OBJECTIVES: To study the mechanism mediating the protective effect of asiaticoside (AS) against myocardial ischemia-reperfusion injury (MIRI) in rats. METHODS: Fifty SD rats were randomized into sham-operated group, MIRI model group and AS treatment group. AS treatment was administered at low, moderate and high doses by daily gavage for 2 weeks before MIRI modeling (n=10). Serum levels of lactate dehydrogenase (LDH), creatine kinase isoenzyme (CK-MB), interleukin-18 (IL-18) and IL-1β, the volume of myocardial infarction and ischemia, and myocardial pathologies of the rats were determined or observed. The protein expression levels of NLRP3, ASC, caspase-1, GSDMD, GSDMD-N, IL-1β and IL-18 in the myocardial tissues were detected using Western blotting. The changes in the expression levels of these proteins were also detected in H9C2 cells with AS pretreatment prior to hypoxia-reoxygenation (H/R) injury. RESULTS: The rats models of MIRI exhibited significant myocardial infarction and ischemia with increased serum levels of LDH and CK-MB and myocardial expressions of NLRP3, ASC, caspase-1, GSDMD, GSDMD-N, IL-1β and IL-18. AS pretreatment effectively reduced myocardial infarction volume in the rat models and significantly reduced serum LDH and CK-MB levels and the protein levels in the myocardial tissue in a dose-dependent manner. In the H9C2 cell model of H/R injury, AS pretreatment significantly suppressed the elevation of the protein expressions of NLRP3, ASC, caspase-1, GSDMD, GSDMD-N, IL-1β and IL-18. Molecular docking studies showed that AS had a strong binding affinity with NLRP3. CONCLUSIONS Asiaticoside can alleviate MIRI in rats possibly by inhibiting NLRP3 inflammasome-mediated pyroptosis.
Animals ; Myocardial Reperfusion Injury/metabolism* ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism* ; Pyroptosis/drug effects* ; Rats, Sprague-Dawley ; Rats ; Inflammasomes/metabolism* ; Triterpenes/pharmacology* ; Interleukin-18/metabolism* ; Male ; Interleukin-1beta/metabolism* ; Caspase 1/metabolism*

Objective:To explore the effect of inflammatory cell levels on the anticoagulant efficacy in patients with liver cirrhosis complicated with portal vein thrombosis (PVT).Methods:A total of 106 patients with liver cirrhosis complicated with PVT who visited the Zhongshan Hospital, Fudan University from 2017 to 2022 were prospectively included. The PVT grade and recanalization were evaluated by imaging. Cox regression was used to analyze the predictive factors of anticoagulation efficacy. The time-dependent receiver operating characteristic (ROC) curve was used to determine the optimal cutoff value of inflammatory cells for predicting anticoagulation efficacy. The Kaplan-Meier method was used to compare the 1-year PVT recanalization rate of patients with different levels of inflammatory cells.Results:Univariate analysis showed that Child-Pugh score ( HR=1.41), D-dimer ( HR=0.98), platelet ( HR=0.98), C-reactive protein to lymphocyte ratio ( HR=1.01), monocyte ( HR=0.21), lymphocyte ( HR=0.34), and prothrombin time( HR=1.32) was related to the improvement of PVT (all P<0.05). Multivariate analysis confirmed that lymphocytes ( HR: 0.41, 95% CI: 0.20-0.85, P=0.016) and prothrombin time ( HR: 1.23, 95% CI: 1.01-1.50, P=0.036) were independent predictors of anticoagulant efficacy. Grouped according to the ROC cutoff value, the 1-year recanalization rate of PVT in the high-level lymphocyte group (4.55% vs 32.84%, P=0.012) and the high-level monocyte group (5.56% vs 31.4%, P=0.028) was significantly lower than that in the low-level group. After excluding patients undergoing splenectomy, the recurrence rate in the high-level lymphocyte group was still lower than that in the low-level group (6.25% vs 33.77%, P=0.038). Conclusions:Among patients with liver cirrhosis accompanied by PVT, high levels of lymphocytes and monocytes are the key factors for the poor efficacy of anticoagulation therapy. For PVT patients with poor anticoagulation efficacy, the therapeutic strategy of anti-inflammatory combined with anticoagulation can be considered for exploration in the future.

