The Blood group that defies the odd; Bombay Blood Group
November 7, 2024 | by ericwanniang.ehw@gmail.com
The Bombay phenotype was discovered by Dr. Bhende in 1952 . It was called Bombay phenotype because it was discovered by this Indian scientist in Bombay, India.
In Bombay phenotytype, there is an inheritance of a double dose of the h gene, producing the very rare genotype hh. Because of this, the ABO genes cannot be expressed, and hence ABH antigens cannot be formed, since there is no H antigen made in the Bombay phenotype.
IN LABORATORY
With Anti H
So this results in RBCs which are devoid of normal ABH antigens and, therefore, fail to react with anti-A, anti-B, and anti-H.
RBCs of the Bombay phenotype (Oh) do not react with the anti-H lectin (Ulex europaeus), whereas the RBCs of O phenotype reacts strongly with ant H lectin . This suggests the absence of H antigen in Bombay phenotytype and its abundance in O phenotype.
With Anti-A, Anti- B
In Forward blood grouping using anti-A and anti-B, the Bombay would phenotype as an O blood group.
Reverse grouping
Whereas in Reverse blood grouping, the Bombay shows strong reaction in A cells, B cells and also O cells suggesting that that there is a presence of Anti A ,Anti B and also potent Anti H in the serum of such individuals. There is also an additional Anti-A,B in the serum of Bombay phenotytype.
Anti-H and Transfusion of blood
Anti-H of Bombay phenotytype is potent and reacts strongly at 37°C. It is an IgM antibody that can bind complement and cause RBC lysis. Transfusing normal group O blood (with the highest concentration of H antigen) to a Bombay recipient (with anti-H in the serum) would cause immediate cell lysis. Therefore, only blood from another Bombay individual will be compatible and can be transfused to a Bombay recipient.
In Bombay phenotytype, ABH substance are also absent in saliva and body fluids.
The underlying molecular defect in Bombay phenotytype is most commonly a mutation in the gene FUT1 (H gene), and thus it produces a silenced gene that is incapable of coding for the enzyme, α(1,2)fucosyltransferase (H transferase). This enzyme is responsible for transferring fucose in an α-1,2 linkage to the terminal galactose of the precursor molecule on RBCs thus forming H antigen.
In Bombay phenotytype there is also an associated mutation in gene FUT2 (Se gene) which normally encodes a very similar α(1,2)fucosyltransferase and normally transfers a fucose to form H antigens in secretions when active.
Characteristics of Bombay phenotytype
- H, A, and B, antigens are absent; no reaction with anti-A, anti-B, or anti-H lectin
- Antibodies present are anti-A, anti-B, anti-A,B, and a potent anti-H in the serum
- Bombay phenotytypes are A, B, H nonsecretor (no A, B, or H substances present in saliva)
- α-2-L-fucosyltransferase (H-enzyme) is absent in serum and H antigen is absent on red cells
- A or B enzymes are present in serum (depending on ABO genotype)
- RBCs of the Bombay phenotype (Oh) do not react with the anti-H lectin (Ulex europaeus)
- RBCs of the Bombay phenotype (Oh) are compatible only with the serum from another Bombay individual
RELATED POSTS
View all