title: An enhanced fibrinolysis prevents the development of multiple organ failure in disseminated intravascular coagulation in spite of much activation of blood coagulation.
abstract: OBJECTIVE
  To investigate the relationship between fibrinolytic enhancement and the development of multiple organ failure (MOF) in disseminated intravascular coagulation (DIC). To detect the useful prognostic index for outcome in DIC.
  
  
  METHODS
  Case-control study.
  
  
  METHODS
  A department of internal medicine in a university hospital, a clinical division for diagnosis and treatment, mainly of respiratory diseases, hematologic diseases, DIC, and other diseases requiring critical care medicine.
  
  
  METHODS
  A total of 69 DIC patients, 31 with MOF.
  
  
  METHODS
  None.
  
  
  RESULTS
  The DIC patients with MOF had more elevated levels of tissue plasminogen activator antigen (t-PA) and plasminogen activator inhibitor antigen (PAI), and more depressed levels of plasmin-alpha2 plasmin inhibitor complex (PIC) and fibrin/fibrinogen degradation products than those without MOF, although no significant difference in thrombin-antithrombin complex (TAT) levels was observed. A fibrinolytic enhancement (shown by PIC) was parallel to an activation of blood coagulation (shown by TAT) in DIC patients without MOF, although no such fibrinolytic enhancement was provoked even by much activation of blood coagulation in DIC patients with MOF. Whereas all the patients without MOF were restored from DIC, 14 of 31 patients with MOF were unable to be restored from DIC and died. A significant increase in plasma levels of t-PA and PAI under the condition of sustained hemostatic activation was observed in the patients who died.
  
  
  CONCLUSIONS
  Enhanced fibrinolysis was considered to be the important defense mechanism in preventing the development of MOF in DIC. The increases in plasma levels of t-PA and PAI were poor prognostic markers in DIC. Further careful study may be useful to clarify whether the fibrinolytic therapy is beneficial in clinical DIC patients with MOF.
authors.affiliation: Department of Internal Medicine (III), Kanazawa University School of Medicine, Takaramachi 13-1, Kanazawa 920-8641, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Asakura
authors.forename: Y
authors.initials: Y
authors.lastname: Ontachi
authors.forename: T
authors.initials: T
authors.lastname: Mizutani
authors.forename: M
authors.initials: M
authors.lastname: Kato
authors.forename: M
authors.initials: M
authors.lastname: Saito
authors.forename: I
authors.initials: I
authors.lastname: Kumabashiri
authors.forename: E
authors.initials: E
authors.lastname: Morishita
authors.forename: M
authors.initials: M
authors.lastname: Yamazaki
authors.forename: K
authors.initials: K
authors.lastname: Aoshima
authors.forename: S
authors.initials: S
authors.lastname: Nakao
mesh_terms: D000933:Antifibrinolytic Agents / Q000097:blood; D016022:Case-Control Studies; D004211:Disseminated Intravascular Coagulation / Q000097:blood* / Q000150:complications; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005341:Fibrinolysin; D005342:Fibrinolysis / Q000502:physiology*; D006801:Humans; D016014:Linear Models; D008297:Male; D009102:Multiple Organ Failure / Q000097:blood* / Q000150:complications; D015849:Plasminogen Inactivators / Q000097:blood; D018709:Statistics, Nonparametric; D010959:Tissue Plasminogen Activator / Q000097:blood; D000979:alpha-2-Antiplasmin
chemical_list: D000933:Antifibrinolytic Agents; D005338:Fibrin Fibrinogen Degradation Products; D015849:Plasminogen Inactivators; D000979:alpha-2-Antiplasmin; C037742:plasmin-plasmin inhibitor complex; D010959:Tissue Plasminogen Activator; D005341:Fibrinolysin