(P-TS-26) Diagnosis of Oh (Bombay) Phenotype in a Pregnant Patient

Background/Case Studies: Bombay phenotype (Oh) represents a rare blood group, in which affected individuals lack the H antigen on the red blood cell (RBC) surface. Two genes, FUT1 and FUT2, code for enzymes needed to produce the H antigen and subsequent type O, A, and B phenotypes. In the Oh phenotype, both enzymes are deficient, leading to the absence of H antigen. The H antigen is required to produce A and B antigens; individuals with this phenotype cannot produce either on the RBC surface or in secretions. They produce specific antibodies to H, A, and B antigens and are incompatible with any non-Bombay phenotype RBCs. We present a case of diagnosis and management of Oh phenotype during pregnancy.

Study

Design/Methods: A 33-year-old G2P1 presented at 24 weeks for routine prenatal care. During her previous pregnancy, an antibody panel demonstrated a panagglutinin of 3/4+ with a negative autologous control and direct antiglobulin test (DAT), IgG and C3. She had no in-house follow-up testing and delivered at an outside facility without complication. Testing was repeated three years later, during her subsequent pregnancy, and showed similar results.

Genotyping performed at a reference lab, ID CORE XT molecular testing, revealed the patient was positive for several high incidence antigens including Kell, k, LuB, JsB, and KpB. A panreactive antibody was identified at saline immediate spine and polyethylene glycol (PEG) indirect antiglobulin test (IAT). Adsorption studies removed anti-H antibodies and subsequently demonstrated no reactivity in either testing modality.

Results/Findings: The persistent panagglutinin represented an anti-H antibody reacting with all cell lines, i.e. H+ cells. A negative DAT demonstrated the findings were not from an autoantibody. The patient’s hemoglobin was within a normal range, arguing against warm autoimmune hemolytic anemia. Outside genotyping revealed the patient was positive for the majority of high incidence antigens, ruling out an alloantibody to a high incidence antigen. Adsorption studies showed the panagglutinin went away once anti-H antibodies were removed from plasma. These findings were consistent with an anti-H antibody and, Oh Rh positive (Bombay) phenotype.

Conclusions: Few reports have documented Oh phenotype during pregnancy (Bullock et al, Transfusion 2018; Krigstein et al, Transfusion 2022). The H antibody is a clinically significant antibody, but it is unclear if it causes HDFN or what titers are significant given the rarity of cases. While Oh phenotype patients can normally auto-donate RBCs, this patient was diagnosed during pregnancy, precluding blood donation. As compatible units may not be available, postpartum hemorrhage should be prevented at all costs; consultation between maternal fetal medicine, hematology and transfusion medicine as well as a clear delivery plan are critical. Her estimated delivery date is 6/29/23; we will report on the outcome after this time.

Importance of research: We describe the identification of Bombay phenotype in a pregnant patient and highlight the potential for hemolytic disease of the fetus and newborn (HDFN) and the difficulty in procuring rare donor units.