FIBRINOLYTIC CHANGES IN A PATIENT WITH TOXIC-SHOCK-SYNDROME - RELEASEOF ACTIVE U-PA

Citation
Ma. Haj et al., FIBRINOLYTIC CHANGES IN A PATIENT WITH TOXIC-SHOCK-SYNDROME - RELEASEOF ACTIVE U-PA, Intensive care medicine, 24(3), 1998, pp. 258-261
Citations number
10
Categorie Soggetti
Emergency Medicine & Critical Care
Journal title
ISSN journal
03424642
Volume
24
Issue
3
Year of publication
1998
Pages
258 - 261
Database
ISI
SICI code
0342-4642(1998)24:3<258:FCIAPW>2.0.ZU;2-S
Abstract
Objective:Definition of the changes in the activators of plasminogen, u-PA and t-PA, and examination of the possible generation of plasmin i n the circulation in over-whelming sepsis. Design: Serial blood analys is starting 4 h after development of symptoms of toxic shock syndrome. Setting: Intensive care unit. Patient: A previously healthy woman und erwent endometrial ablation and rapidly thereafter developed staphyloc occal toxic shock syndrome with organ failure. Measurement and result: t-PA, PAI-1, t-PA-PAI-1. complexes, plasminogen, fibrinogen and plasm in-alpha(2)-antiplasmin complexes were measured serially by ELISA and free u-PA by SDS-PAGE with zymography The onset of symptoms was accomp anied by a rise of t-PA antigen followed rapidly by PAI-1 antigen. Pla smin-alpha(2)-antiplasmin complex was generated in large amounts but d isappeared within hours. From day 3, free u-PA was detectable in the c irculation without plasmin generation. Conclusion: Despite the sustain ed presence of active u-PA in the circulation and of t-PA antigen at t he onset of symptoms, plasmin-alpha(2)-antiplasmin generation was larg ely suppressed by high levels of PAI-1. The suppression of plasmin gen eration by u-PA and t-PA may ensure the persistence of fibrin in the m icrocirculation and so contribute to organ failure.