Objective:To explore the effect of inflammatory cell levels on the anticoagulant efficacy in patients with liver cirrhosis complicated with portal vein thrombosis (PVT).Methods:A total of 106 patients with liver cirrhosis complicated with PVT who visited the Zhongshan Hospital, Fudan University from 2017 to 2022 were prospectively included. The PVT grade and recanalization were evaluated by imaging. Cox regression was used to analyze the predictive factors of anticoagulation efficacy. The time-dependent receiver operating characteristic (ROC) curve was used to determine the optimal cutoff value of inflammatory cells for predicting anticoagulation efficacy. The Kaplan-Meier method was used to compare the 1-year PVT recanalization rate of patients with different levels of inflammatory cells.Results:Univariate analysis showed that Child-Pugh score ( HR=1.41), D-dimer ( HR=0.98), platelet ( HR=0.98), C-reactive protein to lymphocyte ratio ( HR=1.01), monocyte ( HR=0.21), lymphocyte ( HR=0.34), and prothrombin time( HR=1.32) was related to the improvement of PVT (all P<0.05). Multivariate analysis confirmed that lymphocytes ( HR: 0.41, 95% CI: 0.20-0.85, P=0.016) and prothrombin time ( HR: 1.23, 95% CI: 1.01-1.50, P=0.036) were independent predictors of anticoagulant efficacy. Grouped according to the ROC cutoff value, the 1-year recanalization rate of PVT in the high-level lymphocyte group (4.55% vs 32.84%, P=0.012) and the high-level monocyte group (5.56% vs 31.4%, P=0.028) was significantly lower than that in the low-level group. After excluding patients undergoing splenectomy, the recurrence rate in the high-level lymphocyte group was still lower than that in the low-level group (6.25% vs 33.77%, P=0.038). Conclusions:Among patients with liver cirrhosis accompanied by PVT, high levels of lymphocytes and monocytes are the key factors for the poor efficacy of anticoagulation therapy. For PVT patients with poor anticoagulation efficacy, the therapeutic strategy of anti-inflammatory combined with anticoagulation can be considered for exploration in the future.

Objective To investigate whether activation of mitochondrial acetal dehydrogenase 2(ALDH2)alleviates hypoxic pulmonary hypertension by regulating the SIRT1/PGC-1α signaling pathway.Methods Thirty 8-week-old C57 BL/6 mice were randomized into control,hypoxia,and hypoxia+Alda-1(an ALDH2 activator)group(n=10),and the mice in the latter two groups,along with 10 ALDH2 knockout(ALDH2-/-)mice,were exposed to hypoxia(10%O2,90%N2)with or without daily intraperitoneal injection of Alda-1 for 4 weeks.The changes in right ventricular function and pressure(RVSP)of the mice were evaluated by echocardiography and right ventricular catheter test,and pulmonary artery pressure was estimated based on RVSP.Pulmonary vascular remodeling,right ventricular injury,myocardial α-SMA expression,distal pulmonary arteriole muscle normalization,right ventricular cross-sectional area,myocardial cell hypertrophy,and right cardiac hypertrophy index were assessed with HE staining,immunofluorescence staining and WGA staining,and the expressions of ALDH2,SIRT1,PGC-1α,P16INK4A and P21CIP1 were detected.In pulmonary artery smooth muscle cells with hypoxic exposure,the effect of Alda-1 and EX527 on cell senescence and protein expressions was evaluated using β-galactose staining and Western blotting.Results The wild-type mice with hypoxic exposure showed significantly increased RVSP,right ventricular free wall thickness and myocardial expressions of P16INK4A and P21CIP1,which were effectively lowered by treatment with Alda-1 but further increased in ALDH2-/-mice.In cultured pulmonary artery smooth muscle cells,hypoxic exposure significantly increased senescent cell percentage and cellular expressions of P16INK4A and P21CIP1,which were all lowered by treatment with Alda-1,but its effect was obviously attenuated by EX527 treatment.Conclusion ALDH2 alleviates hypoxia-induced senescence of pulmonary artery smooth muscle cells by upregulating the SIRT1/PGC-1α signaling pathway to alleviate pulmonary hypertension in mice.

