Ahmed Alotaibi: Rare Rh Phenotype and Severe Fetal Anaemia
Ahmed Alotaibi, Senior Specialist (Blood bank and blood transfusion) at Afif General Hospital – Riyadh Third Health Cluster (Ministry of Health), shared a post on LinkedIn:
”D-positive, but C− c− E− e−.
What are you looking at?
Most of us think about the Rh system mainly in terms of D positive or D negative.
But this 2026 Frontiers in Immunology case shows how much more complex Rh can be.
A 25-year-old pregnant patient had the extremely rare:
- D− phenotype
- Her red cells expressed D, but lacked the major RhCE antigens:
C− c− E− e−
Why does that matter?
Because exposure to normal RhCE-positive cells through pregnancy or transfusion can lead to formation of anti-Rh17.
In this case, anti-Rh17 was identified at a titre of:
512
The fetus had inherited paternal c and E antigens, making the fetal RBCs RhCE-positive and vulnerable to the maternal antibody.
The result:
Maternal anti-Rh17 antibodies cause fetal red blood cell destruction, leading to severe fetal anaemia.
At 25 plus 5 weeks, fetal anaemia was suspected, and cord blood sampling confirmed a fetal haemoglobin of:
8.9 g/dL
The blood-bank challenge was enormous:
What do you transfuse when almost every donor RBC unit is incompatible?
The fetus ultimately required four intrauterine transfusions:
- 1st: maternal RBCs
- 2nd: rare D−− donor RBCs
- 3rd: maternal RBCs
- 4th: maternal RBCs
The maternal units were carefully prepared, including washing and irradiation.
After each transfusion, fetal haemoglobin improved.
The pregnancy reached 37 weeks, and the baby was delivered with a favourable neonatal outcome.
This case is an important reminder:
D-positive does not mean the rest of the Rh phenotype is typical.
A patient can be D-positive while completely lacking C, c, E and e, creating one of the most difficult compatibility problems in transfusion medicine.”
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