What is the pathophysiology of delayed hemolytic transfusion reactions (DHTR)?

Updated: Sep 08, 2017
  • Author: Douglas Blackall, MD, MPH; Chief Editor: Michael A Kaliner, MD  more...
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DHTRs generally occur 1-2 weeks after transfusion. They represent a secondary immune response in patients previously immunized to a red cell antigen by transfusion or pregnancy. [4] In very rare cases, a brisk primary immune response can result in a DHTR after an initial transfusion. When RBC antibody titers drop below detectable levels (about 50% of the patients with alloimmunization), there is a risk for the transfusion of incompatible units of blood. Transfusion with incompatible RBCs results in restimulation of memory cells and an increase in IgG antibody titer (ie, an anamnestic immune response). Antibodies bind to the surface of RBCs and, depending on the number of antigen-antibody interactions, may activate complement with deposition of C3b. Typically, more than 105 antigenic sites per cell are required for potent complement activation.

RBCs coated with IgG antibodies and/or complement bind to immunoglobulin Fc or C3b receptors present on mononuclear phagocytes and are destroyed by phagocytosis (ie, extravascular hemolysis). IgG antibodies that efficiently activate complement (eg, those in the Kidd blood group system) tend to cause more intense extravascular hemolysis compared to antibodies that do not efficiently activate complement (eg, Rh and Kell system antibodies). Rarely, binding of IgM antibodies to RBCs activates the classic complement pathway and leads to intravascular hemolysis, but this is much more commonly seen in the context of ABO-incompatible transfusions with accompanying acute hemolytic transfusion reactions.

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