Chapter 3 Answers to self-check questions

Haemolytic Disease of the Fetus and Newborn

3.1

Why is the D antigen the most common cause of HDFN?Anti-A and anti-B are very common, why is therefore ABO HDFN not more frequent than it is?

Answers:

  • Between 18-20% of European and North American populations are Rh D negative. Approximately 60% of pregnancies to D-negative mothers will be D-positive fetuses. Coupled with the immunogenicity of D, it is a simple arithmetical fact that more mothers are at risk of HDFN due to anti-D.
  • A and B antigens are not expressed early on fetal erythroid cells, most (but not all) anti-A and anti-B are IgM and cannot cross the placenta. The fetal tissues also express A and B antigens and act as a “sink” for any IgG anti-A or B that enter the fetal system.

 

3.2

  • Why are partial DVI phenotype mothers deliberately serologically typed as D-negative?
  • HDFN due to anti-K of the Kell system can often be very severe early in pregnancy – why is this the case?

Answers:

  • DVI mothers can make clinically significant anti-D when exposed to (normal) D-positive blood. For this reason, it is very important that they receive prophylactic anti-D. it therefore makes good sense to select D typing serological reagents to type mothers as D negative during the pregnancy.
  • The Kell glycoprotein is expressed very early on developing fetal erythroid cells. Anti-K therefore can destroy them, and “suppress’ fetal erythropoiesis early in pregnancy.

 

3.3

  • Why is there a requirement to monitor the levels of fetal erythrocytes leaked into the maternal circulation? How is it performed?
  • What are the similarities and differences between HDFN and NAITP (see chapter 6 before answering this!)

Answers:

    • “Fetal leaks” or feto-maternal haemorrhage (FMH) are monitored to inform the dose of prophylactic anti-D that are given at the end of the pregnancy. They can be quite large in difficult deliveries and thus the amount of anti-D used needs to be adjusted accordingly. FMH are monitored using either the Kliehaeur-Betke test or by flow cytometry.
    • Both are examples of

alloimmune disease of the fetus

  • . This is where the mother becomes immunized to paternally-inherited antigens that are on the surface of fetal erythrocytes or platelets. There are different outcomes in the fetus as a result of anaemia (erythrocytes) or thrombocytopaenia (platelets), which are explained in this chapter and chapter 6.

 

3.4

  • Why is maternal plasma based fetal genotyping preferred in the management of HDFN?
  • Why has the analysis of amniotic fluid largely been abandoned in the management of HDFN and how has it been replaced?

Answers:

  • It is non-invasive. Previously fetal blood sampling was required which has the risk of further FMH into the maternal circulation, inducing further immunization. There is widespread application of prenatal RhD testing using maternal plasma and this can avoid the use of prophylactic anti-D where the fetus is genotyped as RhD negative.
  • See above- the process of amniocentesis can lead to spontaneous miscarriage and further FMH.

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