Elevated factor XIII level and the risk of myocardial infarction in women

Bereczky, Zsuzsanna; Balogh, Emília; Katona, Éva; Czuriga, István; Édes, István; Muszbek, László

doi:10.3324/haematol.10647

Cited by 35 publications

(26 citation statements)

References 10 publications

(1 reference statement)

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“…Further studies should explore if there is any gender-or age-specific difference in the relationship of FXIII level and the risk of VTE. Because elevated FXIII levels represent a risk of myocardial infarction 50 and peripheral arterial disease 51 only in women, genderoriented studies seem especially justified in VTE.…”

Section: The Protection Of Fibrin By Factor XIIImentioning

confidence: 99%

Factor XIII and Venous Thromboembolism

Bereczky

Muszbek

2011

Semin Thromb Hemost

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Plasma factor XIII (FXIII) is a tetrameric zymogen consisting of two potentially active A subunits (FXIII-A) and two carrier/inhibitory B subunits (FXIII-B). In the final phase of the coagulation cascade, FXIII is converted into an active transglutaminase (FXIIIa) by thrombin and Ca (2 + ). FXIIIa strengthens fibrin clot mechanically by cross-linking fibrin chains. In addition, FXIIIa is a key regulator of fibrinolysis, protecting newly formed fibrin from the fibrinolytic machinery by binding α (2)-plasmin inhibitor to the fibrin meshwork. FXIII is essential for maintaining hemostasis; its severe deficiency causes a life-threatening bleeding diathesis. The involvement of FXIII in thrombotic diseases and its association with the risk of these disorders is less clear. The role of FXIII in atherothrombotic diseases has been recently reviewed. This article offers a general overview of the relationship between FXIII and venous thromboembolism (VTE), to collect individual publications on this topic, present conclusions, and examine limitations of published studies. Special attention is given to the association of FXIII-A polymorphism with the risk of VTE, which has provoked considerable interest over the last decade.

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Section: The Protection Of Fibrin By Factor XIIImentioning

confidence: 99%

Factor XIII and Venous Thromboembolism

Bereczky

Muszbek

2011

Semin Thromb Hemost

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“…In a most recent large study involving 955 patients (377 females and 578 males), FXIII activity was measured by an assay that is not influenced by FXIII-A Val34Leu polymorphism. 69 In this study patients were subgrouped according to the presence or absence of CS and according to the presence or absence of positive history of MI. In females, but not in males, adjusted FXIII levels were moderately but significantly elevated in patients with CS and the history of MI.…”

Section: Fxiii In the Acute Phase Of Myocardial Infarctionmentioning

confidence: 99%

Factor XIII and Atherothrombotic Diseases

Muszbek

Bereczky

Bagoly

et al. 2010

Semin Thromb Hemost

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Factor XIII (FXIII) is a protransglutaminase that, after activation, cross-links fibrin chains and several plasma proteins, most importantly alpha (2) plasmin inhibitor, to fibrin. FXIII strengthens the fibrin clot by covalent bonds and protects fibrin from the prompt elimination by the fibrinolytic system. In the last two decades, FXIII has emerged as a key regulator of fibrinolysis. FXIII is also present in platelets, monocytes, and macrophages, but this cellular form does not contribute significantly to maintaining hemostasis. FXIII deficiency is a life-threatening bleeding diathesis whose clinical consequences are well studied. In contrast, the involvement of FXIII in thrombotic disorders and its association with the risk of such diseases are less clear. This review gives an account of the data accumulated mainly in the last decade on the association of FXIII with atherothrombotic diseases and presents conclusions and hypotheses drawn from these data as well as exposing the limitations of the published studies and our knowledge on this topic. The involvement of FXIII in atherogenesis, its role in coronary artery disease, atherothrombotic ischemic stroke, and peripheral artery disease are discussed, with particular reference to the association of FXIII levels and polymorphisms with the risk of these diseases.

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“…The influence of coagulation factors and common polymorphisms in hemostasis/inflammation-related genes on the risk of MI has been studied extensively, with positive and negative results, although none of the polymorphisms studied has shown strong association with the risk of MI. [1][2][3][4] However, novel functional polymorphisms in hemostasis/inflammation genes remain good candidates for a role in the pathogenesis of MI, 5 especially in younger patients in whom angiographically normal coronary arteries are more frequent and a positive family history of premature coronary disease is more prevalent than in older patients. 6,7 Inflammatory processes are a common underlying mechanism leading to coronary heart disease.…”

Section: Introductionmentioning

confidence: 99%