16

CASE 16


DF is a 25-year-old woman, pregnant for the third time. She is known to have blood group A, Rh negative (Rh−) red cells. Her husband is also type A but Rh positive (Rh+). Their first-born child, a boy, was healthy but during the second pregnancy DF was noted to have an indirect Coombs’ titer of 1:32 in her serum. This fetus was followed closely, and a healthy baby girl was induced (vaginal delivery) at 36 weeks of gestation. DF received RhoGam after this delivery. It is now 3 years later and DF is pregnant again. You are monitoring her indirect Coombs’ antibody titer and find it to be 1:32 at 12 weeks and 1:48 at 18 weeks. Amniotic fluid was obtained beginning at 22 weeks of gestation and every 2 weeks thereafter. The amniotic fluid was shown to have increasing amounts of bilirubin (a pigment derived from a breakdown of heme), suggesting hemolysis of fetal red cells. At 28 weeks of gestation, a blood sample obtained from the umbilical vein revealed a hematocrit of 6.2% (normal 45%), confirming profound anemia in the fetus.



QUESTIONS FOR GROUP DISCUSSION



1. The significant point in this case is that the mother is Rh− and the father is Rh+. What is the Rh antigen? What percent of the population is Rh+? What is the potential problem for a fetus whose mother is Rh− and the father is Rh+?

2. Why is the risk of hemolytic disease of the newborn lower during a first pregnancy than for subsequent pregnancies? Include in your discussion how the mother could become sensitized to the Rh antigen during a first pregnancy? At the time of delivery?

3. Explain how maternal anti-Rh antibodies serve as a stimulus for complement-mediated hemolysis of fetal red blood cells. Describe the possible mechanism by which red blood cells would be destroyed after binding of IgG.

4. RhoGam is given to Rh− mothers if there is evidence of bleeding during pregnancy and especially at birth. What is RhoGam?

5. Explain (a) the “older” idea of how RhoGam prevents sensitization of the mother during placental bleeding or during the birthing process and (b) conventional wisdom as to how RhoGam works.

6. Define hematocrit and describe how it is determined. Under what circumstances would the fetal hematocrit continue to drop despite the administration of red blood cells into the umbilical vein?

7. Explain why the fetus was transfused with Rh− packed red blood cells when we already know that the fetus’s red blood cells are Rh+.

8. Explain how ABO incompatibility could reduce the likelihood of an Rh− mother being sensitized to the Rh antigen when carrying a child.

9. What test can be used to determine if the mother has circulating anti-Rh antibodies? At what antibody titer is the fetus considered to be at risk for hemolytic disease?

10. Explain how the serum of an Rh− mother who is pregnant with an Rh+ child gives a negative indirect Coombs’ test but agglutinates Rh+ cell in saline (see Case 15).


RECOMMENDED APPROACH



Implications/Analysis of Family History


The Rh antigen incompatibility between DF and her husband is of significance here because she is pregnant. The Rh antigen, so named because it was first identified on rhesus monkey erythrocytes (red blood cells), is expressed by about 85% of humans. When an Rh− individual becomes exposed (sensitized) to red blood cells expressing the Rh antigens, an immune response is generated because this is a foreign antigen. IgM and IgG anti-Rh antibodies are formed. This is of concern when an Rh− female is pregnant because IgG antibodies cross the placenta (see Etiology).


Differences in red blood cell antigens are more common in the ABO classification. ABO refers to the blood group cell surface glycolipids (antigens) used to classify red blood cells into four major groups: (1) red blood cells with A glycolipids, (2) with B glycolipids, (3) with both A and B glycolipids, and (4) red blood cells that do not express these antigens. Individuals are classed as A, B, or AB positive. Individuals who do not express either the A or B antigens are designated as having “O” blood type. In this case both DF and her husband were “A” positive, and so there was no incompatibility.



Implications/Analysis of Clinical History

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Jun 18, 2016 | Posted by in IMMUNOLOGY | Comments Off on 16

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