Evolution of thrombin formation and fibrinolysis markers, including thrombin-activatable fibrinolysis inhibitor, during severe meningococcemia

Pathophysiol Haemost Thromb. 2005;34(6):284-7. doi: 10.1159/000093109.

Abstract

A 17-year-old girl presented with Neisseria meningitidis sepsis, with evidence of disseminated intravascular coagulation. Substitution therapy with both antithrombin and protein C concentrates was initiated, leading to clinical and biological improvement. Sequential dosages were performed for biological markers including thrombin-activatable fibrinolysis inhibitor (TAFI). Substitution therapy with both antithrombin and protein C concentrates led to a clinical and biological improvement. Biological markers showed a decrease in thrombin generation and in plasminogen activator inhibitor 1 (PAI-1) and a return of TAFI to a normal value. Discontinuation of substitutive treatment was marked by a clinical relapse at 24 h, with thrombin generation and increase in PAI-1, while TAFI remained unchanged. This report shows the evolution of hemostasis markers during septic shock and provides new data concerning the effects of a substitutive therapy.

Publication types

  • Case Reports

MeSH terms

  • Adolescent
  • Biomarkers
  • Blood Coagulation / physiology
  • Carboxypeptidase B2 / metabolism*
  • Female
  • Fibrinolysis / physiology*
  • Humans
  • Meningococcal Infections / blood*
  • Meningococcal Infections / physiopathology
  • Neisseria meningitidis*
  • Sepsis / blood
  • Sepsis / microbiology
  • Severity of Illness Index
  • Thrombin / metabolism*

Substances

  • Biomarkers
  • Carboxypeptidase B2
  • Thrombin