(Circulation. 2000;101:e158.)
© 2000 American Heart Association, Inc.
Circulation Electronic Pages |
Professor of Clinical Chemistry Medical Clinic Nr I, R-3400 Cluj-Napoca, Romania, E-mail hemato@codec.ro
| Introduction |
|---|
Reed and Houng1 demonstrated that factor XIII-mediated
cross-linking plays a critical role in limiting
fibrinolysis in experimentally formed pulmonary
emboli. They suggested that factor XIII could facilitate the growth of
new or forming thrombi. This concept is supported by my
observations, which began 26 years ago and emphasize increased plasma
factor XIII levels in hypertriglyceridemic
patients2 3 4 who also display high plasma fibronectin
concentrations4 and an obviously prolonged dilute blood
clot lysis time.5 Because the in vitro inhibition of
factor XIII by p-chloromercuribenzoate led to an acceleration of clot
lysis,5 I presumed that the association of high plasma
factor XIII levels with impaired fibrinolysis was not
merely casual. My colleagues and I also showed that platelet factor
XIII is unlikely to make any significant contribution to plasma factor
XIII levels.3 However, the significant correlations
between liver-secreted serum cholinesterase and plasma factor XIII and
fibronectin, as well as data obtained in patients with severely
impaired hepatic protein synthesis (decompensated liver cirrhosis) or
compensatively enhanced secretion of plasma proteins (nephrotic
syndrome) provide circumstantial evidence that the liver is the main
contributor to plasma factor XIII and fibronectin.4
Presumably, overloading the liver with lipids in a patient with insulin
resistance would stimulate the synthesis of factor XIII, fibronectin,
and serum cholinesterase. It is also reasonable to presume that thrombi
richer in factor XIII and fibronectin would not only be more
resistant to fibrinolysis but also more readily
attached to the vessel wall. It is hoped that the convincing results
reported by
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2000 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |