Outline the principles of ABO blood grouping and list the consequences of a mismatched transfusion involving these blood groups.

Outline:

·        Agglutinogens

·        Agglutinins

·        Blood typing

·        Transfusion reactions

Essay:

            The membrane of human red cells contain a variety of blood group antigens, which are also called agglutinogens. The most important and best known of these are the A and B antigens, but there are many more. The A and B antigens are inherited as mendelian dominants, and individuals are divided into 4 major blood types on this basis. Type A individuals have the A antigen, type B have the B, type AB have both, and type O have neither. The A and B antigens are actually complex oligosaccharides that differ in their terminal sugar.

            Two genes, one on each of two paired chromosomes, determine the O-A-B blood groups. These two genes are allelomorphic genes that can be any one of three types but only one type on each chromosome: type O, type A, or type B. The type O gene is functionless so that it causes no significant type O agglutinogen on the cells. On the other hand, the type A and type B genes do cause strong agglutinogens on the cells.

            Antibodies against red cell agglutinogens are called agglutinins. When type A agglutinogen is not present in a person’s red blood cells, anti-A agglutinins develop in the plasma. Also when type B agglutinogen is not present in red blood cells, anti-B agglutinins develop in the plasma. The agglutinins are gamma globulins and they are produced by the same cells that produce antibodies to any other antigens. Most of them are IgM and IgG immunoglobulin molecules. These agglutinins enter the body in bacteria and food, initiating the development of the anti-A or anti-B agglutinins.

            Before giving a transfusion, it is necessary to determine the blood type of the recipient and the blood type of the donor blood so that bloods can be appropriately matched. This is called blood typing. The red blood cells are first diluted with saline. One portion is then mixed with anti-A agglutinin and another portion is mixed with anti-B agglutinin. After several minutes, the mixture is observed under a microscope. If the red blood cells have become clumped, an antibody-antigen reaction has resulted. So, if an antibody-antigen reaction is observed in both cases, the red blood type is O and if no reaction is observed, the blood type is AB.

            If donor blood of one blood type is transfused to a recipient of another blood type, a transfusion reaction is likely to occur in which the red blood cells of the donor blood are agglutinated. It is rare that the transfused blood causes agglutination of the recipient’s cells, as the plasma portion of the donor blood immediately becomes dilated by all the plasma of the recipient, thereby decreasing the titer of the infused agglutinins to a level too low to cause agglutination. On the other hand, the infused blood does not dilute the agglutinins in the recipient’s plasma to a major extent. Therefore, the recipient’s agglutinins can still agglutinate the donor cells.

            In a mismatched transfusion of blood groups, the agglutinins attach themselves to the red blood cells, causing the cells to clump together, which is the process of agglutination. Then these clumps plug small blood vessels throughout the circulatory system. During the next few hours to days, either physical distortion of the cells or attack by phagocytic white blood cells destroys the agglutinated cells, releasing hemoglobin into the plasma. The severity of the resulting transfusion reaction may vary from an asymptomatic minor rise in the plasma bilirubin level to severe jaundice and renal tubular damage, which can lead eventually to renal failure and death. The kidney shutdown may be due to toxic substances released by the hemolyzing blood that cause powerful renal constriction. Free hemoglobin is released into the blood and much of the excess leaks through the glomerular membrane into the kidney tubules. As water is reabsorbed, tubular hemoglobin rises so high that it precipitates and blocks many of the tubules. All these add together to cause acute renal shutdown. If the shutdown is complete and fails to open up, the patient dies within a week to 12 days.