Objective To compare the efficacy and safety of endoscopic ligation treatment and endoscopic tissue glue injection for secondary prevention of gastric variceal bleeding.Methods Patients with cirrhosis and esophagogastric variceal bleeding treated with gastric variceal ligation in Zhongshan Hospital,Fudan University,from January 2017 to December 2019 were screened(ligation group).And during the same period,patients underwent endoscopic cyanoacrylate treatment were also screened(tissue glue group).59 patients were included in the two groups after propensity score matching.Univariate and multivariate Cox proportional hazard regression models were used to anslyze risk factors for re-bleeding.Kaplan-Meier curves were plotted to analyze re-bleeding rate and mortality of the two treatment groups.Results There was no statistically significant difference in the eradication rate of esophagogastric varices between the ligation group and the tissue glue group(83.05％vs 79.66％,P=0.778);the ligation group required fewer median endoscopic treatments for variceal eradication(2 vs 3,P=0.017)and a lower average dosage of cyanoacrylate(0.70 mL vs 2.67 mL,P＜0.001).Multivariate Cox regression analysis showed that portal shunt was a risk factor for esophagogastric varices re-bleeding(HR=3.14,95％CI 1.02-9.68,P=0.046),endoscopic variceal ligation was a protective factor against re-bleeding(HR=0.25,95％CI 0.08-0.71,P=0.010).Compared with endoscopic cyanoacrylate injection,endoscopic ligation treatment did not significantly increase the 2-year risk of esophagogastric variceal re-bleeding(18.69％vs 36.29％,P=0.067)or risk of death(1.69％vs 3.39％,P=1.000);patients with GOV1 type had a significantly lower risk of re-bleeding after endoscopic ligation treatment(0 vs 40.27％,P=0.012)and there was a trend towards a lower re-bleeding risk in patients with GOV2 type after endoscopic ligation treatment(13.27％vs 34.16％,P=0.056).Conclusions Endoscopic ligation treatment has higher eradication rate for esophagogastric varices,and does not increase the risk of re-bleeding,death,or other adverse events.Therefore,it can be considered an effective secondary prevention way for patients with gastric varices.

Objective To investigate whether activation of mitochondrial acetal dehydrogenase 2(ALDH2)alleviates hypoxic pulmonary hypertension by regulating the SIRT1/PGC-1α signaling pathway.Methods Thirty 8-week-old C57 BL/6 mice were randomized into control,hypoxia,and hypoxia+Alda-1(an ALDH2 activator)group(n=10),and the mice in the latter two groups,along with 10 ALDH2 knockout(ALDH2-/-)mice,were exposed to hypoxia(10%O2,90%N2)with or without daily intraperitoneal injection of Alda-1 for 4 weeks.The changes in right ventricular function and pressure(RVSP)of the mice were evaluated by echocardiography and right ventricular catheter test,and pulmonary artery pressure was estimated based on RVSP.Pulmonary vascular remodeling,right ventricular injury,myocardial α-SMA expression,distal pulmonary arteriole muscle normalization,right ventricular cross-sectional area,myocardial cell hypertrophy,and right cardiac hypertrophy index were assessed with HE staining,immunofluorescence staining and WGA staining,and the expressions of ALDH2,SIRT1,PGC-1α,P16INK4A and P21CIP1 were detected.In pulmonary artery smooth muscle cells with hypoxic exposure,the effect of Alda-1 and EX527 on cell senescence and protein expressions was evaluated using β-galactose staining and Western blotting.Results The wild-type mice with hypoxic exposure showed significantly increased RVSP,right ventricular free wall thickness and myocardial expressions of P16INK4A and P21CIP1,which were effectively lowered by treatment with Alda-1 but further increased in ALDH2-/-mice.In cultured pulmonary artery smooth muscle cells,hypoxic exposure significantly increased senescent cell percentage and cellular expressions of P16INK4A and P21CIP1,which were all lowered by treatment with Alda-1,but its effect was obviously attenuated by EX527 treatment.Conclusion ALDH2 alleviates hypoxia-induced senescence of pulmonary artery smooth muscle cells by upregulating the SIRT1/PGC-1α signaling pathway to alleviate pulmonary hypertension in mice.

