title: Thrombin-activatable fibrinolysis inhibitor (TAFI) is enhanced in major trauma patients without infectious complications.
abstract: BACKGROUND
  Infectious complications frequently occur after major trauma, leading to increased morbidity and mortality. Thrombin-activatable fibrinolysis inhibitor (TAFI), a procarboxypeptidase in plasma, plays a dual role in regulating both coagulation and inflammation. Activated TAFI (TAFIa) has broad anti-inflammatory properties due to its inactivation of active inflammatory mediators (anaphylatoxins C3a and C5a, bradykinin, osteopontin).
  
  
  OBJECTIVE
  The purpose of this study was to determine if TAFI plays a role in the development of inflammatory complications after major trauma.
  
  
  METHODS
  Upon arrival at the emergency department (ED), plasma levels of TAFI and TAFIa were measured in 26 multiple traumatized patients for 10 consecutive days. Systemic levels of inflammatory mediators, including interleukin-6 (IL-6), procalcitonin (PCT), C-reactive protein (CRP) and leukocytes were determined.
  
  
  RESULTS
  Fifteen patients developed pneumonia and/or sepsis (compl) and 11 had no complications (wo compl). Overall injury severity and age were comparable in both groups. Complications occurred approximately 5 days after trauma. IL-6 increased on day 5, whereas CRP, PCT and leukocytes started to increase on day 6 in the compl-group. Upon arrival at the ED and on days 1 and 4, TAFI levels were significantly lower in the compl-group compared to the wo compl-group (p=0.0215). Similarly, TAFIa was significantly lower on day 4 in the compl-group than in the wo compl-group (p=0.049).
  
  
  CONCLUSIONS
  This pilot study shows that TAFI levels are inversely correlated with inflammation-associated development of complications after major trauma.
authors: Department of Trauma, Hand and Reconstructive Surgery, Hospital of the Goethe University Frankfurt am Main, 60590 Frankfurt, Germany. info@bornarelja.com
authors: B
authors: B
authors: Relja
authors: T
authors: T
authors: Lustenberger
authors: B
authors: B
authors: Puttkammer
authors: H
authors: H
authors: Jakob
authors: J
authors: J
authors: Morser
authors: E C
authors: EC
authors: Gabazza
authors: Y
authors: Y
authors: Takei
authors: I
authors: I
authors: Marzi
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002097:C-Reactive Protein / Q000276:immunology / Q000378:metabolism; D002116:Calcitonin / Q000097:blood / Q000276:immunology; D015740:Calcitonin Gene-Related Peptide; D025901:Carboxypeptidase B2 / Q000097:blood* / Q000276:immunology; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood / Q000276:immunology; D018836:Inflammation Mediators / Q000097:blood / Q000276:immunology; D015850:Interleukin-6 / Q000097:blood / Q000276:immunology; D007958:Leukocyte Count; D008297:Male; D008875:Middle Aged; D009104:Multiple Trauma / Q000097:blood* / Q000150:complications / Q000276:immunology; D010865:Pilot Projects; D011014:Pneumonia / Q000097:blood / Q000209:etiology / Q000276:immunology; D011498:Protein Precursors / Q000097:blood / Q000276:immunology; D018805:Sepsis / Q000097:blood / Q000209:etiology / Q000276:immunology; D013997:Time Factors
chemical_list: C000606589:CALCA protein, human; C508600:IL6 protein, human; D018836:Inflammation Mediators; D015850:Interleukin-6; D011498:Protein Precursors; D002116:Calcitonin; D002097:C-Reactive Protein; D025901:Carboxypeptidase B2; D015740:Calcitonin Gene-Related Peptide