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Cromer Blood Group Systems
It can not be disputed that knowledge of blood groups is of paramount importance to effective administration of scientific as well as biological operations. The Cromer blood groups system was discovered in 1965. It was the named after its very first antibody producer who is also erffered to as Mrs. Cromer. At the time of its identification, the relative anibody was thought to be anti-Go. However, after ten years, it was found out that it has a new and different specificity. It was then that the respective antibody was renamed to anti-Gr.
Normally, the constituent blood group antigens of this Cromer system are carried on in a complement regulatory protein that is also a decay accelerating factor. The respective decay accelerating factor gene is usually located at chromosome Iq32. This according to Daniels and Bromiow constitutes one of the group genes that are referred to as the regulators of complement activation. The respective gene has close to 40kb and contains 11 exons. The decay accelerating factor glycoprotein is typically arranged in four different extra-cellular yet short consensus continuous domains. Each repeat domain usually has sixty amino acid remnants or residues. Through the GPI linkage, the amino acid residues are usually attached to a distinct RBC membrane.
The Cromer blood group system comprises of eleven antigens which have two sets of vital antithetical antigens. According to Hiller, eight of the respective antigens tend to be of high incidence while the remaining three are of a low incidence. The very last exon has a distict hydrophobic C terminal domain that is usually replaced by the GPI postranslationally. When in a secreted DAF form, it is agreed that this segment is likely to be more hydrophilic. The respective antigens are documented to be lacking the Inab phenotype, which is also known as the Cromer null phenotype. By now, it is contended that all the amino acids that are essential for expressing all the antigens are determined. Apart from the Dr, all result from just a single change of an amino acid. In the Dr a negative phenotype, the degree of expression of the respective DAF as well as that of the entire Cromer system antigens is reduced significantly. The CR (a negative) phenotype has been identified to be the least rare of all the other negative phenotypes. Current evidence indicates that apart form one Spanish American lady, the remaining individuals with Cr (a negative) RBCs tends to be Black. A significant percentage of the remaining phenotypes tend to be very rare.
With respect to treatment, it is widely recognized that the Cromer antigens tend to be resistant to any treatment of the RBCs by papain, ficin and sialidase. In addition, they are very sensitive to Chymotrypsin and tend to be weakened by 200mm volume of DDT. This information is imperatively important in clinical procedures of different types. The antibodies in this system on the other hand are very reactive, usually 1gG and neither bind nor complement. The respective antibodies usually culminate in a mild delay of transfusion reactions. However, they do not affect HDN in any way. In incidences where antibody of the patient is directed at an antigen of high incidence, Storry and Reid suggest that the siblings need to be tested for compatibility of blood. Such patients should also urged by clinicians to donate blood to be stored for a long term period whenever their clinical or health status allows.
With respect to expression, Cromer antigens are usually expressed on the relative RBCs of the new born babies. The DAF is usually expressed on the apex of trophoblasts and in most instances; it protects the conceptus from the dangers of antibody mediated hemolysis. However, patients with PNH III conditions do not have their DAF expressed on RBCs. Soluble antigens are usually useful when carrying out hemagglutination tests. However, to obtain optimal results, initial concentration is advised.
The decay accelerating factors usually inhibit assembly as well as accelerate the decay of C5 and C3 convertases. This culminates in decreased deposition of the C3 on RBC surfaces. This greatly reduces complement-mediated hemolysis. Usually, five to six individuals that are known to have the rare Inab phenotype that is also referred to as the null serological phenotype tend to suffer from wide ranging intestinal disorders. Nonetheless, no hematological abnormalities have so far been reported. The antibodies that have specificities in this blood group system do not cause any hemolytic diseases to new born babies.
Emergent research regarding the respective alleles indicates that the epitopes of this blood group system reside in different areas of the sequence of their DAF glycoprotein. Most of them have also been identified to culminate from the single nucleotide substitutions that are found in the SCR domains that characterize the DAF. Further research ascertains that the null Inab phenotype occurs when the membrane surface lacks DAF. According to Daniels, Green, Powell and Ward, DAF is also the most common allele.
Bibliography
Daniels, G. Bromiow, I. Essential guide to blood groups. USA: Wiley-Blackwell, 2006.
Daniels, G., Green, C, Powell, R.Ward, T. Hemagglutination inhibition of Cromer blood group antibodies with soluble recombinant decay accelerating factor. Transfusion. 1998; 38 (4): 332-336.
Lublin, D. Review: Cromer and DAF: role in health and Disease. Immunohematology. 2005; 21(2): 39-47.
Hiller, C. Blood banking and transfusion medicine: Basic principles and practice. USA: Churchill Livingstone, 2006.
Hue-Rowe, K et al. Three new high prevalence antigens in the Cromer blood group system. Transfusion. 2007; 49 (9): 1621-1629
Reid, M. Disappearance of antibodies to Cromer blood group system antigens during mid pregnancy. Vox Sang (1996); 71 (1): 48-50.
Reid, M. International women in transfusion award lecture: Selected lessons learnt from blood groups. ISBT Science Series. 2006; 1 (1): 112-119.
Schenkel-Brunner, H. Human blood groups: Chemical and biochemical basis of antigen specificity. USA: Springer, 2000.
Storry, J. Reid, M. The Cromer blood group system: a review. Immunohematology. 2002; 18 (4), 95-103.
Triulzi, D. Blood transfusion therapy: A physician’s handbook pocket. USA: American Association of Blood banks, 2002.
