RRML - Coagulation factor XIII, impaired fibrinolysis and cardiovascular disease
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Dr. Adrian Man
   
 
Nr. 19(2)/2011
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Coagulation factor XIII, impaired fibrinolysis and cardiovascular disease

Mircea Cucuianu, Ioana Brudaşcă


Abstract:

This review is based on data in the literature also including clinical and laboratory observations reported by one of the review’s authors 38 years ago, demonstrating increased plasma factor XIII activity in patients with hyperlipoproteinemia type IIb and type IV displaying features compatible with the concept of metabolic syndrome. Factor XIII activity was correlated with serum triglyceride levels and also with serum cholinesterase activity, a marker of hepatic protein synthesis. Impaired hepatic protein synthesis subsequent to L-asparaginase therapy in leukemic patients led to an important decrease of both plasma factor XIII and serum cholinesterase activities. It was considered that enhanced hepatic synthesis of factor XIII subunit B occurring in such hypetriglyceridemic subjects would assemble with monocyte-derived subunit A of this factor endowed with transglutaminase activity, thereby stabilizing, transporting and increasing the plasma levels of factor XIII (A2B2) zymogen. Increased plasma factor XIII activity was associated with delayed fibrinolysis in such hypertriglyceridemic patients and in vitro inhibition of factor XIII by parachlormercuribenzoate led to an acceleration of clot lysis. High plasma levels and activity of factor XIII were later reported by British authors in insulin resistant patients. It was also demonstrated that in vivo glycation of fibrinogen occurring in diabetic patients would render a plasmin resistant fibrin clot. The presumptive protection against myocardial infarction exerted by the Val34Leu polymorphism in the subunit A of factor XIII incited many studies with rather controversial results, this protective effect being diminished in insulin resistant patients. Factor XIII exerts bivalent effects on atherogenesis, enhancing thrombotic tendency by reducing fibrinolytic activity, while by the crosslinking of extracellular matrix protein exerted by subunit A in monocytes and histiocytes an atheroma’s fibrous cap would be strengthened thereby reducing its vulnerability and preventing plaque’s rupture.

Keywords: factor XIII,impaired fibrinolysis,metabolic disorders,cardiovascular disease,factor XIII subunit A Val34Leu polymorphism

 
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How to cite
Cucuianu M, Brudaşcă I. Coagulation factor XIII, impaired fibrinolysis and cardiovascular disease. Rev Romana Med Lab. 2011;19(2):119-27