ABSTRACT
Background: The Bombay blood group (Oh phenotype) is a rare blood type characterized by the absence of A, B, and H antigens on red cells, with the presence of potent anti-H antibodies. Pregnancies in women with this phenotype pose significant risks due to the potential for hemolytic disease of the fetus and newborn (HDFN) and the extreme scarcity of compatible blood for transfusion.
Here is the rewritten version with different wording while retaining the original meaning:
Revised Case Description:
We report two instances of pregnant women with the rare Bombay phenotype, focusing on the management of elevated anti-H antibody levels. The first case describes a 23-year-old woman from Bangladesh who delivered a healthy full-term baby following careful monitoring and tailored blood management protocols. The second case involves a 25-year-old Indian woman with an anti-H IgG titer reaching 4000; however, no signs of fetal anemia were detected. The pregnancy was vigilantly observed, with transfusion resources on standby. The baby, delivered via cesarean section, exhibited mild jaundice but did not require a transfusion. These cases underscore the importance of collaborative multidisciplinary care and individualized transfusion planning in managing high-risk pregnancies.
Pregnancies in women with the Bombay blood group demand personalized care strategies, availability of rare blood supplies, and careful, continuous monitoring to ensure the best possible outcomes for both mother and child.
This case underscores the essential importance of collaborative healthcare in handling rare immunohematologic disorders throughout pregnancy.
INTRODUCTION
The Bombay blood group, initially identified in 1952 in Mumbai, India, is a rare blood type resulting from homozygous mutations in the FUT1 gene, which prevents the expression of H antigen on red blood cells (Bhende et al., 1952). People with this phenotype often also have FUT2 gene mutations, making them nonsecretors of ABH antigens. These individuals develop strong naturally occurring anti-H antibodies, posing significant challenges during transfusion and pregnancy due to the potential for hemolytic transfusion reactions and hemolytic disease of the fetus and newborn (HDFN) (Dean, 2005).
Fetal red blood cells can be targeted by maternal anti-H antibodies, particularly if the fetus inherits a functional H gene from the father (Roback et al., 2011). This underscores the importance of early diagnosis, vigilant monitoring, and well-coordinated multidisciplinary management.
Case Reports
Case 1
A 23-year-old Bangladeshi woman (gravida 1, para 0) was referred at 9 weeks of pregnancy following the detection of panreactive antibodies during routine antenatal screening. Serological testing at the regional red cell immunohematology (RCI) center confirmed the Bombay phenotype (Oh, R1r) with the presence of anti-H antibodies. Dithiothreitol (DTT) treatment revealed both IgG and IgM components. Initial antibody titers were 1024 (IgG + IgM) and 256 (IgG). Follow-up titrations showed increasing titers of 2048/512 at 22 and 30 weeks, which later dropped to 256/128 by 34 weeks.
Fetal assessment using middle cerebral artery (MCA) Doppler every two weeks showed no signs of anemia. Molecular testing for FUT1 and FUT2 genes was attempted but could not be completed due to inadequate sample quantity. No additional alloantibodies were identified. A patient blood management (PBM) approach was employed, including iron supplementation and folate monitoring. At 39 weeks, labor was induced, and the patient delivered vaginally with an estimated blood loss of 400 mL. The neonate (blood group A D–) had a normal hemoglobin level (159 g/L) and mildly raised bilirubin (36 mmol/L). The direct antiglobulin test (DAT) was moderately positive, and no eluate was performed.
Case 2
A 25-year-old Indian woman, pregnant for the first time, was referred at 19 weeks of gestation. She was identified as having the Bombay phenotype (Oh, R1R1) with anti-H antibodies. Her initial IgG antibody titer at 24 weeks measured 512. Genetic testing confirmed homozygous mutations in FUT1 and a deletion in exon 2 of FUT2, confirming her as a nonsecretor. Repeat testing at 32 weeks indicated a significant increase in anti-H titer to 4000 (IgG), prompting biweekly MCA Doppler monitoring. Despite the elevated titers, no signs of fetal anemia were observed.
Discussion
The presence of anti-H antibodies in expectant mothers with the Bombay phenotype poses a significant clinical concern. These antibodies, often naturally occurring and capable of crossing the placenta due to their IgG nature, can cause hemolytic disease of the fetus and newborn (HDFN) if the fetus inherits a functional H gene from the father (Daniels, 2013). However, as demonstrated in these cases, not all fetuses are affected.
Close monitoring through serial antibody titrations and MCA Doppler assessments was instrumental in preventing complications in both cases. The downward trend in titers in Case 1 may reflect a natural decline, while the sharp increase in Case 2 required intensified surveillance. These experiences highlight the importance of individualized monitoring plans.
Due to the extreme rarity of Bombay phenotype donors, ensuring readiness for transfusion is essential. This includes coordination with regional blood centers and the National Frozen Blood Bank. Although neither case required intrauterine transfusion, having a structured plan in place was crucial. Employing PBM strategies—such as antenatal iron supplementation and intraoperative cell salvage—can help reduce the dependence on donor blood (Shander et al., 2014).
Author Name
Suchana Mallick