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Transjugular intrahepatic portosystemic shunt (TIPS), a highly effective procedure reducing portal hypertension, has been in use for over seven decades and is now a cornerstone in managing portal hypertension-related complications such as variceal bleeding and ascites. Historically, TIPS has dealt with two main challenges: ensuring stent patency and preventing post-TIPS hepatic encephalopathy. The introduction of PTFE-coated stents markedly reduced the risk of TIPS dysfunction and stent patency is no longer a major concern. However, despite improved patient selection criteria, hepatic encephalopathy continues to be a significant and persistent issue. In addition, the broader application of TIPS in recent decades has brought to light additional, albeit less common, complications, such as post-TIPS heart failure. This review offers a comprehensive overview of TIPS historical evolution, advancements in technique, and its application in the treatment of portal hypertension. [ABSTRACT FROM AUTHOR]

Background: Patients with hepatocellular carcinoma (HCC) and cirrhosis can present with features of severe portal hypertension, which can be worsened further by portal vein tumoral thrombosis (PVTT). Due to the technical difficulties and short survival of these patients, HCC was traditionally considered a relative contra-indication for transjugular intrahepatic portosystemic shunt (TIPS). However, there is an increasing body of evidence, mainly from China, supporting the use of TIPS in HCC. The present study aimed at analyzing the efficacy and safety of TIPS in patients with HCC. Methods: From 2000 through May 2023, MEDLINE, Embase and Scopus were searched for studies analyzing the outcome of TIPS in HCC. Technical and clinical success, adverse events (AE) and mortality were the main outcomes assessed. With the use of a random effects model, the event rates were combined. Results: Total 19 studies with 1498 patients were included in the final analysis. The pooled technical and clinical success rates with TIPS in HCC were 98.8% (98.0–99.7) and 94.1% (91.2–97.0), respectively. After TIPS, ascites was controlled in 89.2% (85.1–93.3) of the cases, while rebleeding was observed in 17.2% (9.4–25.0) of cases on follow-up. The pooled incidence of overall AE, serious AE and post-TIPS hepatic encephalopathy (HE) was 5.2% (2.5–7.9), 0.1% (0.0–0.4) and 25.1% (18.7–31.5), respectively. On follow-up, 11.9% (7.8–15.9) of the patients developed shunt dysfunction requiring re-intervention. Conclusion: The present analysis supports the feasibility, safety and efficacy of TIPS in the management of portal hypertension in patients with HCC. [ABSTRACT FROM AUTHOR]

ABSTRACT Background Aims Materials and Methods Discussion Conclusion Portal hypertension (PH) is a critical complication in patients with hepatic diseases. Its accurate evaluation is essential for early diagnosis, risk stratification, and management. Endoscopic ultrasound (EUS) has emerged as a promising diagnostic tool, offering high‐resolution imaging of the portal venous system, hepatic vasculature, and surrounding structures.This review aims at providing an overview of the evolving role of EUS in PH evaluation in patients with liver disease.A systematic search was conducted in PubMed and Google Scholar until 31 May 2024. Relevant studies were identified using keywords related to EUS and PH. Additional references were included based on expert knowledge and citation analysis. Only full‐length papers and abstracts in English were considered. Results: EUS demonstrates significant utility in PH assessment, offering high‐resolution imaging and advanced tools like contrast enhancement (CE) and shear‐wave elastography (SWE) for evaluating liver stiffness and correlating it with PH severity. EUS‐guided portal pressure gradient (PPG) measurement provides a less invasive method for evaluating PH, potentially offering a safer alternative to conventional techniques.EUS offers unique advantages in PH assessment, enabling comprehensive evaluation in a single session. Despite its potential, limitations such as invasiveness, sedation‐related variability, and restricted availability persist. Emerging techniques require further validation in larger cohorts and standardised training.EUS is a valuable diagnostic tool for PH evaluation, with the potential to improve outcomes through earlier diagnosis and better stratification. Addressing its limitations through further research and standardised protocols is critical to optimize its clinical utility.Trial Registration: NCT04115046, NCT05728697, NCT05097963 and NCT03155282 [ABSTRACT FROM AUTHOR]

Background: Chronic total occlusion (CTO) of the portal vein is one of the main causes of portal hypertension, which may result in life-threatening complications often managed by interventional radiology (IR). The aim of this study is to report the innovative experience with percutaneous revascularization therapy in the management of portal vein CTO in paediatric and adult patients. Materials and methods: From January 2020 to December 2023 consecutive paediatric and adult patients with severe portal hypertension resulting from portal vein CTO who underwent attempts at percutaneous recanalization were retrospectively reviewed. Technical aspects including the percutaneous approach, portal vein stenting, transjugular intrahepatic portosystemic shunt (TIPS) creation, varices embolization and clinical outcomes including adverse events and control of portal hypertension were analyzed. Technical success was defined as at least partial restoration of the portal vein patency at the final angiogram. Clinical success was defined as the improvement of clinical-laboratory signs of portal hypertension and control for variceal bleeding. Results: Fifteen patients (median age = 21 years, range = 59 years; 10 males; 5 children) with portal vein CTO underwent a total of 25 percutaneous revascularization procedures. Nine patients (60%; 5 children, 4 adults) were liver transplant recipients. All patients except one had cavernous transformation of the extra-hepatic portal vein, involving the spleno-mesenteric confluence in 5 cases. Technical success was achieved in 13/15 (87%) patients of whom 8 had portal revascularization through the placement of an extra-hepatic stent; indeed, in six cases, a TIPS was performed to achieve sustained portal vein patency. Embolization of varices and/or cavernoma was performed in 12 patients. Adverse events occurred in 2/15 (splenic artery perforation and hemoperitoneum, one each) managed without sequelae. Technical success led to clinical success in all the 13/15 (87%) cases, with a median follow-up of 20 months (IQR 4–34 months). Conclusion: CTO can be managed effectively by interventional radiology. Restored portal flow physiology alone is possible in most patients, while TIPS may be required in a small proportion of them, to prolong portal vein patency and control portal hypertension. [ABSTRACT FROM AUTHOR]

Background: Primary sclerosing cholangitis (PSC) is an idiopathic cholestatic liver disease that may lead to biliary strictures and destruction. It is associated with p-ANCA positivity and inflammatory bowel disease, typically ulcerative colitis. The aim of this study is to investigate the trends of inpatient healthcare utilization and mortality from 2008 to 2017 in the United States. Methods: The Nationwide Inpatient Sample (NIS) was examined to identify adult patients diagnosed with PSC between 2008 and 2017. Data on patient demographics, resource utilization, mortality, and PSC-related complications were collected. STATA version 16.0 was employed to perform forward stepwise multivariate regression analysis, generating adjusted odds ratios for both primary and secondary outcomes. Primary outcomes included the inpatient mortality rate and healthcare resource utilization (length of stay, total charges, and trends over the study period). Secondary outcomes focused on trends in associated comorbidities and malignancies in patients with PSC. Results: The average total charge increased by 32.2% ± 2.12 from USD 61,873 ± 2567 in 2008 to USD 91,262 ± 2961 in 2017. Concurrently, the average length of stay declined from 8.07 ± 0.18 days in 2008 to 7.27 ± 0.13 days in 2017. The APR-DRG severity of illness and risk of death significantly increased (major or extreme) during the study period (2008 to 2017), with severity rising from 73.6% to 82.7% (coefficient: 0.21, 95% CI: 0.13–0.28) and risk of death from 45.3% to 60.9% (coefficient: 0.15, 95% CI: 0.08–0.23). The proportion of patients with HCC increased from 1.3% to 7.9% (coefficient: 2.13, 95% CI: 1.9–2.8). Conversely, the percentage of patients with cholangiocarcinoma (CCA) decreased from 5.1% to 2.8% (coefficient: −0.36, 95% CI: −0.25 to −0.46). Conclusions: There was rising mortality and healthcare resource utilization among patients with PSC from the years 2008 to 2017. These trends were paralleled by increasing rates of decompensated cirrhosis, HCC, and liver transplants. However, the incidence of CCA decreased during this time period. African American patients with PSC had worse inpatient mortality outcomes and healthcare utilization as compared to white patients. Further studies are warranted to investigate a possible causal link amongst these trends. [ABSTRACT FROM AUTHOR]

Background: Elevated spleen stiffness may be seen in patients with portal hypertension due to cirrhosis. In patients with Fontan physiology, elevated liver stiffness has been shown to correlate poorly with liver fibrosis. It is unknown whether spleen stiffness may instead serve as a surrogate marker of liver fibrosis in these patients. Objective: To compare spleen stiffness determined by shear wave elastography (SWE) with histological findings of an ultrasound-guided liver biopsy in patients who had undergone Fontan palliation as a potential surrogate for Fontan-associated liver disease. Materials and methods: This was an IRB-approved single-center, retrospective study. Patients with Fontan palliation who had undergone both a spleen SWE study and a percutaneous liver biopsy between 2016 and 2020 were included. Biopsy, performed during cardiac catheterization, within 3 months of the SWE was required for inclusion. Using Kruskal–Wallis tests, spleen stiffness was compared with three liver biopsy scoring methods: Ishak, METAVIR, and congestive hepatic fibrosis score (CHFS). When available, Pearson's correlation was also used to compare collagen deposition determined using Sirius Red stain (%SR) with SWE values. A P-value < 0.05 was considered statistically significant. Results: Twenty-two patients (15 males) were included in the study, with a median age of 17 years (IQR is 14.8–20.5 years; age range: 7 years to 30.2 years). The median spleen stiffness was 2.94 m/s (IQR: 2.57–3.61 m/s; range: 1.48–4.27 m/s). The median Fontan pressure was 11 mm Hg (IQR: 10–13.3 mm Hg; range: 7–19 mm Hg) obtained within a median of 10 days (IQR: 1–41 days) of SWE. Splenic stiffness did not correlate with the extent of fibrosis determined by histology (all P > 0.05). There was also no statistically significant correlation between the %SR staining and SWE-determined spleen stiffness (Pearson's correlation of 0.165, P = 0.59, n = 13). Conclusions: In this preliminary study, SWE spleen stiffness values did not correlate with biopsy-determined scoring of liver fibrosis in patients with Fontan physiology. [ABSTRACT FROM AUTHOR]

