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Theodore F. Logan, MD; Mohamed A. Virji, MD, PhD; William E. Gooding, MS; Franklin A. Bontempo, MD; Marc S. Ernstoff, MD; John M. Kirkwood, MD
Pittsburgh Cancer Institute Pittsburgh, Pa

JAMA. 1994;271(6):427-428.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.

—We read with interest the excellent article by Levi et al¹ reviewing the pathogenetic mechanisms of the activation of coagulation and fibrinolysis in sepsis. It is noted that plasminogen activator activity can result from the activation of the contact-activated (intrinsic) coagulation pathway. However, several studies are cited that suggest that the activation of fibrinolysis was independent of activation of the coagulation system in sepsis. The temporal relationship between the appearance of tumor necrosis factor- (TNF-) after endotoxin and the increase in fibrinolytic activity as well as the abolition of fibrinolytic activation in endotoxin-treated chimpanzees given pentoxifylline, suggested that TNF- was the mediator of this effect. We would like to suggest further insight into the mechanism of TNF-induced fibrinolytic activation.

In a phase I (uncontrolled) study of TNF- in human cancer patients, we have recently demonstrated the release of tissue-type plasminogen activator (t-PA, an endothelial product as . . . [Full Text PDF of this Article]

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