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Increased prothrombin activation in a patient with congenital afibrinogenemia is reversible by fibrinogen substitution.

Abstract
We describe a patient with congenital afibrinogenemia who showed elevated prothrombin activation fragments (F1 + 2) indicating increased thrombin formation. This finding was unexpected since it has hitherto been thought that patients with congenital hypo- or afibrinogenemia have no evidence of increased utilization or accelerated consumption of coagulation factors. No other possible reasons for the elevation of F 1 + 2 were found. Upon fibrinogen substitution F1 + 2 decreased and were again increasing when fibrinogen concentration in plasma fell to very low levels. These findings raise the question of whether increased thrombin formation should be understood as a compensatory mechanism in congenital afibrinogenemia.
AuthorsW Korte, A Feldges
JournalThe Clinical investigator (Clin Investig) Vol. 72 Issue 5 Pg. 396-8 (May 1994) ISSN: 0941-0198 [Print] Germany
PMID8086775 (Publication Type: Case Reports, Journal Article)
Chemical References
  • Fibrin Fibrinogen Degradation Products
  • Peptide Fragments
  • fibrin fragment D
  • prothrombin fragment 1.2
  • Prothrombin
  • Fibrinogen
Topics
  • Adolescent
  • Afibrinogenemia (blood, drug therapy)
  • Enzyme Activation
  • Female
  • Fibrin Fibrinogen Degradation Products (analysis)
  • Fibrinogen (therapeutic use)
  • Humans
  • Peptide Fragments (analysis)
  • Prothrombin (analysis, metabolism)

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