von Zabern I, Ehlers M, Grunwald U, Mauermann K, Greinacher A
Institute of Immunology and Transfusion Medicine, University of Greifswald, Germany.
Transfusion. 1998 May;38(5):459-68. doi: 10.1046/j.1537-2995.1998.38598297215.x.
In vitro studies suggest that mediators of systemic inflammatory response syndrome are generated in the course of hemolytic transfusion reactions. Evidence for the in vivo significance of these findings is given by the present clinical and laboratory analysis of a severe delayed hemolytic transfusion reaction (DHTR).
A 67-year-old patient (blood group O, D-negative) with a negative pretransfusion antibody screen received a massive transfusion because of arterial bleeding (Day 1). The transfusion of group O, D-positive red cell concentrates was unavoidable because of limited supplies. At Day 10, the patient developed a DHTR with symptoms of septic-toxic syndrome and signs of hemolysis; he received an exchange transfusion. Serologic markers, as well as proinflammatory and anti-inflammatory mediators, were monitored at the onset of the DHTR and during the exchange transfusion.
At Day 10, the direct antiglobulin test was positive; anti-D was present, most likely as the result of an anamnestic immune response. Interleukin (IL)-1 was not detectable; all other mediators monitored were elevated: IL-1 receptor antagonist, tumor necrosis factor, IL-6, IL-8, IL-10, neopterin, elastase, C3a-desArg, C-reactive protein, and fibrinogen. Most of the values declined during the exchange transfusion, which was followed by an improvement of the clinical presentation.
Mediators of systemic inflammatory response syndrome were released in the course of a DHTR caused by anti-D. Severe clinical symptoms could be treated successfully by exchange transfusion.
