Abstract
Background: Non-alcoholic fatty liver disease (NAFLD) is a pathological condition, ranging from fatty liver to chronic steatohepatitis (NASH), liver cirrhosis, and eventually to hepatocellular carcinoma. Recent findings suggest that patients with NAFLD have an increased risk of cardiovascular events and thromboembolism, which is independent of metabolic diseases that are frequently associated with NAFLD, such as diabetes, hyperlipidemia, and obesity. Methods: We evaluated 30 NAFLD patients, before and after weight loss. Plasma levels of C-reactive protein (CRP), fibrinogen, plasminogen activator inhibitor-1 (PAI-1), von Willebrand factor (VWF), homocysteine, coagulation protein S, Thrombin activable fibrinolysis inhibitor (TAFI), and factor VII (FVII) were assessed to evaluate whether they should be responsible of the prothrombotic state of NAFLD after weight loss. Results: At baseline, patients affected by NAFLD had a significantly higher levels of CRP, fibrinogen, PAI-1, VWF antigen, and FVII levels. After weight reduction, we observed a significant drop of inflammatory and prothrombotic markers, as well as glucometabolic, lipid profile. Conclusion: These findings provide evidence for a link between NAFLD/NASH and thromboembolism. The association seems to be linked with primitive thrombotic state and hypercoagulation due to increased levels of coagulation factors and reduced levels of PAI-1. This hypercoagulation state might explain increased levels of thrombosis and splanchnic thrombosis observed in NASH correlated cirrhosis.
Highlights
Non-alcoholic fatty liver disease (NAFLD) is a pathological condition, ranging from fatty liver (FL) to chronic steatohepatitis (NASH), liver cirrhosis, and eventually to hepatocellular carcinoma (HCC) [1].Nonalcoholic fatty liver disease (NAFLD), on its whole spectrum of conditions ranging from steatosis to steatohepatitis and cirrhosis, is the most frequent liver disease in developed countries, regarded as the liver manifestation of the metabolic syndrome [2]
Liver biopsy was performed during observational time in four cases, showing NASH in two cases and liver cirrhosis in two cases
The present study indicates that patients affected by NAFLD have elevated levels of C-reactive protein (CRP), fibrinogen, plasminogen activator inhibitor-1 (PAI-1), von Willebrand factors, and F VII, which are known to be associated with an increased risk of thrombosis
Summary
Non-alcoholic fatty liver disease (NAFLD) is a pathological condition, ranging from fatty liver (FL) to chronic steatohepatitis (NASH), liver cirrhosis, and eventually to hepatocellular carcinoma (HCC) [1].Nonalcoholic fatty liver disease (NAFLD), on its whole spectrum of conditions ranging from steatosis to steatohepatitis (nonalcoholic steatohepatitis; NASH) and cirrhosis, is the most frequent liver disease in developed countries, regarded as the liver manifestation of the metabolic syndrome [2]. Non-alcoholic fatty liver disease (NAFLD) is a pathological condition, ranging from fatty liver (FL) to chronic steatohepatitis (NASH), liver cirrhosis, and eventually to hepatocellular carcinoma (HCC) [1]. Several studies indicate that NAFLD, especially in its necroinflammatory form (NASH), is associated with a systemic proinflammatory/prothrombotic state, leading to atherothrombosis such as cardiovascular disease. Non-alcoholic fatty liver disease (NAFLD) is a pathological condition, ranging from fatty liver to chronic steatohepatitis (NASH), liver cirrhosis, and eventually to hepatocellular carcinoma. Plasma levels of C-reactive protein (CRP), fibrinogen, plasminogen activator inhibitor-1 (PAI-1), von Willebrand factor (VWF), homocysteine, coagulation protein S, Thrombin activable fibrinolysis inhibitor (TAFI), and factor VII (FVII) were assessed to evaluate whether they should be responsible of the prothrombotic state of NAFLD after weight loss. We observed a significant drop of inflammatory and prothrombotic markers, as well as glucometabolic, lipid profile
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