ABSTRACT Background and Aims Methods Results Conclusion Portal hypertension is the main pathophysiological driver of decompensation in patients with liver cirrhosis. Epithelial cell death markers, m30 and m65, correlate with hepatic injury and predict outcomes across various stages of liver disease. We aim (i) to evaluate whether portal hypertension itself contributes to liver outcome‐relevant epithelial injury, and (ii) to analyse the capacity of m30/m65 to predict outcome in patients receiving a transjugular intrahepatic portosystemic shunt (TIPS) for refractory ascites.Sixty‐six patients undergoing TIPS placement for refractory ascites and 20 patients with compensated cirrhosis as controls were prospectively enrolled in this monocentric cohort study. Epithelial cell death markers were analysed pre‐TIPS, as well as 1–3 and 6–9 months post‐TIPS. The capacity of baseline levels of m30/m65 in predicting six‐month transplant‐free survival rates was analysed by multivariable Cox proportional hazards regression.Levels of m30 and m65 were higher in patients with decompensated cirrhosis (pre‐TIPS) compared with compensated cirrhosis (controls). Following correction of portal hypertension by TIPS and recompensation, both markers decreased over time, reaching levels comparable to patients with compensated cirrhosis. On multivariable analysis, pre‐TIPS baseline levels of m30 and m65 were not predictive for six‐month survival.Correction of portal hypertension via TIPS reduces levels of epithelial cell death markers, indicating that portal hypertension is a driver of outcome‐relevant, hepatic cell death in patients with decompensated cirrhosis. Baseline m30/m65 values do not affect six‐month survival rates, which suggests that TIPS placement overcomes the unfavourable spontaneous prognosis otherwise indicated by elevated baseline m30/65 levels. [ABSTRACT FROM AUTHOR]

Cardiovascular complications are common in patients with severe liver disease and are an important cause of peri-operative and post-transplant morbidity and mortality. Cirrhotic cardiomyopathy (CCM), often found in advanced liver disease, is characterized by diastolic dysfunction, systolic dysfunction, and electrophysiological abnormalities. While CCM may not cause symptoms at rest, it can become evident during stressful activities, such as surgery. Liver transplantation, while being the definitive treatment for end-stage liver disease (ESLD), carries significant cardiovascular risks. Preoperative cardiac evaluation is essential for assessing these risks and planning appropriate management. Cardiac imaging, particularly echocardiography, plays a crucial role in evaluating liver transplant candidates, helping to identify conditions such as CCM, pulmonary hypertension, hepatopulmonary syndrome, and others. Currently, liver transplant anesthetists must acquire echocardiographic knowledge and skills to evaluate the cardiocirculatory conditions of the transplanted patient, especially in the pre-operative phase, but also intra-operatively and post-operatively. [ABSTRACT FROM AUTHOR]

Background: Solid pseudopapillary neoplasm (SPN) is a low-grade malignant tumor that occurs in 60% of all pediatric pancreas tumors. Radical tumor resection is essential; however, spleen preservation is also crucial to prevent overwhelming post-splenectomy infection. In contrast, spleen preservation is not always possible, because left-sided portal hypertension (LSPH) can cause splenic vein stenosis or occlusion induced by pancreatic tumor. We herein report on a pediatric patient of LSPH due to SPN in the pancreatic tail. Case presentation: A 12-year-old girl was admitted to our hospital with left upper quadrant abdominal pain. A solid mass was palpated in the left costal region. The patient showed slight anemia (Hb: 11.8 g/dL) and elevation of inflammatory reaction (CRP: 5.98 mg/dL) without positive tumor markers. A radiological examination revealed that a 9 cm-sized mass with hemorrhagic necrosis in the pancreatic tail. Splenic venous flow was not detected and collateral draining into the left gastric vein and left renal veins were developed with splenomegaly. LSPH was involved at the time of diagnosis. The tumor was diagnosed with SPN, hence tumor resection with spleen preservation was performed. Six months after surgery, the patient developed a left quadrant abdominal pain that worsened during exercise. There was no improvement of splenic venous flow and splenomegaly. LSPH remained with splenomegaly, which possibly triggered the patient's abdominal pain. The patient underwent splenectomy 9 months after the tumor resection. After the splenectomy, the patient's abdominal pain disappeared without any recurrence 8-year post-surgery. Conclusions: LSPH has not been a major focus in previous SPN pediatric patients, although most symptomatic LSPH patients required splenectomy. Careful post-operative observation for LSPH is important for pediatric SPN patients. [ABSTRACT FROM AUTHOR]

ABSTRACT Background Aims Methods Results Conclusions The accuracy of current criteria for ruling out large oesophageal varices (LEV) and other endoscopic lesions of portal hypertension (PH) may be compromised by obesity and MASLD/MASH.In the US multicentre SHUNT‐V study, we evaluated the disease severity index (DSI) for detecting LEV and other lesions of PH at endoscopy.Subjects were adults with compensated cirrhosis scheduled for endoscopy to screen for varices. DSI was calculated from clearances of labelled cholates after oral and intravenous administration. DSI ≤ 18.3 was evaluated as a cut‐off for ruling out LEV with acceptance criteria of negative likelihood ratio < 0.52 and sensitivity > 85%.SHUNT‐V enrolled 306 subjects; 275 had both DSI and endoscopy, and 238 had Child–Pugh A cirrhosis (52.1% MASLD/MASH, 25.2% chronic hepatitis C and 15.6% alcoholic liver disease; 87% were overweight, 64% were obese and 54% had diabetes). AUROCs for DSI ranged from 0.81 to 0.82 for LEV and 0.79 to 0.80 for all significant PH lesions. DSI 18.3 had sensitivity 96.3%–100% for LEV and 97.3%–100% for all significant PH lesions. If DSI ≤ 18.3 were used as the sole determinant to defer EGD, 27%–35% of EGDs could have been avoided with 0%–3.7% of LEV and 0%–2.7% of all significant PH lesions missed.HepQuant DSI predicts the likelihood of LEV and significant PH lesions across a spectrum of patient characteristics and disease aetiologies. DSI, based on liver function and portal‐systemic shunting, can aid in the decision to defer endoscopy for varices in patients with Child–Pugh A cirrhosis.Trial Registration: The SHUNT‐V study was registered at ClinicalTrials.gov (NCT03583996) [ABSTRACT FROM AUTHOR]

Background: Radical cystectomy is typically recommended for managing bladder cancer, with ileal conduit diversion being a prevalent form of urinary diversion. Stomal variceal haemorrhage is a rare complication of ileal bladder diversion and poses diagnostic and therapeutic challenges that can escalate to life-threatening circumstances. Hepatic cirrhosis and cancer liver metastasis-induced portal hypertension are considered the main causes of stomal varices. However, the real-world expertise in the pathophysiology of, diagnostic approach to, and overall management strategy for stomal variceal haemorrhage in ileal conduit diversion is limited. Case presentation: Herein, we present a rare case of a 77-year-old man with bladder cancer who developed stomal variceal haemorrhage after undergoing radical cystectomy and ileal conduit urinary diversion. Imaging revealed that the peristomal varices communicated with the subcutaneous veins of the abdominal wall without apparent portal hypertension. Transhepatic coil embolization of bleeding stomal varices was successfully performed via a transhepatic antegrade approach. No complications or stomal variceal haemorrhage occurred during a 6-month follow-up period. Conclusion: Transhepatic coil embolization may be considered an initial therapeutic option for patients who experience stomal variceal haemorrhage. Comprehensive management of underlying liver disease and portal hypertension is needed at follow-up visits. We describe successful experience with the precise treatment of this rare and atypical disease, conduct a thorough review of the pertinent literature, and deliberate on optimized diagnostic and therapeutic procedures. [ABSTRACT FROM AUTHOR]

