RELEASE OF MEDIATORS OF SYSTEMIC INFLAMMATORY RESPONSE SYNDROME IN THE COURSE OF A SEVERE DELAYED HEMOLYTIC TRANSFUSION REACTION CAUSED BY ANTI-D

BACKGROUND: In vitro studies suggest that mediators of systemic inflam matory response syndrome are generated in the course of hemolytic tran sfusion reactions. Evidence for the in vivo significance of these find ings is given by the present clinical and laboratory analysis of a sev ere delayed hemolytic transfusion reaction (DHTR). CASE REPORT: A 67-y ear-old patient (blood group O, D-negative) with a negative pretransfu sion antibody screen received a massive transfusion because of arteria l bleeding (Day 1). The transfusion of group O, D-positive red cell co ncentrates was unavoidable because of limited supplies. At Day 10, the patient developed a DHTR with symptoms of septic-toxic syndrome and s igns of hemolysis; he received an exchange transfusion. Serologic mark ers, as well as proinflammatory and anti-inflammatory mediators, were monitored at the onset of the DHTR and during the exchange transfusion . RESULTS: At Day 10, the direct antiglobulin test was positive; anti- D was present, most likely as the result of an anamnestic immune respo nse. Interleukin (IL)-1 was not detectable; all other mediators monito red were elevated: IL-l receptor antagonist, tumor necrosis factor, IL -5, IL-8, IL-10, neopterin, elastase, C3a-desArg, C-reactive protein, and fibrinogen. Most of the values declined during the exchange transf usion, which was followed by an improvement of the clinical presentati on. CONCLUSIONS: Mediators of systemic inflammatory response syndrome were released in the course of a DHTR caused by anti-D. Severe clinica l symptoms could be treated successfully by exchange transfusion.