Urgent Transfusion in a New Patient with Rare Blood Type

Background/Case Studies: Bombay is a rare blood group characterized by the absence of H substance at

the surface of RBCs leading to naturally occurring anti-H antibodies. Anti-H presents the risk of severe

hemolytic transfusion reactions in these patients. The case presented is of a 32-year-old female of Middle

Eastern origin, who presented with a traumatic vertebral fracture with spinal cord compression and required

urgent neurosurgery. Her presenting hemoglobin was 84 g/L. She had no previous group and screen on

record, had never been transfused and had a history of a remote miscarriage.

Study Design/Methods: Forward blood group with an automated gel-method instrument revealed the

following reactions: negative with anti-A, unable to interpret (?) with anti-B, 4+ with anti-D. Reverse

grouping revealed the following reactions: 4+ with A1-cells and an unexpected 1+ with B-cells. The antibody

screen and 11 cell panel in gel (Micro Typing Systems) 2+; the panel, with enhancement reacted 3+ in

Ficin. The auto control was negative. A second panel and pre-warm panel produced the same findings. An

antibody reacting at 37C against a high-frequency antigen was suspected. Patient specimen was sent for

investigation to the reference lab (RL), which performed blood group by manual tube test, antibody

identification with panels by manual tube PEG-IAT method; RL also sent a sample for ABH sequencing

(Sanger).

Results/Findings: A thawed frozen plasma sample from a previous Bombay patient 12 years prior showed

no reactivity against the patient's RBCs; positive control included. A frozen Bombay RBC unit was ordered

urgently from the blood supplier and was crossmatch compatible. The patient underwent surgery and was

transfused with a single unit of RBC for peri-operative bleeding. She was treated with erythropoietin and IV

iron post-operatively and did not require any further transfusions. The investigation at the RL showed mixed

field reaction on forward blood typing with anti-B and anti-A,B and negative reaction with anti-A commercial

reagents. The RL reverse grouping showed 4+ with all O H+ and A1 red cells, but 2+ with B cells. The autocontrol

and group O H- cells did not react, confirming anti-H and suggesting Para-Bombay group. ABH

sequencing revealed a normal B allele (ABO*B.01) while genotyping of FUT1 revealed a null allele

(FUT1*01N.12) and weak H allele (FUT1*01W.23). FUT2 genotyping (FUT2*01N.02) predicted a nonsecretor

(sese) phenotype.

Conclusions: This patient with non-secretor status, variant H production, clinically significant anti-H, greatly

reduced B antigen expression, should be treated as a Bombay (Oh) for transfusion purposes. She was

counselled and provided with an antibody card and a letter. This case illustrates the importance of timely

communication with the clinical team about the risks and benefits of transfusion pending antibody

identification, as it could have proved fatal in this case.

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