ABSTRACT Background Aims Methods Results Conclusions Transjugular intrahepatic portosystemic shunt (TIPSS) is highly effective for treatment of variceal bleeding; however, factors contributing to rebleeding complications remain unclear.In this study, we aim to determine risk factors for recurrent portal hypertensive gastrointestinal bleeding following TIPSS.Utilising the Advancing Liver Therapeutic Approaches multicentre database, we retrospectively identified adult patients who underwent TIPSS for secondary prophylaxis of variceal bleeding and had a gastrointestinal rebleeding event within 1 year. We developed multivariable logistic regression models to identify clinical/procedural characteristics associated with rebleeding.We identified 476 patients, predominately middle‐aged (mean age 57), male (62%) and White (65%), with mean MELD‐Na 16. 16% (n = 77) had a rebleeding event; these patients were more likely to be male (p = 0.016), with higher serum creatinine (p = 0.005), MELD‐Na (p = 0.0002), portal hypertensive gastropathy on pre‐TIPSS upper endoscopy (p = 0.000) and with higher incidence of TIPSS revision (p = 0.000). There were no significant differences in type of TIPSS endoprosthesis, concurrent embolotherapy, and post‐TIPSS pressure gradients between those who experienced rebleeding and those who did not. After adjusting for TIPSS revision, multivariable analysis revealed MELD‐Na and presence of portal hypertensive gastropathy on pre‐TIPSS endoscopy were independently associated with rebleeding.In this retrospective analysis of a multicentre, nationally representative database, we found that apart from TIPSS‐related factors, high MELD‐Na and portal hypertensive gastropathy on pre‐TIPSS endoscopy were independent predictors of rebleeding within 1 year following TIPSS. These variables may be used to identify high‐risk patients who may require additional monitoring following TIPSS. [ABSTRACT FROM AUTHOR]

Background: The advent of antibody-drug conjugates (ADCs) represents a landmark advance in cancer therapy, permitting targeted delivery of a potent cytotoxic agent to tumor cells with minimal damage to surrounding cells. Although ADCs can induce sustained therapeutic responses in heavily pretreated patients, they can also cause significant toxicity and thus require careful monitoring. The prototype ADC, ado-trastuzumab emtansine (T-DM1) is comprised of a humanized, monoclonal human epidermal growth factor receptor 2 (HER2)-directed antibody, trastuzumab, linked to the cytotoxic agent, DM1, and is used for the treatment of early-stage and advanced HER2-positive breast cancer. Liver toxicities, including transaminitis and nodular regenerative hyperplasia resulting in portal hypertension have been described. We report a case series of four patients who developed hepatopulmonary syndrome (HPS) during treatment with T-DM1. HPS is characterized by hypoxemia, portal hypertension, and intrapulmonary shunting, and it can be associated with severe hypoxic respiratory failure. HPS secondary to noncirrhotic portal hypertension occurring with long-term exposure to T-DM1 has not previously been reported. Case series presentation: Four patients who received T-DM1 in our institutional cohort (n=230) developed HPS, which can be associated with severe hypoxic respiratory failure. Each patient diagnosed with HPS received >50 doses of T-DM1. Only one patient at diagnosis had resting hypoxia, while the other three patients became hypoxic with exertion only. Discontinuation of T-DM1 led to clinical improvement in hypoxia in three of the four patients. The spectrum of liver injury that occurs with long-term use of T-DM1 remains incompletely defined. Conclusions: As T-DM1 is approved for use in the management of early-stage operable and advanced breast cancer, awareness of HPS as a potential complication of long-term administration of T-DM1 is necessary. The emergence of dyspnea alone or combined with low oxygen saturation and signs of hypoxemia (clubbing or elevated hemoglobin) should raise clinical suspicion and prompt evaluation for HPS. Cancer care team members should be vigilant regarding the potential for new and serious side effects associated with novel targeted therapies, which may emerge years beyond initial regulatory approval. [ABSTRACT FROM AUTHOR]

Background: Acute kidney injury (AKI) is one of the common complications of liver cirrhosis. It occurs in nearly 20% of patients with cirrhosis who are hospitalized. Prior literature demonstrated that the AKI occurrence in patients with cirrhosis is independently associated with higher mortality. However, there are data assessing predictors and outcomes of AKI resolution in hospitalized patients with cirrhosis. Therefore, the aim of the current study was to identify clinical predictors of AKI resolution among inpatients with cirrhosis that are easily obtained and to evaluate the clinical outcomes of those patients. Methods: The current study is a retrospective cohort of patients with cirrhosis who were hospitalized and had AKI between 2012 and 2020 at a tertiary referral center. Patients included in this study were identified using the International Classification of Diseases 9 codes and then they were manually verified by two independent chart reviewers. AKI was classified according to the AKI Network (AKIN) serum creatinine (Cr) criteria, with AKIN resolution defined as AKIN stage 1 or lower at the time of discharge, while unresolved AKIN was defined as AKIN stage 2 or 3 at the time of discharge. For univariate analysis, Fisher's exact and the two-sample T-test were utilized. For multivariable analysis, stepwise logistic regression was performed to evaluate variables associated with AKIN resolution. Survival curves were estimated and compared using the Kaplan–Meier method and Log-Rank Test. A p-value cutoff of 0.05 was used for statistical significance. Results: Between 2012 and 2020, there were 140 patients who were included (59% males). The majority of patients had viral hepatitis (54%) as the cirrhosis etiology with 80% of them having hepatitis C virus. Most patients had fluid-responsive AKI (49%), and stage 1 AKIN (69%). In terms of outcomes, the majority of patients (117 patients; 84%) had AKIN resolution at the time of discharge. In the multivariable analysis, after adjusting for clinical meaningful variables, our study shows that higher albumin value at the time of admission (adjusted Odds Ratio "aOR" = 3.28; p = 0.01) and non-metabolic dysfunction-associated steatotic liver disease (non-MASLD) cirrhosis (aOR = 9.43; p < 0.01) were variables associated with higher odds of AKIN resolution at the time of discharge. Conversely, we show that a higher Cr value at the time of admission was associated with lower odds of AKIN resolution at the time of discharge (aOR = 0.31; p < 0.01). When evaluating mortality, patients with unresolved AKIN at the time of discharge had higher rates of in-hospital mortality (p < 0.01) compared to those with resolved AKIN. Survival curve analyses using the Kaplan–Meier method indicated that patients with resolved AKIN experienced higher 90-day survival rates (p < 0.01). Additionally, those with resolved AKIN demonstrated greater transplant-free survival compared to patients with unresolved AKIN at both the 1-year (p = 0.04) and 3-year (p < 0.01) follow-ups. Conclusions: When evaluating clinical predictors of AKIN resolution in admitted patients with cirrhosis, our study showed that a higher admission albumin value and non-MASLD etiology of cirrhosis were associated with higher odds of AKIN resolution at the time of discharge. Conversely, a higher admission Cr value was associated with lower odds of AKIN resolution at the time of discharge. We also demonstrate that AKIN resolution during index admission was associated with improved short- and long-term transplant-free survival (up to 3 years). Our findings warrant external validation in larger cohorts to further evaluate the impact of inpatient AKI resolution on cirrhosis outcomes. Our findings can help clinicians predict AKIN outcomes and encourage more aggressive management of AKI, especially in high-risk patients, which can improve mortality. [ABSTRACT FROM AUTHOR]

Objectives Patients with liver cirrhosis are prone to develop severe bacterial infections. Pharmacokinetics (PK) of antibiotics in cirrhosis are potentially affected by impaired biotransformation phases 0–3 and consequences of portal hypertension such as portovenous shunting, ascites formation and/or acute kidney injury (AKI). We aimed to elucidate to what extent PK of selected antibiotics and, therefore, dosage recommendations are affected in adults with cirrhosis. Methods We performed a systematic search in PubMed, Embase, Cochrane and CINAHL on effects of cirrhosis on PK profiles of ceftriaxone, fosfomycin, gentamicin, meropenem, nitrofurantoin, piperacillin/tazobactam and vancomycin in adults. Antibiotics were selected based on the lack of specific dosing recommendations for adults with cirrhosis. We included studies reporting on ≥1 of the following PK parameters: AUC, half-life (t ½), CL, volume of distribution (V d), peak (C max) or trough concentrations (C min). Results We identified 15 studies (ceftriaxone, n  = 5; gentamicin, n  = 3; meropenem n  = 5; vancomycin, n  = 2), including 379 patients with cirrhosis, of which two were of high quality. No eligible studies were identified for fosfomycin, nitrofurantoin or piperacillin/tazobactam. Ceftriaxone unbound concentration increased in cirrhosis, but was mitigated by increased renal CL. Gentamicin levels in ascitic fluid were comparable to those in plasma. Meropenem PK parameters were not altered in cirrhosis without AKI, but in the presence of AKI a decrease in CL was observed. In contrast, vancomycin CL decreased in advanced cirrhosis. Conclusions Available data in studies of mostly moderate quality suggest that PK of ceftriaxone, meropenem and vancomycin are altered in cirrhosis. More advanced PK studies are needed to provide specific dosing recommendations. [ABSTRACT FROM AUTHOR]

This is the English version of the guidelines for the diagnosis and treatment of idiopathic portal hypertension, extrahepatic portal obstruction, and Budd–Chiari syndrome, which were established and revised in 2018 by the Aberrant Portal Hemodynamics Study Group under the jurisdiction of the Ministry of Health, Labor, and Welfare in Japan. These guidelines are excerpts, and the full version consists of 86 clinical questions and explanations, totaling 183 pages in Japanese. [ABSTRACT FROM AUTHOR]