Objective:A cohort of patients with oxaliplatin-associated portal hypertension was established and compared with patients with hepatitis B or schistosomiasis-associated cirrhotic portal hypertension to explore the course, disease features and prognosis of endoscopic treatment.Methods:From January 1, 2014 to December 31, 2021, patients diagnosed with portal hypertension and gastroesophageal varices after oxaliplatin chemotherapy at Zhongshan Hospital of Fudan University were selected (oxaliplatin general group). The patients who received endoscopic treatment for the first time because of esophagogastric variceal bleeding in the oxaliplatin general group were included in the oxaliplatin group. From January 1, 2014 to December 31, 2016, patients who initially received endoscopic treatment for the first time because of esophagogastric variceal bleeding due to hepatitis B or schistosomiasis-associated cirrhotic portal hypertension at Zhongshan Hospital of Fudan University were enrolled (hepatitis B group and schistosomiasis group). The history of oncology and chemotherapy, laboratory results, imaging and pathological findings were collected, and the clinical features were analyzed. Clinical data were collected, and the clinical features, 3-year cumulative non-bleeding rate and survival rate after endoscopic treatment of the 3 groups including oxaliplatin group, hepatitis B group and schistosomiasis group were compared. Kaplan-Meier survival curve was drawn to estimate treatment effects, and log-rank method was performed to test the differences in survival curves. Chi-square test and Mann-Whitney U test were used for statistical analysis. Results:There were 93 patients in oxaliplatin general group, with a median chemotherapy course of 8 (ranged from 6 to 10) cycles, and the median time from the end of chemotherapy to the diagnosis of gastroesophageal varices was 4 (ranged from 2 to 6) years. There were 55 patients in oxaliplatin group, 191 cases in hepatitis B group and 96 cases in schistosomiasis group. There were 78.5% (73/93) of patients in the oxaliplatin group classified as Child-Pugh grade A, and 33 patients (35.5%) with portal vein thrombosis. The abdominal imaging showed no obvious liver cirrhosis such as liver shrinkage and uneven surface. The pathology of 11 patients with liver biopsy in the oxaliplatin general group showed mainly vascular injury and fibrous deposition in the confluent area with lymphocytic infiltration, mild hepatocellular injury, and no pseudolobule formation. In terms of baseline characteristics, direct bilirubin, alanine transaminase, and aspartate transaminase levels of patients in the oxaliplatin group were all lower than those of the hepatitis B group and schistosomiasis group (4.8 (3.9, 6.5) μmol/L vs. 6.4 (4.7, 9.0) and 6.5 (4.4, 9.4) μmol/L; 17 (13, 22) U/L vs. 22 (15, 31) and 19 (15, 27) U/L; 22 (19, 25) U/L vs. 28 (22, 39) and 29 (22, 42) U/L), while albumin and prealbumin levels and the proportion of patients with Child-Pugh grade A were all higher than those of the hepatitis B group and schistosomiasis group (39.0 (35.0, 42.5) g/L vs. 34.0 (30.0, 38.3) and 33.8 (29.5, 36.0) g/L; 0.160 (0.130, 0.197) g/L vs. 0.120 (0.090, 0.150) and 0.110 (0.080, 0.140) g/L; 74.5% (41/55) vs. 55.5% (106/191) and 42.7% (41/96)), and the differences were all statistically significant ( U=3 298.50, 2 749.00, 2 159.00, 7 759.00, 5 822.50, χ2=6.92 and U=1 622.00, 1 878.50, 1 305.50, 3 989.00, 3 264.50, χ2=16.36; all P<0.05). The 3-year rebleeding risk in the oxaliplatin group was higher than that in the hepatitis B group ( HR=1.80, 95% confidence interval 1.07 to 3.02, P=0.026), but the difference was not statistically significant compared with that of the schistosomiasis group ( HR=1.04, 95% confidence interval 0.61 to 1.78, P=0.874). There were no statistically significant differences in the 3-year cumulative survival rate between the oxaliplatin group and the hepatitis B group and schistosomiasis group (96.4% (53/55) vs. 94.8% (181/191) and 95.8% (92/96), both P>0.05). Conclusions:The pathology of liver injury in patients with oxaliplatin-associated portal hypertension are mainly vascular injury and fibrous deposition in the confluent area. The efficacy of endoscopic treatment to prevent rebleeding in patients with oxaliplatin-associated portal hypertension is significantly inferior to that in patients with hepatitis B-associated portal hypertension, but comparable to that in patients with schistosomiasis-associated portal hypertension.

