Factor V Leiden and Inflammation

Abstract

<jats:p>Factor V Leiden, is a variant of human factor V (FV), also known as proaccelerin, which leads to a hypercoagulable state. Along these years, factor V Leiden (FVL) has been studied from the pathophysiologic point of view, and research has been focused on finding clinical approaches for the management of the FVL associated to a trombophilic state. Less attention has been paid about the possible role of FVL in inflammatory conditions known to be present in different disorders such as uremia, cirrhosis, liver transplantation, depression as well as sepsis, infection or, inflammatory bowel disease (IBD). Whether platelet FVL will increase the activation of coagulation and/or in which proportion is able to determine the final outcome in the previously mentioned inflammatory conditions is a subject that remains uncertain. This paper will review the association of FVL with inflammation. Specifically, it will analyze the important role of the endothelium and the contribution of other inflammatory components involved at both the immune and vascular levels. This paper will also try to emphasize the importance of being a FVL carrier in associations to diseases where a chronic inflammation occurs, and how this condition may be determinant in the progression and outcome of a specific clinic situation.</jats:p>

Thrombophilic genetic factors PAI-1 4G-4G and MTHFR 677TT as risk factors of alcohol, cryptogenic liver cirrhosis and portal vein thrombosis, in a Caucasian population

“…The role of Factor V Leiden @@is important in chronic inflammation and this condition may have a role in the hepatic fibrogenesis, throughout the activation of stellate cells (Perez-Pujol et al, 2012); this THRGF was not significantly correlated to any clinical variable, in the present study.…”

“…The role of hypercoagulability in the liver fibrogenesis is well known, and many authors are studying this argument for many years (Adinolfi et al, 2005;Toniutto et al, 2008;Assy et al, 2005;Anstee et al, 2011;Perez-Pujol et al, 2012;Maharshak et al, 2011). PAI-1 has an active role in liver fibrosis in rats (Zhang et al 1999), through a pathogenic mechanism leading to the stellate cell activation, today considered the key of liver fibrogenesis (AbdulHameed et al, 2014).…”

“…Many studies were published on the role of these THRGFs in the development the PVT (Janssen et al, 2000;Balta et al, 2002;Primignani et al, 2005;Primignani and Mannucci, 2008;Tsantes et al, 2008;Parikh et al, 2010) and liver fibrosis of various etiology (Adinolfi et al, 2005;Toniutto et al, 2008;Assy et al, 2005;Anstee et al, 2011;Perez-Pujol et al, 2012;Maharshak et al, 2011), but never to date, to our knowledge, in the same study, in a consecutive series of patients with liver cirrhosis. …”

Pulmonary Embolism in a Young Male with Tuberculosis and Factor V Leiden

“…In fact, it has been suggested that the inflammatory response may further increase the thrombotic risk in FVL patients. Damage of the endothelium as well as exposure of adhesion molecules may play a major role in upregulating the thrombophilic state in this group of patients [30]. Last but not least, the risk of PE is only mildly elavated in FVL carriers.…”

Genotipos frecuentemente asociados a trombofilias

“…El factor V de la coagulación (FV), proacelerina o factor lábil, es sintetizado en el hígado, no es activo enzimáticamente, circula por el plasma libre como una cadena polipeptídica simple en una forma procoagulante inactiva y actúa como cofactor de la APC en la inactivación del factor VIIIa (36)(37)(38). El gen que codifica para el FV se encuentra en el brazo largo del cromosoma 1 (1q23).…”