Background and Aims: The role of histamine in advanced chronic liver disease (ACLD) is poorly understood. We investigated plasma histamine levels across ACLD stages and their prognostic value. Methods: We included patients with evidence of ACLD, defined by portal hypertension (hepatic venous pressure gradient [HVPG] ≥6 mmHg) and/or a liver stiffness measurement by transient elastography ≥10 kPa, who underwent HVPG measurement between 2017 and 2020. Acute‐on‐chronic liver failure (ACLF) and/or liver‐related death were defined as composite endpoint. Results: Of 251 patients, 82.5% had clinically significant portal hypertension (median HVPG: 17 mmHg [interquartile range (IQR) 12–21]) and 135 patients (53.8%) were decompensated at baseline. Median plasma histamine was 8.5 nmol/L (IQR: 6.4–11.5), 37.1% of patients showed elevated values (>9.9 nmol/L). Histamine levels did not differ significantly across Child‐Turcotte‐Pugh (CTP) stages nor strata of model for end‐stage liver disease (MELD) or HVPG. Histamine levels correlated with markers of circulatory dysfunction (i.e. sodium, renin and aldosterone). During a median follow‐up of 29.2 months, 68 patients developed ACLF or liver‐related death. In univariate as well as in multivariate analysis (adjusting for age, sex, HVPG as well as either MELD, clinical stage, and serum albumin or CTP and serum sodium), elevated histamine levels remained associated with the composite endpoint. CTP‐based multivariate model adjusted sub‐distribution hazard ratio (asHR): 1.010 (95% CI: 1.004–1.021), p <.001; MELD‐based multivariate model asHR: 1.030 (95% CI: 1.017–1.040), p <.001. Conclusion: High levels of histamine were linked to circulatory dysfunction in ACLD patients and independently associated with increased risks of ACLF or liver‐related death. Further mechanistic studies on the link between histamine signalling and development of hyperdynamic circulation and ACLF are warranted. [ABSTRACT FROM AUTHOR]

Background: Portal hypertension leads to lethal complications in liver cirrhosis. Oxidative stress induced hepatic vascular dysfunction, which exaggerated vasoconstriction and increases hepatic vascular resistance (HVR). Gut dysbiosis further exacerbates portal hypertension. Fructooligosaccharides are prebiotics with potent antioxidant effect. This study aimed to evaluate the roles of fructooligosaccharides in portal hypertension‐related vascular dysregulation and gut microbiome. Methods: Sprague–Dawley rats received bile duct ligation to induce cirrhosis or sham operation as controls. The rats then randomly received fructooligosaccharides or vehicle for 4 weeks. Experiments were performed on the 29th day after operations. Results: Fructooligosaccharides did not affect portal pressure. Interestingly, fructooligosaccharides significantly attenuated HVR (p =.03). Malondialdehyde, an oxidative stress marker, reduced significantly in the liver in fructooligosaccharides‐treated group. In addition, superoxide dismutase and trolox equivalent antioxidant capacity increased in the treatment group. On the other hand, vasodilatation‐related protein expressions, GTPCH and phospho‐eNOS, enhanced significantly. Fructooligosaccharides had no adverse vasodilatation effects on splanchnic vascular system or porto‐systemic collateral systems. Locomotor function was not affected by fructooligosaccharides. Faecal microbiota analysis showed that Negativicutes, Selenomonadales and Lactobacillus salivarius reduced in the fructooligosaccharides‐treated group. Conclusion: In conclusion, fructooligosaccharides attenuate hepatic vascular dysfunction in cirrhotic rats via at least partly, ameliorate of dysbiosis and oxidative stress. [ABSTRACT FROM AUTHOR]

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a leading cause of advanced chronic liver disease (ACLD). Portal hypertension drives hepatic decompensation and is best diagnosed by hepatic venous pressure gradient (HVPG) measurement. Here, we investigate the prognostic value of HVPG in MASLD-related compensated ACLD (MASLD-cACLD). This European multicentre study included patients with MASLD-cACLD characterised by HVPG at baseline. Hepatic decompensation (variceal bleeding/ascites/hepatic encephalopathy) and liver-related mortality were considered the primary events of interest. A total of 340 patients with MASLD-cACLD (56.2% male; median age 62 [55-68] years, median MELD 8 [7-9], 71.2% with diabetes) were included. Clinically significant portal hypertension (CSPH: i.e. , HVPG ≥10 mmHg) was found in 209 patients (61.5%). During a median follow-up of 41.5 (27.5-65.8) months, 65 patients developed hepatic decompensation with a cumulative incidence of 10.0% after 2 years (2Y) and 30.7% after 5 years (5Y) in those with MASLD-cACLD with CSPH, compared to 2.4% after 2Y and 9.4% after 5Y in patients without CSPH. Variceal bleeding did not occur without CSPH. CSPH (subdistribution hazard ratio [SHR] 5.13; p < 0.001) was associated with an increased decompensation risk and a higher HVPG remained an independent risk factor in the multivariable model (adjusted SHR per mmHg: 1.12, p < 0.001). Liver-related mortality occurred in 37 patients at a cumulative incidence of 3.3% after 2Y and 21.4% after 5Y in CSPH. Without CSPH, the incidence after 5Y was 0.8%. Accordingly, a higher HVPG was also independently associated with a higher risk of liver-related death (adjusted SHR per mmHg: 1.20, p < 0.001). HVPG measurement is of high prognostic value in MASLD-cACLD. In patients with MASLD-cACLD without CSPH, the short-term risk of decompensation is very low and liver-related mortality is rare, while the presence of CSPH substantially increases the risk of both. While the incidence of compensated advanced chronic liver disease (cACLD) due to metabolic dysfunction-associated steatotic liver disease (MASLD) is increasing worldwide, insights into the impact of clinically significant portal hypertension (CSPH) on the risk of liver-related events in MASLD-cACLD remain limited. Based on the findings of this European multicentre study including 340 MASLD-cACLD patients, we could show that increasing HVPG values and the presence of CSPH in particular were associated with a significantly higher risk of first hepatic decompensation and liver-related mortality. In contrast, the short-term incidence of decompensation in patients with MASLD-cACLD without CSPH was low and the risk of liver-mortality remained negligible. Thus, HVPG measurements can provide important prognostic information for individualised risk stratification in MASLD-cACLD and may help facilitate the study of novel and promising treatment possibilities for MASLD. [Display omitted] • HVPG measurement can identify patients with MASLD-cACLD at risk of liver-related events. • CSPH drives decompensation and liver-related death in MASLD-cACLD. • The risk of liver-related events in MASLD-cACLD without CSPH is low. • HVPG can facilitate risk-stratification and treatment decisions in MASLD-cACLD. [ABSTRACT FROM AUTHOR]

The objective of this study was to investigate the subharmonic response of Lumason (also known as SonoVue; Bracco, Milan, Italy) to static and dynamic ambient pressures, with a direct comparison to Sonazoid (GE HealthCare, Oslo, Norway) and Definity (Lantheus Medical Imaging, MA, USA). The subharmonic responses of contrast agents can be exploited to perform subharmonic-aided pressure estimation. The subharmonic response of each ultrasound contrast agent was evaluated in both a static and dynamic tank using a commercially available Logiq E10 clinical ultrasound scanner (GE HealthCare) equipped with subharmonic imaging (SHI) and an acoustic power-optimization algorithm. A C1-6 curvilinear array that transmits at 2.5 MHz and receives at 1.25 MHz in SHI mode was used to acquire the subharmonic signals. Data was transferred offline into MATLAB (MathWorks) to perform linear regression analysis and statistical testing for significance of the slopes (i.e. , agent sensitivity). Sonazoid and Definity showed an inverse linear dependency between subharmonic signal and hydrostatic pressure at all pressure ranges (static and dynamic) tested, with maximum sensitivity under 50 mmHg in the static tank (−0.190 and −0.194 dB/mmHg for Sonazoid and Definity, respectively). Lumason exhibited a tri-phasic subharmonic behavior, beginning with a linear trend from 0 to 90 mmHg (sensitivity = 0.069 dB/mmHg), followed by a plateau from 100 to 130 mmHg, and an inverse linear trend from 140 to 200 mmHg (sensitivity = −0.137 dB/mmHg). The subharmonic response of Lumason is tri-phasic and differs from Sonazoid and Definity. Further investigation is needed to solidify understanding of the subharmonic behavior of Lumason to identify its usefulness for subharmonic-aided pressure estimation. [ABSTRACT FROM AUTHOR]

Background: Endoscopic variceal ligation and sclerotherapy are recommended for esophagogastric variceal bleeding (EGVB) in cirrhosis but can be complicated by early rebleeding and death. This study aimed to identify noninvasive markers accurately predicting early rebleeding and mortality after endoscopic hemostasis for EGVB. Methods: Among 116 patients with endoscopically confirmed EGVB and endoscopic hemostasis, various noninvasive markers were calculated, and their predictive accuracy was compared by receiver‐operating characteristic curve analysis. Endpoints included 5‐day rebleeding, 5‐day mortality, 6‐week rebleeding, and 6‐week mortality. Results: The median age was 63 years. Child‐Pugh class B and C patients accounted for 40.5% and 34.5%, respectively. Only the aspartate aminotransferase‐to‐platelet ratio index (APRI) significantly predicted 5‐day rebleeding, with an area under the curve (AUC) of 0.777 (95% confidence interval [CI]: 0.537–1). The model for end‐stage liver disease‐Na (MELD‐Na) score showed good predictive accuracy for 5‐day mortality (AUC: 0.839, 95% CI: 0.681–0.997), 6‐week rebleeding (AUC: 0.797, 95% CI: 0.663–0.932), and 6‐week mortality (AUC: 0.888, 95% CI: 0.797–0.979). Conclusions: Patients with cirrhosis with a high APRI and MELD‐Na score were at high risk of early rebleeding and death after EGVB. Allocating appropriate monitoring and care for those patients is necessary. [ABSTRACT FROM AUTHOR]

