Increased fibrosis progression rates in hepatitis C patients carrying the prothrombin G20210A mutation

Abstract

Carriage of the PT20210 mutation is related to an increased rate of liver fibrosis in HCV patients.

Prothrombotic genetic risk factors are associated with an increased risk of liver fibrosis in the general population

“…In this large population-based study, presence of the FVL mutation or prothrombin Our results confirm the observations of previous studies showing that the presence of FVL, prothrombin G20210A or blood group type non-O was associated with an increased rate of development or progression of liver fibrosis in patients with chronic hepatitis C [18,19,21,22].…”

“…In addition, presence of FVL caused a significant acceleration of liver fibrogenesis when exposing mice to chronic liver injury [20]. An increased rate of liver fibrosis development was also observed in patients with hepatitis C carrying the prothrombin G20210A gene variant [21]. Finally, increased severity of liver fibrosis was observed in chronic hepatitis C patients with blood group type non-O, the most common prothrombotic genetic risk factor [12,22].…”

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 same is true for the Prothrombin 20210A mutation that previously was found to be correlated to an increased rate of liver fibrosis in HCV patients (Maharshak et al, 2011).…”

“…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. …”