Secondary Prophylaxis of Cirrhotic Gastric Variceal Bleeding: Addition of Non-Selective Beta-Blockers to Endoscopic Combined Treatment.

Background: It remains unclear whether the addition of non-selective beta-blockers (NSBB) provides further benefit after combined use of tissue adhesive and endoscopic variceal ligation for bleeding gastroesophageal varices.

Objective: This is the first cohort study comparing the secondary prophylactic efficacy of adding NSBB to combined endoscopic treatment in cirrhotic patients with gastric varices (without inclusion of isolated gastric varices [IGVs], which are rare in patients with cirrhosis without splanchnic thrombosis).

Methods: We retrospectively analyzed two matched large cohorts of cirrhotic patients with gastric varices who received combined endoscopic treatment and were assigned to receive NSBB treatment or not as secondary prophylaxis.

Increased Factor VIII Activity Is Predictive of the Occurrence of Portal Vein Thrombosis in Cirrhosis.

Background:  The aim of this study was to identify the role of factor VIII (FVIII) in portal vein thrombosis (PVT) occurrence in cirrhotic patients with gastroesophageal variceal bleeding.

Methods:  A total of 453 cirrhotic patients with gastroesophageal varices were enrolled. Computed tomography was performed at baseline and patients were divided into PVT and non-PVT groups ( = 131 vs.

Platelet-derived TGF-β1 is related to portal vein thrombosis in cirrhosis by promoting hypercoagulability and endothelial dysfunction.

Background: Portal vein thrombosis (PVT) is a serious complication of cirrhosis accompanied by unclear pathogenesis. Transforming growth factor-beta (TGF-β) has been implicated in atherosclerosis and venous thrombosis whereas study regarding its part in PVT is lacking. The aim of this study was to explore the role of cytokine TGF-β1 in PVT and the potential mechanism.

Endoscopic Treatment as the Rescue Therapy for Recurrent Bleeding after Transjugular Intrahepatic Portosystemic Shunt (TIPS).

Background: Transjugular intrahepatic portosystemic shunt (TIPS) is suggested as the salvage therapy for gastroesophageal variceal bleeding in cirrhosis. However, rebleeding might occur in some patients after TIPS. Currently, there is a lack of evidence in the endoscopic management of recurrent bleeding in these patients.

SCAP Mediated GDF15-Induced Invasion and EMT of Esophageal Cancer.

GDF15 is a potential biomarker for patients with esophageal cancer (EC). However, the mechanistic role of GDF15 in the invasion and metastasis of EC remains poorly understood. We determined the expression and function of GDF15 in esophageal cancer cells (ESCCs) and in patient tissue samples using western blotting, migration, and invasion assays, immunohistochemistry, Co-IP assays, and quantitative real-time-PCR.

Positive consequences of splenectomy for patients with schistosomiasis-induced variceal bleeding.

Background: Patients with hepatic schistosomiasis are at high risk of gastroesophageal variceal bleeding, which is highly torrential and life threatening. This study aimed to assess the effects of splenectomy on patients with schistosomiasis-induced variceal bleeding, especially those influences related to overall survival (OS) rate.

Methods: From January 2005 to December 2018, 112 patients with schistosomiasis-induced varices were enrolled.

Endoscopic treatment of gastroesophageal variceal bleeding after oxaliplatin-based chemotherapy in patients with colorectal cancer.

BACKGROUND : Oxaliplatin, used as first-choice treatment for colorectal cancer (CRC), induces sinusoidal endothelial injury and portal hypertension. This study investigated the characteristics of oxaliplatin-induced portal hypertension and evaluated the efficacy of endoscopic management of gastroesophageal variceal bleeding. METHODS : We performed a retrospective, multicenter, case-control study between January 2010 and December 2018.

Simvastatin Mitigates Apoptosis and Transforming Growth Factor-Beta Upregulation in Stretch-Induced Endothelial Cells.

Portal hypertension is a common clinical symptom of digestive disorders. With an increase in portal pressure, the portal vein will continue to dilate. We aimed to determine whether continuous stretch induced by portal hypertension may impair the function of endothelial cells (ECs) in the portal vein and aggravate the progress of portal hypertension and explore its mechanism.