Transfusion Reactions Are Type II Reactions

A large number of proteins and glycoproteins on the membrane of red blood cells are encoded by different genes, each of which has a number of alternative alleles. An individual possessing one allelic form of a blood-group antigen can recognize other allelic forms on transfused blood as foreign and mount an antibody response. In some cases, the antibodies have already been induced by natural exposure to similar antigenic determinants on a variety of microorganisms present in the normal flora of the gut. This is the case with the ABO blood-group antigens (Figure 16-13a).

Antibodies to the A, B, and O antigens, called isohemag-glutinins, are usually of the IgM class. An individual with blood type A, for example, recognizes B-like epitopes on intestinal microorganisms and produces isohemagglutinins to the B-like epitopes. This same individual does not respond to A-like epitopes on the same intestinal microorganisms because these A-like epitopes are too similar to self and a state of self-tolerance to these epitopes should exist (Figure 16-13b). If a type A individual is transfused with blood containing type B cells, a transfusion reaction occurs in which the anti-B iso-hemagglutinins bind to the B blood cells and mediate their

(a) Galactose

Lipid or protein

Fucose ( y A—Acetylglucosamine O antigen

A-Acetylgalactosamine Galactose

A antigen B antigen

(b)

Genotype

Blood-group phenotype

Antigens on erythrocytes (agglutinins)

Serum antibodies (isohemagglutinins)

AA or AO

A

A

Anti-B

BB or BO

B

B

Anti-A

AB

AB

A and B

None

OO

O

None

Anti-A and anti-B

ABO blood group. (a) Structure of terminal sug- blood antigens. (b) ABO genotypes and corresponding phenotypes, ars, which constitute the distinguishing epitopes, in the A, B, and O agglutinins, and isohemagglutinins.

ABO blood group. (a) Structure of terminal sug- blood antigens. (b) ABO genotypes and corresponding phenotypes, ars, which constitute the distinguishing epitopes, in the A, B, and O agglutinins, and isohemagglutinins.

FIGURE 16-13

destruction by means of complement-mediated lysis. Antibodies to other blood-group antigens may result from repeated blood transfusions because minor allelic differences in these antigens can stimulate antibody production. These antibodies are usually of the IgG class.

The clinical manifestations of transfusion reactions result from massive intravascular hemolysis of the transfused red blood cells by antibody plus complement. These manifestations may be either immediate or delayed. Reactions that begin immediately are most commonly associated with ABO blood-group incompatibilities, which lead to complement-mediated lysis triggered by the IgM isohemagglutinins. Within hours, free hemoglobin can be detected in the plasma; it is filtered through the kidneys, resulting in hemoglobinuria. Some of the hemoglobin gets converted to bilirubin, which at high levels is toxic. Typical symptoms include fever, chills, nausea, clotting within blood vessels, pain in the lower back, and hemoglobin in the urine. Treatment involves prompt termination of the transfusion and maintenance of urine flow with a diuretic, because the accumulation of hemoglobin in the kidney can cause acute tubular necrosis.

Delayed hemolytic transfusion reactions generally occur in individuals who have received repeated transfusions of ABO-compatible blood that is incompatible for other blood-group antigens. The reactions develop between 2 and 6 days after transfusion, reflecting the secondary nature of these reactions. The transfused blood induces clonal selection and production of IgG against a variety of blood-group membrane antigens, most commonly Rh, Kidd, Kell, and Duffy. The predominant isotype involved in these reactions is IgG, which is less effective than IgM in activating complement. For this reason, complement-mediated lysis of the transfused red blood cells is incomplete, and many of the transfused cells are destroyed at extravascular sites by agglutination, op-sonization, and subsequent phagocytosis by macrophages. Symptoms include fever, low hemoglobin, increased biliru-bin, mild jaundice, and anemia. Free hemoglobin is usually not detected in the plasma or urine in these reactions because RBC destruction occurs in extravascular sites.

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