibody can cross the placenta and cause hemolytic disease of the newborn,exam 2?
    6 years ago
  • barbara
    How does erythroblastosis fetalis develop?
    3 years ago
  • elisabeth h
    Can hemoly disease of a newborn prevents mothers B cell activation and memory cell formation?
    2 years ago

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