Purpose: To assess the technical and clinical outcomes of percutaneous embolization for high-flow mesenteric vein to gonadal vein (MGV) portosystemic shunts. Methods: In this HIPPA-compliant, review board-approved study, patients who underwent embolization of MGV shunts between 2011 and 2023 were included. Patient demographic data, embolization technique, clinical outcomes, and complications were retrieved from the electronic health records. Technical success was defined as complete occlusion of the shunt on follow-up imaging. Clinical outcomes assessed were resolution/improvement of hepatic encephalopathy, improvement in liver function, changes to liver volumes, and occurrence of adverse events. Results: Eight patients (mean age 59.5, 75% female) with nine MGV shunts were included. The indications for shunt embolization included medically refractory hepatic encephalopathy, bleeding duodenal varices, and transplant liver dysfunction. The mean maximum shunt diameter was 23.3 mm. Embolization was most commonly performed with a combination of coils and N-butyl cyanoacrylate or vascular plugs. Complete MGV shunt thrombosis was achieved in 7/9 shunts post-embolization, and symptom improvement was noted in 7/8 patients. Child–Pugh scores improved post-embolization in 6/9 patients by a median of 3 points. Liver volumes also increased by a mean of 20.8 ± 17.7% post-embolization. Minor adverse events included new onset ascites, partial mesenteric/portal vein thrombosis, and new gastroesophageal varices without bleeding in four patients. Conclusion: Embolization of MGV shunts is technically feasible and effective for treatment of hepatic encephalopathy and increasing hepatopetal portal perfusion. There was an improvement in Child–Pugh scores and an increase in liver volumes in the majority of patients post-embolization. [ABSTRACT FROM AUTHOR]

PURPOSE Computed tomography (CT)-based body composition parameters and the hepatic venous pressure gradient (HVPG) are key characteristics in patients with liver cirrhosis. The present study aims to explore the correlation between CT-based body composition parameters and HVPG, as well as the difference in HVPG between patients with and patients without sarcopenia. METHODS A literature search for studies reporting the correlation between HVPG and CT-based body composition parameters published in English up to August 2023 in four databases, Embase, MEDLINE (via PubMed), Web of Science, and Cochrane Library, was conducted. The correlation coefficient between HVPG and CT-based body composition parameters was the primary outcome, and the difference in the HVPG value between the sarcopenia and non-sarcopenia groups was the secondary outcome. A meta-analysis was conducted using a random-effects models. The methodologic quality was assessed using the Quality Assessment of Diagnostic Studies instrument. RESULTS A total of 652 articles were identified, of which nine studies (n = 1,569) met the eligibility criteria. Among them, seven studies reported the primary outcome via the muscle index, five via the skeletal muscle index (SMI), two via the psoas-muscle-related index (PRI), and three via two adipose tissue indexes. A total of five studies reported the secondary outcome: four via SMI and one via PRI. No evidence of a significant correlation was determined between the various body composition parameters and the HVPG value, either in the muscle index or the adipose tissue index. Higher HVPG values were observed in patients with sarcopenia than in patients without sarcopenia [pooled standardized mean difference (SMD): 0.628 (-0.350, 1.606), P < 0.001; I² = 92.8%; P < 0.001] when an Asian sarcopenia definition was adopted. In contrast, when a Western cut-off value was applied, the HVPG value was higher in patients without sarcopenia than in patients with sarcopenia [pooled SMD: -0.201 (-0.366, -0.037), P = 0.016; I² = 0.00%; P = 0.785]. CONCLUSION No sufficient evidence regarding a correlation between the CT-based body composition and HVPG value was discovered. The difference in the HVPG value between the sarcopenia and non-sarcopenia groups was likely dependent on the sarcopenic cut-off value. [ABSTRACT FROM AUTHOR]

PURPOSE This meta-analysis aimed to evaluate the diagnostic accuracy of computed tomography (CT) for detecting gastroesophageal varices (GEVs) and identify high-risk GEVs in patients with cirrhosis. METHODS A comprehensive search of databases identified 28 studies reporting on CT-based diagnosis for GEVs confirmed via endoscopy. Meta-analyses were conducted to calculate pooled sensitivity (SEN) and pooled specificity (SPE), positive likelihood ratio (PLR) and negative likelihood ratio (NLR), diagnostic odds ratio (DOR), and the area under the curve (AUC). RESULTS Based on the number of patients (or varices), the pooled SEN, SPE, PLR, NLR, DOR, and AUC of CTbased diagnosis were estimated at 0.91 (0.92), 0.81 (0.45), 4.82 (1.67), 0.11 (0.17), 42.47 (10.26), and 0.93 (0.94), respectively, for any GEV and at 0.89 (0.89), 0.90 (0.79), 8.86 (4.28), 0.12 (0.14), 75.71 (30.19), and 0.95 (0.85), respectively, for high-risk GEVs. Subgroup analyses indicated that CT had a higher diagnostic accuracy for esophageal varices compared with gastric varices (AUC: 0.93 vs. 0.89, P < 0.05), and the 64-slice CT yielded superior SEN compared with 16-slice and <16-slice CT (AUC: 0.97 vs. 0.92 and 0.82, respectively, P < 0.05). Prospective studies demonstrated higher diagnostic accuracy than retrospective studies (AUC: 0.95 vs. 0.90, P < 0.05). Regarding variceal size, a cut-off of 3 mm and 5 mm discriminated between low- and high-risk individuals, respectively, with high diagnostic accuracy (AUC: 0.992 vs. 0.997, P > 0.05). CONCLUSION CT demonstrates promising diagnostic accuracy for identifying gastroesophageal varices and distinguishing high-risk GEVs in patients with cirrhosis. Further research to validate optimal variceal size cut-offs is warranted to enhance clinical utility. CLINICAL SIGNIFICANCE Such a high diagnostic accuracy of CT scans for predicting varices is clinically meaningful for patients with cirrhosis accompanied by portal hypertension. If high-risk varices are identified at CT scans, early intervention would be helpful to reduce the risk of variceal bleeding. [ABSTRACT FROM AUTHOR]

Aims: Splenic vein occlusion (SpVO) due to a pancreatic tumor may result in the development of collateral circulation and left‐sided portal hypertension. This study aimed to investigate the impact of SpVO on distal pancreatectomy (DP) and provide insights about the management of such cases. Methods: This retrospective analysis included 124 patients who underwent DP from 2014 to 2022. A subgroup analysis was performed on 88 patients who underwent DP for pancreatic ductal adenocarcinoma (PDAC). Results: SpVO was found in 26 (20.8%) patients. The patients with SpVO had significantly larger splenic volumes and lower platelet counts. Compared to the patients with patent splenic veins (SpVs), the patients with SpVO underwent significantly longer operations (p = 0.006), with a higher incidence of postoperative complications (p = 0.002). We classified the collateral routes associated with SpVO into five patterns. The most common pattern was the left gastroepiploic vein type, which was associated with a tumor of the pancreatic body. In patients with PDAC, SpVO was associated with larger tumors, microscopic vascular permeation, and peritoneal recurrence. However, the differences between overall and recurrence‐free survival rates in the patients with SpVO vs those with patent SpVs were not significant. Conclusions: SpVO causes left‐sided portal hypertension, which can be a risk for perioperative complications in DP. Operative planning based on the classification of collateral flow patterns may help prevent intraoperative congestion and perioperative complications. [ABSTRACT FROM AUTHOR]

ABSTRACT Background and Aims Method Results Conclusions NOD2 mutations are associated with impaired gut mucosal barrier function. According to the systemic inflammation hypothesis, bacterial translocation is central in the development of decompensation. The aim was to evaluate whether the presence of NOD2 variants is associated with the development of first decompensation.Secondary analysis of prospectively collected consecutive patients with compensated cirrhosis, who were screened between 2014 and 2018. Patients with and without NOD2 variants were compared and stratified analysis according to the presence of varices was performed.360 patients [239 (66%) men, median age 61 (53–69) years, 70 (19%) with NOD2 variants, 90 (25%) with varices] were followed for a median of 9 (4–16) months. Similar baseline characteristics were observed across NOD2 status groups, except for beta‐blocker use (45% vs. 32% amongst variant carriers vs. non‐carriers, p = 0.05). During follow‐up, 34 patients (12%) developed their first decompensation, with no differences according to NOD2 status [HR 1.75 (95% CI 0.84–3.67)]. On multivariate analysis, only MELD remained an independent predictor of decompensation. Amongst patients with varices (n = 90), 18 (24.4%) carried a NOD2 variants, with a higher incidence of first decompensation [HR 3.00 (95% CI 1.08–8.32)], primarily due to ascites [HR 3.32 (95% CI 1.07–10.32)]. In this subgroup, MELD [HR 1.18 (95% CI 1.06–1.32)] and NOD2 variants [HR 2.91 (95% CI 0.95–8.89)] were determined to be independent predictors of decompensation.The presence of NOD2 risk variants leads to a greater incidence of first decompensation only in compensated patients with varices. [ABSTRACT FROM AUTHOR]

