title: Release of mediators of systemic inflammatory response syndrome in the course of a severe delayed hemolytic transfusion reaction caused by anti-D.
abstract: BACKGROUND
  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).
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Institute of Immunology and Transfusion Medicine, University of Greifswald, Germany.
authors.forename: I
authors.initials: I
authors.lastname: von Zabern
authors.forename: M
authors.initials: M
authors.lastname: Ehlers
authors.forename: U
authors.initials: U
authors.lastname: Grunwald
authors.forename: K
authors.initials: K
authors.lastname: Mauermann
authors.forename: A
authors.initials: A
authors.lastname: Greinacher
mesh_terms: D018806:APACHE; D000209:Acute-Phase Proteins / Q000032:analysis; D000368:Aged; D001663:Bilirubin / Q000097:blood; D001787:Blood Group Incompatibility / Q000150:complications*; D003404:Creatinine / Q000097:blood; D017707:Erythrocyte Transfusion / Q000009:adverse effects*; D004912:Erythrocytes / Q000276:immunology; D005434:Flow Cytometry; D006454:Hemoglobins / Q000032:analysis; D006461:Hemolysis / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis; D018836:Inflammation Mediators / Q000097:blood / Q000378:metabolism*; D007518:Isoantibodies / Q000097:blood / Q000276:immunology; D007770:L-Lactate Dehydrogenase / Q000097:blood; D007958:Leukocyte Count; D008297:Male; D010976:Platelet Count; D012204:Rh-Hr Blood-Group System / Q000276:immunology*; D018746:Systemic Inflammatory Response Syndrome / Q000378:metabolism*; D013997:Time Factors; D017186:Titrimetry; D014508:Urea / Q000097:blood
chemical_list: D000209:Acute-Phase Proteins; D006454:Hemoglobins; D007074:Immunoglobulin G; D018836:Inflammation Mediators; D007518:Isoantibodies; D012204:Rh-Hr Blood-Group System; D014508:Urea; D003404:Creatinine; D007770:L-Lactate Dehydrogenase; D001663:Bilirubin