Carvedilol has limited research on decompensated cirrhosis. This study compared the effects of carvedilol, traditional nonselective beta blockers (NSBBs), including propranolol and nadolol, and other interventions in patients using carvedilol or traditional NSBBs for secondary prophylaxis of variceal hemorrhage (VH) and portal hypertension (PH)-related complications.

A systematic search of databases, including PubMed, Embase, Cochrane Library, and Scopus, was conducted through October 2023. Randomized controlled trials (RCTs) evaluating carvedilol or traditional NSBBs for secondary prophylaxis of VH were included. The outcomes were the occurrence of VH and portal PH-related complications, including new or worsening ascites, hepatic encephalopathy, spontaneous bacterial peritonitis, and hepatorenal syndrome. A network meta-analysis was performed using a random-effects model.

A total of 60 RCTs involving 5,600 patients with a median Child Pugh score of 8.0 (range 6.8-10) were included. The risk of carvedilol plus variceal band ligation (VBL) on VH was lower than placebo (relative risk (RR) 0.24; 95% confidence interval (CI): 0.10-0.57), and the risk of carvedilol on new or worsening ascites was lower than placebo (RR = 0.10, 95%CI; 0.01-0.93). Traditional NSBBs plus VBL also had preventive effects on VH compared to placebo (RR = 0.31, 95%CI; 0.18-0.54). However, there were no differences between carvedilol and traditional NSBBs in other outcomes.

Carvedilol can prevent PH-related complications, including VH and new or worsening ascites, in cirrhosis patients with a history of VH. No significant differences were observed between the effects of carvedilol and traditional NSBBs, both combined with VBL.

To investigate the association between overt hepatic encephalopathy (OHE) and liver pathology after transjugular intrahepatic portosystemic shunt (TIPS) creation in cirrhotic patients. From July 2015 to April 2024, 73 patients from 4 hospitals in China who received TIPS creation and liver biopsy were retrospectively enrolled in this study. Based on whether OHE occurred within 3 months after TIPS creation, the patients were categorized into OHE (n = 29) and non-OHE (n = 44) groups. The liver pathology was assessed by hematoxylin-eosin (H&E), Sirius red staining, immunohistochemistry, and immunofluorescence. Liver pathology by H&E staining showed typical features of liver cirrhosis (including disordered structure and pseudolobule formation) in all the patients. No marked difference was observed in extracellular matrix (ECM) deposition between the OHE and non-OHE groups. However, the patients in the OHE group had a higher level of liver and systemic inflammation than in the non-OHE group. And there was a strong correction between intrahepatic macrophage infiltration and serum inflammatory indicators. Additionally, the OHE group had more liver neovascularization, which was consistent with liver inflammation. The emergence of OHE after TIPS creation is closely associated with liver pathology, especially in liver inflammation and angiogenesis, but not in ECM deposition.

Patients with cirrhosis-associated and portal hypertension-associated complications may benefit from TIPS and/or liver transplantation. In many patients, the decision of whether or not TIPS should be placed prior to liver transplantation is fairly clear-cut. Nevertheless, there are some patients in whom the decision can be more complex. On one hand, TIPS is easily available in contrast to liver transplantation, and patients with TIPS may have clinical improvement. On the other hand, although TIPS may improve the situation of the patient, this improvement may not be sufficient to significantly improve the quality of life. Furthermore, TIPS malposition may be challenging for liver transplantation surgery. This review approaches the advantages and disadvantages of TIPS placement in patients who are candidates for liver transplantation and proposes decision pathways for patients with complications of portal hypertension on the liver transplant waiting list.

Portal hypertension is a hemodynamic abnormality that complicates the course of cirrhosis, as well as other diseases that affect the portal venous circulation. The development of portal hypertension compromises prognosis, especially when it rises above a certain threshold known as clinically significant portal hypertension (CSPH). In the consensus conference on Portal Hypertension promoted by the Spanish Association for the Study of the Liver and the Hepatic and Digestive diseases area of the Biomedical Research Networking Center (CIBERehd), different aspects of the diagnosis and treatment of portal hypertension caused by cirrhosis or other diseases were discussed. The outcome of this discussion was a set of recommendations that achieved varying degrees of consensus among panelists and are reflected in this consensus document. The six areas under discussion were: the relevance of CSPH and the non-invasive methods used for its diagnosis and that of cirrhosis, the prevention of the first episode of decompensation and its recurrence, the treatment of acute variceal bleeding and other complications of portal hypertension, the indications for the use of TIPS, and finally, the diagnosis and treatment of liver vascular diseases.

Portal hypertension is a hemodynamic abnormality that complicates the course of cirrhosis, as well as other diseases that affect the portal venous circulation. The development of portal hypertension compromises prognosis, especially when it rises above a certain threshold known as clinically significant portal hypertension (CSPH). In the consensus conference on Portal Hypertension promoted by the Spanish Association for the Study of the Liver and the Hepatic and Digestive diseases area of the Biomedical Research Networking Center (CIBERehd), different aspects of the diagnosis and treatment of portal hypertension caused by cirrhosis or other diseases were discussed. The outcome of this discussion was a set of recommendations that achieved varying degrees of consensus among panelists and are reflected in this consensus document. The six areas under discussion were: the relevance of clinically significant portal hypertension and the non-invasive methods used for its diagnosis and that of cirrhosis, the prevention of the first episode of decompensation and its recurrence, the treatment of acute variceal bleeding and other complications of portal hypertension, the indications for the use of TIPS, and finally, the diagnosis and treatment of liver vascular diseases.