Background: Portal vein pressure (PVP) is crucial in the diagnosis, treatment monitoring, and prognosis of portal hypertension (PHT). At present, the hepatic venous pressure gradient (HVPG) and the portal vein pressure gradient (PPG) are the main approaches for portal pressure measurement. However, HVPG and PPG are limited in application due to invasive operations and high requirements for medical conditions. A more convenient way to measure portal pressure is demanded. Objectives: To detect whether the endoscopic variceal pressure (EVP) could predict the PVP. Design: This is a single-center retrospective study that detects whether the EVP could predict the PVP. Methods: Thirty-six patients were considered eligible for pre-emptive transjugular intrahepatic portosystemic shunt (TIPS) and were willing to accept the endoscopy-TIPS hybrid surgery (continuous operation within 24 h) from April 2023 to October 2023 retrospectively. EVP was measured in the procedure of the modified sandwich method. HVPG, PPG, and PVP were measured following TIPS operation. EVP was compared with HVPG, PPG, and PVP in groups divided by different sarin classifications and whether portal vein thrombosis (PVT) or not. Results: EVP was successfully measured and recorded in all. Totally, HVPG was lower than PPG, PPG was lower than PVP, and EVP manifested between PPG and PVP. In the PVT group, HVPG was lower than PPG, PPG was lower than EVP, and EVP manifested between PPG and PVP. In the non-PVT group, HVPG was lower than PPG, PPG was lower than PVP, and EVP manifested between PPG and PVP. In the gastroesophageal varices group, HVPG was lower than PPG, and PPG was lower than EVP. Conclusion: As a novel way for prediction, EVP measurement might be useful and convenient in PHT. Moreover, it might be closer to the PVP. [ABSTRACT FROM AUTHOR]

Background: Recent studies have highlighted that TACE in conjunction with Lenvatinib (TACE-L) offers a promising adjunct therapy for advanced HCC patients, outperforming TACE plus Sorafenib (TACE-S). However, there has been a lack of research comparing these two regimens for intermediate HCC. Aims: This study aims to address the research gap by evaluating the efficacy of TACE-L versus TACE-S in intermediate HCC patients. Methods: A retrospective analysis was conducted on a cohort of consecutive intermediate HCC patients who received either TACE-L or TACE-S from November 2018 to December 2022. Portal vein width was assessed using abdominal NMRI or Doppler ultrasonography, and inflammatory markers were derived from routine blood counts. The primary outcomes of interest were overall survival (OS), progression-free survival (PFS), objective response rate (ORR), disease control rate (DCR), and adverse drug reactions (ADRs). Results: The study included 117 patients, with 56 in the TACE-S group and 61 in the TACE-L group. The TACE-S group demonstrated superior OS (HR = 1.704, 95% CI: 1.012–2.870, p = 0.045) compared to the TACE-L group. No significant difference was observed in PFS (HR:1.512, 95% CI: 0.988–2.313, p = 0.057) between the two groups. Subgroup analyses revealed that male patients, those with cirrhosis, and those with more than four tumors had better OS and PFS in the TACE-S group than in the TACE-L group. Inflammatory markers were comparable between the groups. The TACE-S group experienced a higher incidence of palmar-plantar erythrodysesthesia syndrome (PPE) (14/56 [25%] vs. 5/61 [8.1%], p = 0.014) but a lower incidence of hypertension (3/56 [5.3%] vs. 11/61 [18%], p = 0.035) compared to the TACE-L group. Conclusions: In patients with intermediate HCC, TACE-S was found to be more effective in terms of OS than TACE-L. No significant disparity was noted in PFS between the two treatment groups. [ABSTRACT FROM AUTHOR]

Background: Hepatic inflammation in patients with hepatocellular carcinoma (HCC) remains unclear. This study aimed to construct a clinically expedient predictive model to grade hepatic inflammation in HCC patients. Methods: This is a two-center retrospective cohort study of HCC patients comprising Derivation cohort and External Validation cohort of 1201 and 505 patients, respectively. Variables of liver inflammation identified through uni- and multi-variate logistic regression analyses were incorporated into predictive nomograms and applied to Derivation cohort, subject to internal and external validation. Results: Liver fibrosis severity score, portal hypertension severity, and model for end-stage liver disease-sodium independently predicted hepatic inflammation grade. Performance for distinguishing G1 and non-G1 (≥ G2) patients was good with C-index of 0.810 and 0.817 in Derivation and External Validation cohort, respectively. The nomogram performed poorly to predict grade G2, G3 and G2 + G3, but performed well to predict G4. Conclusions: Our nomogram exhibited good performance for scaling hepatic inflammation (G1 and G4) in HCC, and could be employed as adjunctive diagnostic tools to guide HCC management strategy. [ABSTRACT FROM AUTHOR]

Background: Hepatic venous pressure gradient (HVPG) is considered the gold standard for diagnosing portal hypertension (PHT). Laparoscopic splenectomy plus esophagogastric devascularization (LSED) is an important surgery for treating PHT. However, the variation trend of HVPG after surgery is not clear. Moreover, whether HVPG can provide precise prognostic information for patients undergoing surgery remains to be further studied. This study aimed to investigate the independent prognostic value of HVPG in LSED. Methods: From January 2016 to March 2023, 135 patients with PHT underwent LSED at our hospital were retrospectively evaluated. We analyzed the correlations between clinical indicators and history of upper gastrointestinal bleeding (UGIB). Among them, 57 patients remeasured postoperative HVPG. We further investigated the postoperative alterations of HVPG and correlative factors, as well as the relationship between the HVPG and postoperative UGIB. Results: In this study, we found that 94 patients with preoperative UGIB (16.27 ± 5.73 mmHg) had a higher baseline HVPG than the other 41 patients without (14.02 ± 5.90 mmHg) (p = 0.04). The mean postoperative HVPG significantly decreased (-3.57 ± 8.09 mmHg, p = 0.001) compared to the baseline, and 66% of patients (38/57) experienced a decreased HVPG-response after surgery. The baseline HVPG and preoperative CTP class B were associated with the decreased HVPG-response (p<0.05). Additionally, patients with postoperative HVPG decreased>20% from baseline exhibited better recurrent hemorrhage-free survival rates than those without (log-rank, p = 0.013). Conclusion: We found that LSED led to a significantly decreased HVPG, and patients with postoperative HVPG decreased >20% obtained better UGIB-free survival benefits than those without. [ABSTRACT FROM AUTHOR]

Purpose: To compare clinical outcomes of transjugular intrahepatic portosystemic shunt (TIPS) created with the single covered-uncovered stent (Viatorr TIPS Endoprosthesis) versus covered stent (Fluency) versus a combination of covered and uncovered stent. Materials and methods: From May 2016 and July 2019, a total of 180 liver cirrhosis patients with recurrent variceal bleeding underwent TIPS creation with single covered-uncovered stent (n = 63) or covered stent (n = 41) or a covered and uncovered stent combination (n = 76). Shunt dysfunction, rebleeding, overt hepatic encephalopathy and mortality was estimated using the Kaplan–Meier method and compared with the log-rank test. Results: The difference of baseline characteristics among these three groups were not significant. The included patients had a median age of 51 years (IQR 43–61), and 101 (56.1%) were men. The 1-year and 2-year shunt dysfunction rates were 1.6% and 3.2% in the single covered-uncovered stent group, 7.3% and 7.3% in the covered stent group and 5.3% and 6.6% in the combination group, respectively. There was no significant difference among groups [Hazard Ratio (HR) (95%CI): 1 vs 2.29 (0.38 − 13.72) vs 2.10 (0.41 − 10.83); P = 0.913]. No significant differences in the incidence of all-cause rebleeding were observed between the groups at 1 year (Viatorr vs Fluency vs combination: 11.1% vs 17.1% vs 10.5%) as well as 2 years (15.9% vs 17.1% vs 11.8%), with the HR (95%CI) being 1 vs 1.27 (0.5—3.21) vs 0.74 (0.30–1.82); P = 0.475). The 1-year and 2-year incidence of overt hepatic encephalopathy were 30.2% and 30.2% in the single covered-uncovered stent group, 22.0% and 22.0% in the covered stent group and 25.0% and 25.0% in the combination group, respectively. However, there was no significant difference among these three groups (P = 0.402). In addition, there was no significant difference in the 1-year and 2-year mortality (6.3% and 7.9% vs. 4.9% and 9.8% vs. 6.6% and 9.2%, P = 0.606). Conclusion: No significant difference was observed among different stent groups. Fluency covered stent and the generic bare stent/Fluency covered stent was not an unreasonable alternative to the Viatorr stent for TIPS creation. [ABSTRACT FROM AUTHOR]

ABSTRACT Background and Aims Methods and Results Metabolic dysfunction‐associated steatotic liver disease (MASLD) is a heterogenous clinical and histopathological entity, where multiple metabolic co‐factors are intertwined with high interindividual variability. The impact and severity of each factor (including obesity and type 2 diabetes) define a systemic dysmetabolism that can lead to either advanced liver disease and its complication (including hepatocellular carcinoma and clinical events related to portal hypertension) or extrahepatic events: incident cardiovascular disease, chronic kidney disease and extrahepatic cancers. The balance between environmental factors and genetic susceptibility has unique implications in MASLD: the intermittent injury of metabolic co‐factors, their fluctuation over time and their specific management, are counterbalanced by the presence of gene variants that can significantly impact the disease at multiple levels. The I148M variant in the PNPLA3 gene is the most investigated genetic susceptibility that induces a more severe steatohepatitis, enhanced fibrogenesis and can shape the incidence of long‐term clinical events regardless of, or worsened by, other metabolic risk factors.In this review, we will summarise the updated evidence on the natural history of MASLD accounting for classical metabolic risk factors, the role of PNPLA3 in clinical sub‐phenotyping (e.g., ‘lean MASLD’), impact on disease severity and fibrosis progression, as well as its role for prognostication, alone or in combination with non‐invasive tools into polygenic risk scores. [ABSTRACT FROM AUTHOR]