Objective:A cohort of patients with oxaliplatin-associated portal hypertension was established and compared with patients with hepatitis B or schistosomiasis-associated cirrhotic portal hypertension to explore the course, disease features and prognosis of endoscopic treatment.Methods:From January 1, 2014 to December 31, 2021, patients diagnosed with portal hypertension and gastroesophageal varices after oxaliplatin chemotherapy at Zhongshan Hospital of Fudan University were selected (oxaliplatin general group). The patients who received endoscopic treatment for the first time because of esophagogastric variceal bleeding in the oxaliplatin general group were included in the oxaliplatin group. From January 1, 2014 to December 31, 2016, patients who initially received endoscopic treatment for the first time because of esophagogastric variceal bleeding due to hepatitis B or schistosomiasis-associated cirrhotic portal hypertension at Zhongshan Hospital of Fudan University were enrolled (hepatitis B group and schistosomiasis group). The history of oncology and chemotherapy, laboratory results, imaging and pathological findings were collected, and the clinical features were analyzed. Clinical data were collected, and the clinical features, 3-year cumulative non-bleeding rate and survival rate after endoscopic treatment of the 3 groups including oxaliplatin group, hepatitis B group and schistosomiasis group were compared. Kaplan-Meier survival curve was drawn to estimate treatment effects, and log-rank method was performed to test the differences in survival curves. Chi-square test and Mann-Whitney U test were used for statistical analysis. Results:There were 93 patients in oxaliplatin general group, with a median chemotherapy course of 8 (ranged from 6 to 10) cycles, and the median time from the end of chemotherapy to the diagnosis of gastroesophageal varices was 4 (ranged from 2 to 6) years. There were 55 patients in oxaliplatin group, 191 cases in hepatitis B group and 96 cases in schistosomiasis group. There were 78.5% (73/93) of patients in the oxaliplatin group classified as Child-Pugh grade A, and 33 patients (35.5%) with portal vein thrombosis. The abdominal imaging showed no obvious liver cirrhosis such as liver shrinkage and uneven surface. The pathology of 11 patients with liver biopsy in the oxaliplatin general group showed mainly vascular injury and fibrous deposition in the confluent area with lymphocytic infiltration, mild hepatocellular injury, and no pseudolobule formation. In terms of baseline characteristics, direct bilirubin, alanine transaminase, and aspartate transaminase levels of patients in the oxaliplatin group were all lower than those of the hepatitis B group and schistosomiasis group (4.8 (3.9, 6.5) μmol/L vs. 6.4 (4.7, 9.0) and 6.5 (4.4, 9.4) μmol/L; 17 (13, 22) U/L vs. 22 (15, 31) and 19 (15, 27) U/L; 22 (19, 25) U/L vs. 28 (22, 39) and 29 (22, 42) U/L), while albumin and prealbumin levels and the proportion of patients with Child-Pugh grade A were all higher than those of the hepatitis B group and schistosomiasis group (39.0 (35.0, 42.5) g/L vs. 34.0 (30.0, 38.3) and 33.8 (29.5, 36.0) g/L; 0.160 (0.130, 0.197) g/L vs. 0.120 (0.090, 0.150) and 0.110 (0.080, 0.140) g/L; 74.5% (41/55) vs. 55.5% (106/191) and 42.7% (41/96)), and the differences were all statistically significant ( U=3 298.50, 2 749.00, 2 159.00, 7 759.00, 5 822.50, χ2=6.92 and U=1 622.00, 1 878.50, 1 305.50, 3 989.00, 3 264.50, χ2=16.36; all P<0.05). The 3-year rebleeding risk in the oxaliplatin group was higher than that in the hepatitis B group ( HR=1.80, 95% confidence interval 1.07 to 3.02, P=0.026), but the difference was not statistically significant compared with that of the schistosomiasis group ( HR=1.04, 95% confidence interval 0.61 to 1.78, P=0.874). There were no statistically significant differences in the 3-year cumulative survival rate between the oxaliplatin group and the hepatitis B group and schistosomiasis group (96.4% (53/55) vs. 94.8% (181/191) and 95.8% (92/96), both P>0.05). Conclusions:The pathology of liver injury in patients with oxaliplatin-associated portal hypertension are mainly vascular injury and fibrous deposition in the confluent area. The efficacy of endoscopic treatment to prevent rebleeding in patients with oxaliplatin-associated portal hypertension is significantly inferior to that in patients with hepatitis B-associated portal hypertension, but comparable to that in patients with schistosomiasis-associated portal hypertension.