Esophageal variceal bleeding is a severe complication often associated with portal hypertension, commonly due to liver cirrhosis. Prevention and treatment of this condition are critical for patient outcomes. Preventive strategies focus on reducing portal hypertension to prevent varices from developing or enlarging. Primary prophylaxis involves the use of non-selective beta-blockers, such as propranolol or nadolol, which lower portal pressure by decreasing cardiac output and thereby reducing blood flow to the varices. Endoscopic variceal ligation (EVL) may also be employed as primary prophylaxis to prevent initial bleeding episodes. Once bleeding occurs, immediate treatment is essential. Initial management includes hemodynamic stabilization followed by pharmacological therapy with vasoactive drugs such as octreotide or terlipressin to control bleeding. Endoscopic intervention is the cornerstone of treatment, with techniques such as EVL or sclerotherapy applied to directly manage the bleeding varices. In cases where bleeding is refractory to endoscopic treatment, transjugular intrahepatic portosystemic shunt may be considered to effectively reduce portal pressure. Long-term management after an acute bleeding episode involves secondary prophylaxis using beta-blockers and repeated EVL sessions to prevent rebleeding, complemented by monitoring and managing liver function to address the underlying disease. In light of new scientific evidence, including the findings of the study by Peng et al, this editorial aims to review available strategies for the prevention and treatment of esophageal varices.

Esophageal-gastric variceal bleeding (EGVB) is a serious complication in patients with liver cirrhosis, characterized by high mortality and rebleeding rates. The effect of sequential endoscopic therapy on patient mortality and rebleeding rates remains unclear.

This study aimed to evaluate the effects of sequential endoscopic therapy on mortality and rebleeding rates in patients with EGVB.

In this single-center retrospective study, 373 hospitalized cases of EGVB caused by liver cirrhosis, collected between November 2019 and November 2023, were divided into four groups according to different treatment methods: a sequential endoscopy group, emergency endoscopy group, emergency endoscopy plus transjugular intrahepatic portosystemic shunt (TIPS) group and control group.

Mortality and rebleeding rates were compared among the four groups using statistical analyses.

The mortality and rebleeding rates of the sequential endoscopy group (3.7% and 19%, respectively) were significantly lower than those of the emergency endoscopy (22% and 36%, respectively), emergency endoscopy plus TIPS (33% and 28%, respectively), and control groups (33% and 51%, respectively) (p = 0.013 and p = 0.013, respectively).

Sequential endoscopic therapy may significantly reduce the mortality and rebleeding rates of patients with EGVB compared to other conventional treatment strategies. The findings of the study could help develop approaches benefiting EGVB treatment.

Hepatic venovenous communications (HVVC) is detectable in more than one-third of cirrhotic patients, where portal hypertension (PHT) tends to present more severely. We aimed to explore the prognostic implications of HVVC in patients with sinusoidal PHT treated by transjugular intrahepatic portosystemic shunt (TIPS).

The multicenter data of patients (2020-2022) undergoing balloon-occluded hepatic venography during TIPS were retrospectively analyzed. Pre-TIPS total bile acids (TBA) levels in portal, hepatic and peripheral veins were compared between groups. The primary endpoint was the development of overt hepatic encephalopathy (HE) within one year after TIPS.

183 patients were eligible and classified by the presence (n = 69, 37.7 %) or absence (n = 114, 62.3 %) of HVVC. The agreement between wedged hepatic venous pressure and portal venous pressure was poor in HVVC group (intraclass correlation coefficients [ICC]: 0.141, difference: 13.4 mmHg, p < 0.001), but almost perfect in non-HVVC group (ICC: 0.877, difference: 0.4 mmHg, p = 0.152). At baseline, patients with HVVC had lower Model for end-stage liver disease scores (p < 0.001), blood ammonia levels (p < 0.001), TBA concentrations in the hepatic (p = 0.011) and peripheral veins (p = 0.049) rather than in the portal veins (p = 0.516), and a higher portosystemic pressure gradient (p = 0.035), suggesting more effective intrahepatic perfusion in this group. Within 1-year post-TIPS, HVVC group had a lower incidence of overt HE (11.7 % vs. 30.5 %, p = 0.004, HR: 0.34, 95 % CI: 0.16-0.74, absolute risk difference [ARD]: -17.4) and an improved liver transplantation-free survival rate (97.1 % vs. 86.8 %, p = 0.021, HR: 0.16, 95 % CI: 0.05-0.91, ARD: -10.3).

For patients with sinusoidal PHT treated by TIPS, the presence of HVVC was associated with a reduced risk of overt HE and a potential survival benefit.