ABSTRACT Background and Aims Methods Results Conclusions We sought to characterise the impact of GLP‐1RA on adverse liver outcomes (ALO) among patients with alcohol‐associated liver disease (ALD) and Type 2 diabetes mellitus (T2DM).Patients with T2DM newly diagnosed with ALD between 2013 and 2020 were identified using IBM MarketScan database and were categorised by GLP‐1RA exposure. Overlap propensity score weighting (OPSW) followed by Poisson regression models was used to analyse adjusted risk of ALO, a composite endpoint defined by first occurrence of hepatic decompensation (HD), portal hypertension (PH), hepatocellular carcinoma (HCC) or liver transplantation (LT) relative to GLP‐1RA.Among 14 730 patients, most individuals were male (n = 9752, 66.2%) with median age of 57 (IQR 52–61) years; 2.2% (n = 317) of patients had GLP‐1RA exposure. Overall, 32.0% (n = 4717) of patients experienced HD, 15.9% (n = 2345) had PH, 3.8% (n = 563) developed HCC, while 2.5% (n = 374) underwent transplantation. Non‐GLP‐1RA patients had higher incidence of HD (32.2% vs. 22.4%) and HCC (3.9% vs. 0.3%) versus patients taking GLP‐1RA (both p < 0.001); in contrast, there was no difference in incidence of PH (14.5% vs. 16.0%) and LT (1.3% vs. 2.6%) (both p > 0.05). After OPSW, overall incidence of ALO was lower in GLP‐1RA cohort (GLP‐1RA: 12.0%, 95%CI 9.0–16.0 vs. non‐GLP‐1RA: 21.0%, 95%CI 20.0–22.0) with an absolute incidence risk reduction of 9.0% (95%CI 3.0%–15.0%) associated with GLP‐1RA. GLP‐1RA was most strongly associated with lower likelihood of HD with reduced adjusted incidence rate of 0.56 (95%CI 0.36–0.86) relative to non‐GLP‐1RA individuals.GLP‐1RA may have a hepatoprotective impact among patients with ALD and T2DM. [ABSTRACT FROM AUTHOR]

Summary: Background and Aims: Non‐selective beta‐blockers (NSBB) are a well‐established treatment in patients with clinically significant portal hypertension. However, their potential role after insertion of a transjugular intrahepatic portosystemic shunt (TIPS) still needs to be determined. Of note, recent studies suggested that favourable anti‐inflammatory effects of NSBB might be independent from pressure reduction. This study aimed to evaluate whether NSBB‐treatment is associated with amelioration of systemic inflammation (SI), hepatic decompensation and survival after TIPS‐insertion. Methods: In a retrospective study comprising 305 consecutive patients, we investigated the impact of NSBB‐intake at TIPS‐placement on periinterventional cirrhosis‐associated complications and continued NSBB‐treatment after discharge on complications including hepatic decompensation and mortality during 1‐year follow‐up, employing multivariable competing‐risk‐analyses. In a prospective cohort including 45 patients, we performed a comprehensive analysis of SI analysing 48 soluble inflammatory markers (SIMs) at baseline plus 3 and 6 months after TIPS‐insertion. Results: Overall, 175 (57.4%) patients received NSBB‐therapy prior to TIPS‐insertion; upon discharge, this decreased to 131 (22.9%), with 36 (27.5%) discontinuing NSBB within 1‐year follow‐up. Neither NSBB‐therapy at TIPS‐insertion nor treatment‐continuation after discharge were associated with lower risks for hepatic decompensation, individual cirrhosis‐associated complications or mortality neither in the periinterventional period nor during follow‐up. Similarly, in the prospective cohort NSBB‐intake was not linked to lower levels or a more prominent change of WBC, CRP or any other SIM at any of the investigated time points. Conclusion: NSBB‐therapy at the time of TIPS‐insertion and its (dis‐)continuation afterwards seems to have no significant impact on SI, development of hepatic decompensation and survival. [ABSTRACT FROM AUTHOR]

Hepatitis B and Hepatitis C are viral causes of Hepatitis that lead to significant worldwide mortality and morbidity through the sequelae of fibrosis and hepatocellular carcinoma. In this review, we have summarized recent studies that have examined the effects of antiviral therapy on the regression of fibrosis and the reduction in mortalities associated with the viruses. Antiviral therapy significantly decreases mortality and induces the regression of fibrosis. [ABSTRACT FROM AUTHOR]

Key Clinical Message: The occurrence of terlipressin‐induced skin necrosis in cirrhotic patients is a rare but serious adverse event that warrants further investigation. Clinicians should be aware of this potential complication in cirrhotic patients receiving terlipressin therapy and closely monitor for any signs of skin necrosis. Early recognition and prompt intervention are crucial in preventing further complications and improving patient outcomes. Further research is needed to better understand the risk factors associated with terlipressin‐induced skin necrosis and to develop effective preventive strategies. Overall, healthcare providers should exercise caution when prescribing terlipressin to cirrhotic patients, weighing the potential benefits against the risks of this rare but significant adverse event. Terlipressin is commonly used to manage conditions related to portal hypertension, such as hepatorenal syndrome and esophageal variceal bleeding. Despite its therapeutic benefits, terlipressin can rarely lead to severe ischemic complications involving the skin vasculature, known as terlipressin‐induced skin necrosis. We present a 50‐year‐old male with cirrhosis and acute variceal bleeding who developed skin necrosis following terlipressin administration. We performed a comprehensive review of the literature by analyzing 18 case reports/case series comprising 22 cirrhotic patients with terlipressin‐induced skin necrosis. Among these individuals, we found a mean age of 51 years with a male predominance (78%). Further analysis showed that the onset of skin necrosis ranged from 2 to 5 days post‐terlipressin initiation, with bolus administration being predominant (85.7%). The underlying pathophysiological mechanisms of terlipressin‐induced skin ischemia are still elusive but primarily attributed to the vasoconstrictive and thrombogenic effects. Management involves terlipressin discontinuation and supportive care. Physicians should be aware of this potential complication in patients receiving terlipressin and closely observe for any signs of skin rash. [ABSTRACT FROM AUTHOR]

Background: Abnormal glycosylation is associated with tumors. The clinical value of serum glycans in assessing progression of hepatocellular carcinoma (HCC) patients remains a challenge. Methods: A study dynamically comparing levels of fifteen lectin‐specific glycans between preoperative and postoperative serum of 65 HCC patients was conducted via lectin biochip technology. Multivariable logistic regression analysis was used to address associations between serum glycan levels and clinicopathological characteristics. Kaplan–Meier analysis was used to evaluate the impacts of serum glycan levels on overall survival (OS) and progression‐free survival (PFS) of the HCC patients. Results: HCC patients presented significantly higher levels of the lectin‐specific glycans in preoperative serum than disease‐free individuals (p < 0.001 − p = 0.029), except ConA. The glycans in preoperative sera were significantly related to tumor size, pTNM, metastasis, BCLC stage, portal hypertension (PHT), and platelet count (PLT), respectively (p < 0.05). Multivariate logistic analyses indicated that tumor size and pTNM independently impact on glycan‐specific lectins either LTL, UEA‐I, VVL, NPL, WGA, PNA, MAL‐I, SNA, or PHA‐L (p = 0.003 − p = 0.044); BCLC stage and PLT were independent factors influencing the serum glycans recognizable DSA (p = 0.024) and SNA (p = 0.050), respectively. Surgical excision of tumor mass significantly reduced glycan levels in sera. Tumor differentiation, albumin, and ABO type significantly revealed independent influence on glycan‐specific lectins, such as RCA‐I (p = 0.024), VVL (p = 0.024), and Con A (p = 0.026) in the postoperative serum. HCC patients with high levels of VVL‐binding glycans significantly benefited from a longer OS time (p = 0.016, HR: 0.460, 95% CI: 0.237–0.892) and a better PFS time (p = 0.004; HR: 0.435, 95% CI: 0.237–0.799), respectively. Conclusion: Serum glycans could reflect surgical outcomes in at‐risk patients and become valuable biomarkers in evaluating the progression of HCC patients. [ABSTRACT FROM AUTHOR]

Simple Summary: Hepatocellular carcinoma (HCC) associated with portal vein thrombosis (PVT) represents an advanced stage of the tumor, with a subsequently poor prognosis and reduced therapeutic perspectives. These patients could present severe complications such as ascites, metastases, an increase in portal hypertension and potentially fatal gastrointestinal bleeding. The intricate molecular patterns at the basis of the development of TVP could also represent possible biomarkers in the early detection of patients at high risk of PVT. Hepatocellular carcinoma (HCC) represents the sixth most diagnosed cancer worldwide and is the second leading cause of cancer-related death in the world. The association of HCC and portal vein thrombosis (PVT) represents an advanced stage of the tumor. PVT has a prevalence of about 25–50% in HCC, determining poor prognosis and a remarkable reduction in therapeutic perspectives in these patients, leading to severe complications such as ascites, metastasis, an increase in portal hypertension and potentially fatal gastrointestinal bleeding. The aim of this review is to evaluate the molecular mechanisms that are at the basis of PVT development, trying to evaluate possible strategies in the early detection of patients at high risk of PVT. [ABSTRACT FROM AUTHOR]

