Fibrinolytic changes in a patient with toxic shock syndrome; release of active u-PA

Haj, M. A.; Robbie, Linda A.; Croll, A.; Adey, Gillian; Bennett, B. M.

doi:10.1007/s001340050561

Cited by 8 publications

(2 citation statements)

References 9 publications

(8 reference statements)

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“…Fifteen % had systemic fibrinolytic activity with predominance of t-PA activity while 85% had increased systemic anti-fibrinolytic activity with predominance of PAI-1 activity. These findings are supported in part by previous adult reports (19)(20)(21).…”

Section: Discussionsupporting

confidence: 89%

The Tissue Factor and Plasminogen Activator Inhibitor Type-1 Response in Pediatric Sepsis-induced Multiple Organ Failure

Green¹,

Doughty²,

Kaplan³

et al. 2002

Thromb Haemost

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SummaryCytokines increase endothelial tissue factor (TF) and tissue plasminogen activator inhibitor type -1 (PAI-1) expression in vitro. Tissue factor interacts with factor VII to facilitate thrombosis and PAI-1 inhibits fibrinolysis by endogenous plasminogen activators.Because cytokine release is increased in children with sepsisinduced multiple organ failure (MOF), we hypothesized a cytokine associated increase in circulating TF and PAI-1 antigen release, and systemic activity in these patients.One hundred and seven consecutive children, who met the criteria for sepsis, and 10 critically ill children without sepsis, were enrolled in the study. Plasma TF and PAI-1 antigen and activity levels, Interleukin-6 antigen levels (IL-6), nitrite + nitrate levels (marker of nitric oxide production) and number of organs failing were measured on days 1-3 of sepsis.Increased TF and PAI-1 antigen, and PAI-1 activity levels were associated with increasing IL-6 and nitrite + nitrate levels (p <0.05), the development of MOF (p <0.05), and mortality (p <0.05). Increased systemic PAI-1 activity was associated with cardiovascular, renal, and hepatic failure (p <0.05). Increased systemic TF activity was associated with the development of coagulopathy (p <0.05) and tended to be associated with mortality (p =0.06, power .77)A shift to an anti-fibrinolytic endothelium phenotype characterizes children who develop sepsis-induced MOF and mortality. Children with coagulopathy have a shift to a pro-coagulant phenotype. These findings support potential therapeutic roles for PAI-1 and TF pathway inhibitors in reversal of this devastating pathophysiologic process.

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Section: Discussionsupporting

confidence: 89%

The Tissue Factor and Plasminogen Activator Inhibitor Type-1 Response in Pediatric Sepsis-induced Multiple Organ Failure

Green¹,

Doughty²,

Kaplan³

et al. 2002

Thromb Haemost

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show abstract

“…The major endogenous inhibitor of tPA and uPA, plasminogen activator inhibitor 1 (PAI-1), is markedly increased in pleural loculation (26 -28), myocardial infarction (29 -34), acute respiratory distress syndrome, and sepsis (35)(36)(37). High levels of PAI-1 inhibit the fibrinolytic system and promote thrombosis and uncontrolled fibrin deposition (38,39).…”

mentioning

confidence: 99%

Effects of Extracellular DNA on Plasminogen Activation and Fibrinolysis

Komissarov¹,

Florova²,

Idell³

2011

Journal of Biological Chemistry

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Background: Elevated levels of extracellular DNA and aberrant fibrinolysis occur in a range of severe diseases. Results: DNA competes with fibrin for fibrinolytic enzymes. DNA stimulates fibrin-independent plasminogen activation and increases enzyme susceptibility to serpins. Conclusion: DNA is a macromolecular template that both potentiates and inhibits fibrinolysis. Significance: Understanding the interaction of DNA with the fibrinolytic system could improve the outcomes of fibrinolytic therapy.

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Endometrial ablation: postoperative complications

Sharp¹

2012

American Journal of Obstetrics and Gynecology

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Fibrinolytic changes in a patient with toxic shock syndrome; release of active u-PA

Cited by 8 publications

References 9 publications

The Tissue Factor and Plasminogen Activator Inhibitor Type-1 Response in Pediatric Sepsis-induced Multiple Organ Failure

The Tissue Factor and Plasminogen Activator Inhibitor Type-1 Response in Pediatric Sepsis-induced Multiple Organ Failure

Effects of Extracellular DNA on Plasminogen Activation and Fibrinolysis

Endometrial ablation: postoperative complications

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