hh blood group

The serum contained antibodies that attacked all red blood cells of normal ABO phenotypes.

Since anti-H immunoglobulins can activate the complement cascade, it will lead to the lysis of red blood cells while they are still in the circulation, provoking an acute hemolytic transfusion reaction.

[citation needed] This very rare phenotype is generally present in about 0.0004% (about 4 per million) of the human population, though in some places such as Mumbai (formerly Bombay) locals can have occurrences in as much as 0.01% (1 in 10,000) of inhabitants.

The resulting antigens are oligosaccharide chains, which are attached to lipids and proteins that are anchored in the red blood cell membrane.

More specifically, the minimum requirement for H antigenicity is the terminal disaccharide fucose-galactose, where the fucose has an alpha(1-2)linkage.

This antigen is produced by a specific fucosyl transferase (Galactoside 2-alpha-L-fucosyltransferase 2) that catalyzes the final step in the synthesis of the molecule.

Because both parents must carry this recessive allele to transmit this blood type to their children, the condition mainly occurs in small closed-off communities where there is a good chance of both parents of a child either being of Bombay type, or being heterozygous for the h allele and so carrying the Bombay characteristic as recessive.

Other examples may include noble families, which are inbred due to custom rather than local genetic variety.

In theory, the maternal production of anti-H during pregnancy might cause hemolytic disease (HDN) in a fetus who did not inherit the mother's Bombay phenotype.

IgM does not cross the placenta and thus does not coat the fetal RBCs that would elicit the Hemolytic disease of the newborn