Objective:This study aimed to evaluate the rebleeding risk and prognosis of patients being treated after acute esophageal varices bleeding by two different treatment strategies: sclerosing agent combined with tissue glue injection, esophageal varices ligation (EVL), through comparing the therapeutic effects and securities.Methods:A total of 76 patients who underwent endoscopy and received treatment in Zhongshan Hospital Affiliated to Fudan University due to acute esophageal variceal bleeding were included retrospectively. 6 patients with active bleeding and 70 patients with thrombus in esophagus varices under gastroscopy. Among them, 21 cases were treated with sclerosing agent combined with tissue glue injection (sclerosing tissue glue group), and 55 cases were treated with EVL (EVL group). The emergency endoscopic diagnosis and treatment of the two groups were compared, and the risk factors of rebleeding 6 months after endoscopic treatment were analyzed by univariate and multivariate analysis.Results:All patients received endoscopic treatment successfully. During the follow-up period of 6 months after endoscopic treatment, rebleeding occurred in 13 cases. Kaplan Meier analysis showed that the 6-month rebleeding rate in the sclerosing tissue glue group was significantly higher than that in the EVL group (41.6% vs 12.3%, P=0.011). There were 8 deaths in total. Kaplan Meier analysis showed that there was no significant difference in 6-month mortality between the two groups (17.5% vs 10.1%, P=0.616). Multivariate analysis further showed that malignant tumor ( HR=3.700, 95% CI: 1.187-11.536, P=0.024) and treatment mode of esophageal variceal bleeding ( HR=4.834, 95% CI: 1.443-16.193, P=0.011) were independent risk factors for rebleeding 6 months after endoscopic treatment of acute esophageal variceal bleeding. Conclusions:This study found that EVL and the combining injection of lauromacrogol and cyanoacrylate could be used in emergent hemostatic treatment for acute esophageal varices bleeding. Moreover, EVL is the prioritized approach in endoscopic emergency treatment with a lower rebleeding rate and fewer complications. Sclerotherapy combined with tissue glue can be used as one of the measures of emergency treatment, which is not better than ligation.

Objective:To explore whether portal vein thrombosis affects the efficacy of endoscopic treatment in preventing re-bleeding from ruptured gastroesophageal varices in hepatitis B-related liver cirrhosis.Methods:Hospitalized patients who received endoscopic therapy to prevent re-bleeding from ruptured gastroesophageal varices due to hepatitis B-related liver cirrhosis during 2013 to 2017 were selected, and followed up for 1 year after treatment for re-bleeding and survival status. Patients were divided into thrombotic and non-thrombotic group according to whether they were combined with portal vein thrombosis at the time of initial admission. The baseline data characteristics of the two groups were analyzed. The 1-year re-bleeding rate and survival rate of the two groups were compared by Kaplan-Meier survival analysis. The other risk factors for re-bleeding after endoscopic variceal therapy were evaluated by univariate and multivariate regression.Results:A total of 124 cases with re-bleeding from ruptured gastroesophageal varices due to hepatitis B-related liver cirrhosis were included. The average age was 50.7 years old. 81.5% (101 cases) were male, and 24.2% (30 cases) were combined with portal vein thrombosis. There were no statistically significant differences between the thrombotic and the non-thrombotic group in the average age, gender, liver function classification, transjugular portal pressure gradient, antiviral treatment, and non-selective β-blockers. Kaplan-Meier analysis of the re-bleeding rate after endoscopic treatment indicated that the incidence of non-bleeding in patients with thrombotic group at 60 days, 180 days and 1 year was significantly lower than that in the non-thrombotic group [86.7%, 80.0%, 56.7% vs. 95.7%, 93.6%, 87.2% ( P = 0.000 1)]. Analysis of the location of portal vein thrombosis showed that the bleeding rate in the main portal trunk, left and right branches and superior mesenteric vein had increased significantly after endoscopic treatment, while the splenic vein had no effect on the bleeding after endoscopic treatment. Univariate and multivariate regression analysis indicated that age (HR 1.05, 95% CI: 1.01-1.09, P = 0.02) and thrombosis in the main portal trunk, left and right branches (HR 4.95, 95% CI: 2.05-11.95, P < 0.01) were independent risk factors for re-bleeding at 1 year after endoscopic treatment. Conclusion:Portal vein thrombosis is an independent risk factor that affects the efficacy of endoscopic treatment in preventing re-bleeding from ruptured gastroesophageal varices in hepatitis B-related liver cirrhosis and the risk of re-bleeding increases significantly after endoscopic treatment in patients with thrombosis.