Abstract
Objective: Definition of the changes in the activators of plasminogen, u-PA and t-PA, and examination of the possible generation of plasmin in the circulation in overwhelming sepsis.
Design: Serial blood analysis starting 4 h after development of symptoms of toxic shock syndrome.
Setting: Intensive care unit.
Patient: A previously healthy woman underwent endometrial ablation and rapidly thereafter developed staphylococcal toxic shock syndrome with organ failure.
Measurement and result: t-PA, PAI-1, t-PA-PAI-1 complexes, plasminogen, fibrinogen and plasmin-α2-antiplasmin complexes were measured serially by ELISA and free u-PA by SDS-PAGE with zymography. The onset of symptoms was accompanied by a rise of t-PA antigen followed rapidly by PAI-1 antigen. Plasmin-α2-antiplasmin complex was generated in large amounts but disappeared within hours. From day 3, free u-PA was detectable in the circulation without plasmin generation.
Conclusion: Despite the sustained presence of active u-PA in the circulation and of t-PA antigen at the onset of symptoms, plasmin-α2-antiplasmin generation was largely suppressed by high levels of PAI-1. The suppression of plasmin generation by u-PA and t-PA may ensure the persistence of fibrin in the microcirculation and so contribute to organ failure.
References
McWilliam NA, Robbie LA, Bardie CJ, Adey GD, Prasad S, Bennett B, Booth NA (1996) Evidence for an active fibrinolytic system in normal human bone marrow. Br J Haematol 93: 170–176
Bennett B, Croll A, Ferguson K, Booth NA (1990) Complexing of tissue plasminogen activator with alpha2macroglobulin and C I inhibitor. Studies on patients with defibrination and a fibrinolytic state after electroshock or complicated labor. Blood 75: 671–676
Williams GR (1990) The toxic shock syndrome. BMJ 300: 960
Bergdoll MS, Crass BA, Reiser RF, Robbins RN, Davis JP (1981) A new staphylococcal enterotoxin, F, associated with toxic shock syndrome Staphylococcus aureus isolates. Lancet 1: 1017–1021
Pintucci G, Iacoviello L, Amore C, Evangelista V, Cerletti C, Donati (1992) Cathepsin G, a polymorphonuclear cell protease, affects the fibrinolytic system by releasing PAI-1 from endothelial cells and platelets. Ann NY Acad Sci 667:286–288
Haj MA, Robbie LA, Adey GD, Bennett B (1995) Inhibitors of plasminogen activator in neutrophils and mononuclear cells from septic patients. Thromb Haemost 74:1528–1532
Sprengers ED, Princen HMG, Kooistra T, Van Hinsbergh VWM (1985) The inhibition of plasminogen activators by human hepatocytes and hepatoma cell line Hp G 92. J Lab Clin Med 105: 751–758
Pralong G, Calandra T, Glauser MP, Schellekens J, Verhoef J, Bachmann F, Kruithof EKO (1989) Plasminogen activator inhibitor 1; a new prognostic marker in septic shock. Thromb Haemost 61: 459–469
Philippe J, Offner F, Declerck PJ, Leroux-Roels G, Vogelaers D, Baele G, Collen D (1991) Fibrinolysis and coagulation in patients with infectious disease and sepsis. Thromb Haemost 65: 291–299
Philippe J, Doojewaard G, Offner F, Turion P, Baele G, Leroux-Roels G (1992) Granulocyte elastase, tumour necrosis factor alpha and urokinase levels as prognostic markers in severe infection. Thromb Haemost 68:19–23
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Haj, M.A., Robbie, L.A., Croll, A. et al. Fibrinolytic changes in a patient with toxic shock syndrome; release of active u-PA. Intensive Care Med 24, 258–261 (1998). https://doi.org/10.1007/s001340050561
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s001340050561