Objective:To investigate the correlation between thromboelastography (TEG) and portal vein thrombosis in patients with cirrhotic esophagogastric varices.Methods:210 hospitalized patients with cirrhotic esophagogastric varices treated in Zhongshan Hospital Affiliated to Fudan University from December 2016 to December 2017 were retrospectively included. They were divided into portal vein thrombosis group (PVT group) and non portal vein thrombosis group (NPVT group) according to whether they were complicated with portal vein thrombosis. The correlation between the results of TEG coagulation reaction time (R value), coagulation time (K value), αAngle, maximum amplitude (MA) and coagulation composite index (CI) and portal vein thrombosis was analyzed. The characteristics of coagulation status in patients with portal vein thrombosis in cirrhosis were compared.Results:A total of 91 patients (43.3%) were complicated with portal vein thrombosis. The R value in the PVT group was significantly lower than that of NPVT group [5.49(5.22-5.77) vs 5.98(5.76-6.20), P=0.006]. Logistic regression analysis showed that Child Pugh grade ( OR=2.883, 95% CI: 1.630-5.098, P<0.001) and R value ( OR=0.739, 95% CI: 0.575-0.950, P=0.018) were independently associated risk factors of PVT. The R value of patients was significantly correlated with Child Pugh grade ( r=0.147, P=0.034), platelet ( r=-0.358, P<0.001), prothrombin time (PT) ( r=0.334, P<0.001) and international standardized ratio (INR) ( r=0.328, P<0.001). Conclusions:The decrease of TEG-R value is closely related to PVT in liver cirrhosis.

Non-alcoholic fatty liver disease (NAFLD) is a chronic liver disease caused by abnormal accumulation of fat in the hepatocytes. Its prevalence is rising globally and has become the most common cause of chronic liver disease worldwide. The pathogenesis of NAFLD is multifaceted, involving insulin resistance, genetic and epigenetic factors, chronic systemic inflammation, mitochondrial dysfunction, endoplasmic reticulum stress, diet, gut microbiota, and other significant contributors. This article primarily delves into the mechanisms of mitochondrial dysfunction and endoplasmic reticulum stress in the development of NAFLD, aiming to provide new insights and therapeutic strategies for NAFLD.