PREVALENCE OF BLOOD GROUPA2 AMONG GROUPAAND AB DONORS

Abstract

The ABO blood group antigens are clinically signicant and their discovery by Landsteiner in 1900 paved way for the performance of safe blood transfusions. These antigens are characterized by their distinct carbohydrate structures attached to the glycoprotein or glycolipid membranes of red blood cells (RBCs). Their expression can also be detected on various human cell and tissue surfaces including sensory neurons, vascular endothelium and platelets. [1] Subgroups of the ABO antigens occur and are characterized by reduced quantities of the antigens on the RBCs and saliva of secretors. [2] Landsteiner & Levine subdivided blood group A into their principal subgroups, A1 and A2. The presence of Asubgroups is due to genetic variations in the coding region which leads to diminished amounts of A substance and higher amounts of H substance on red blood cells. There are weaker subgroups than A2 which do not frequently occur but when present; they show a characteristic decreased Aantigen sites on their RBC and a corresponding increased H antigen activity. [3] The difference between subgroups A1 and A2 is seen in their reactivity with the Dolichos biflorus lectin. The Dolichos lectin specically agglutinates A1 cells, leaving the A2 cells unagglutinated. The ABO antibodies occur naturally in the sera of individuals who do not have the corresponding antigens and can cause haemolysis in-vivo. They are mostly immunoglobulin M (IgM). These antibodies through complement activation can cause severe, life-threatening transfusion reactions due to incompatible ABO blood transfusions. Anti-A1 antibody appears as an atypical cold agglutinin in the sera of few people with group A2 or A2B who do not have the corresponding antigen.[4] One to eight percent of persons with blood group A2 and about 22-35% of persons with group A2B have serum anti-A1. These antibodies may cause discrepancies in ABO blood grouping which can further result in HTR.[5] Rare cases of haemolytic transfusion reaction due to anti-A1 have been reported.[4] It is estimated that about 80% of individuals with antigen A are A1 while the remaining 20% are A2. [5] Among Indians, the frequency of subgroup A2 among group A individuals is 6.58% whiles that of A2B among group AB is 8.99%.[6] Knowledge of the frequency and distribution of blood subgroup A2 will help to enhance blood compatibility testing, population genetic studies, investigation of transfusion reactions, studying disease associations and resolving some medico-legal issues.[7]