INTRODUCTION: The 2021 American Association for the Study of Liver Disease (AASLD) Practice Guidance recommends albumin infusion when removing ≥5 L of ascites to prevent post-paracentesis circulatory dysfunction. However, the optimal criteria and scenarios for initiating albumin infusion subsequent to therapeutic paracentesis (TP) have been subject to limited scientific inquiry. METHODS: Weconducted a retrospective cohort study at aUSacademic healthcare center. Participants received elective, outpatient TP between July 2019 andDecember 2022. Patientswith spontaneous bacterial peritonitis, post-TP clinical adjustments, and/or hospitalization were excluded. The institution strictly followed the AASLD Guidance. We used a sharp regression discontinuity (RD) design to estimate the effect of albumin infusion at the AASLD Guidance-recommended cutoff of 5 L on serum creatinine and sodium trajectory after TP. RESULTS: Over the study period, 1,457 elective TPs were performed on 235 unique patients. Albumin infusion at the threshold of 5 L of ascites removal reduced serum creatinine levels by 0.046 mg/dL/d (95% confidence interval 0.003-0.116, P 5 0.037) and increased serum sodium levels by 0.35 mEq/L/d (95%confidence interval 0.15-0.55, P 5 0.001) compared with those who did not receive albumin infusion. The RD plots indicated worsened serum creatine/sodium levels after draining 3 L of fluid, approaching levels similar to or worse than with albumin infusion at 5 L or more. DISCUSSION: OurRDmodels supported the 2021 AASLD Guidance with robust estimation of causal effect sizes at the cutoff level of 5 L. Nevertheless, the findings also highlight the need to further evaluate the efficacy of albumin infusion in patients who undergo elective TP and have 3-5 L of ascites removed. [ABSTRACT FROM AUTHOR]

Background and Aims: Adaptive immunity is gaining a significant role in progression of metabolic dysfunction‐associated steatotic liver disease (MASLD). B‐cell activity can be assessed by serum‐free light chains (sFLCs) k and λ levels. The objective of the present investigation is to examine the utility of sFLCs as non‐invasive biomarkers for the stratification of MASLD. Methods: We enrolled a consecutive cohort from an outpatient liver unit. Diagnosis of metabolic dysfunction‐associated steatohepatitis (MASH) was made with liver biopsy according to current guidelines. Compensated advanced chronic liver disease (cACLD) and clinically significant portal hypertension (CSPH) were defined according to Baveno VII criteria. sFLCs were measured by turbidimetry using an immunoassay. Results: We evaluated 254 patients, 162/254 (63.8%) were male. Median age was 54 years old, and the median body mass index was 28.4 kg/m2. A total of 157/254 (61.8%) subjects underwent liver biopsy: 88 had histological diagnosis of MASH, 89 were considered as simple metabolic dysfunction‐associated steatotic liver (MASL) and 77/254 (30.3%) patients with compensated metabolic dysfunction‐associated cirrhosis. By using Baveno VII criteria, 101/254 (39.7%) patients had cACLD; among them, 45/101 (44.5%) had CSPH. Patients with cACLD showed higher sFLC levels compared with patients without cACLD (p <.01), and patients with CSPH showed higher sFLC levels than patients without CSPH (p <.01). At multivariable analysis, sFLCs were associated with cACLD (p <.05) independently from γ‐globulins and other known dysmetabolic risk factors. κFLC was associated with CSPH (p <.05) independently from γ‐globulins and other known dysmetabolic risk factors. Conclusion: sFLCs could be a simple biomarker for stratification of cACLD in MASLD patients. [ABSTRACT FROM AUTHOR]

Background Around 5% of patients with cirrhosis of the liver develop hepatic hydrothorax (HH). For patients with refractory HH (RHH), transjugular intrahepatic portosystemic shunt (TIPS) has been investigated in small studies. Hence, the present meta-analysis aimed to summarize the current data on the outcome of TIPS in patients with RHH. Methods From inception through June 2023, MEDLINE, Embase, and Scopus were searched for studies analyzing the outcome of TIPS in RHH. Clinical response, adverse events (AEs), mortality, and shunt dysfunction were the primary outcomes assessed. The event rates with their 95% confidence interval were calculated using a random-effects model. Results A total of 12 studies (n = 466) were included in the final analysis. The pooled complete and partial response rates were 47.2% (35.8–58.5%) and 25.5% (16.7–34.3%), respectively. The pooled incidences of serious AEs and post-TIPS liver failure after TIPS in RHH were 5.6% (2.1–9.0%) and 7.6% (3.1–12.1%), respectively. The pooled incidences of overall hepatic encephalopathy (HE) and severe HE nonresponsive to standard treatment after TIPS in RHH were 33.2% (20.0–46.4%) and 3.6% (0.4–6.8%), respectively. The pooled 1-month and 1-year mortality rates were 14.0% (8.3–19.6%) and 42.0% (33.5–50.4%), respectively. The pooled incidence of shunt dysfunction after TIPS in RHH was 24.2% (16.3–32.2%). Conclusion RHH has a modest response to TIPS in patients with cirrhosis, with only half having a complete response. Further studies are required to ascertain whether early TIPS can improve the outcome of patients with cirrhosis and HH. [ABSTRACT FROM AUTHOR]

Background and aims: The placement of Transjugular intrahepatic portosystemic shunt (TIPS) results in a sudden increase in central circulating blood volume, which requires proper regulation of the cardiovascular system. We aimed to investigate the impact of TIPS on cirrhotic cardiomyopathy (CCM). Method: A consecutive case series of patients with cirrhosis who underwent TIPS were evaluated by echocardiography and pressure measurements before, immediately after TIPS and 2–4 days later (delayed). Furthermore, all patients underwent a one-year follow-up. Results: In this study, 107 patients were enrolled, 38 (35.5%) with CCM. Echocardiography revealed an increase in postoperative left ventricular filling pressure accompanied by an elevation in left ventricular ejection fraction (LVEF). However, patients in the CCM group exhibited lower LVEF and mean arterial pressure (MAP) compared to the non-CCM group. Post-TIPS, CCM patients showed increased right atrium pressure (RAP) that normalized within 2–4 days, whereas non-CCM patients had lower RAP than baseline. Compared to patient without CCM, CCM patients revealed lower immediate (16.7 ± 4.4 vs. 18.9 ± 4.8, p = 0.022) and delayed 15.9 ± 3.7 vs. 17.7 ± 5.3, p = 0.044) portal vein pressures (PVP) and portal pressure gradients (PPG) (7.7 ± 3.4 vs. 9.2 ± 3.6, p = 0.032 and 10.1 ± 3.1 vs. 12.3 ± 4.9, p = 0.013). The 1-year mortality rates were 13.2% for CCM patients and 4.3% for non-CCM patients (log-rank test, p = 0.093), with MELD score, and preoperative RAP significantly associated with the mortality. Conclusion: Cirrhotic patients with CCM exhibit lower PVP and PPG immediately after TIPS and 2–4 days later, without significantly impacting one-year survival outcomes. [ABSTRACT FROM AUTHOR]

Objective: Portal hypertension leads to hepatic artery dilatation and a higher risk of bleeding. We tried to identify the bleeding risk after gastroesophageal varices (GOV) treatment using hepatic artery diameter of contrast-enhanced CT. Methods: Retrospective retrieval of 258 patients with cirrhosis who underwent contrast-enhanced CT from January 2022 to May 2023 and endoscopy within one month thereafter at Hainan Affiliated Hospital of Hainan Medical University. Cirrhotic patients before GOV treatment were used as the test cohort (n = 199), and cirrhotic patients after GOV treatment were used as the validation cohort (n = 59). The grading and bleeding risk was classified according to the endoscopic findings. Arterial-phase images of contrast-enhanced CT were used for coronal reconstruction, and the midpoint diameter of the hepatic artery was measured on coronal images. The optimal cutoff value for identifying bleeding risk was analyzed and calculated in the test cohort, and its diagnostic performance was evaluated in the validation cohort. Results: In the test cohort, hepatic artery diameters were significantly higher in high-risk GOV than in low-risk GOV [4.69 (4.31, 5.56) vs. 3.10 (2.59, 3.77), P < 0.001]. With a hepatic artery diameter cutoff value of 4.06 mm, the optimal area under the operating characteristic curve was 0.940 (95% confidence interval: 0.908–0.972), with a sensitivity of 0.887, a specificity of 0.892, a positive predictive value of 0.904, and a negative predictive value of 0.874 for identifying bleeding risk in the test cohort, while in the validation cohort, the sensitivity was 0.885, specificity was 0.939, positive predictive value was 0.920, and negative predictive value was 0.912. Conclusion: Hepatic artery diameter has high diagnostic performance in identifying bleeding risk after GOV treatment. [ABSTRACT FROM AUTHOR]

Portal hypertension (PH) is one of the most frequent complications of chronic liver disease. The peripheral 5-hydroxytryptamine (5-HT) level was increased in cirrhotic patients. We aimed to elucidate the function and mechanism of 5-HT receptor 1A (HTR1A) in the portal vein (PV) on PH. PH models were induced by thioacetamide injection, bile duct ligation, or partial PV ligation. HTR1A expression was detected using real-time polymerase chain reaction, in situ hybridization, and immunofluorescence staining. In situ intraportal infusion was used to assess the effects of 5-HT, the HTR1A agonist 8-OH-DPAT, and the HTR1A antagonist WAY-100635 on portal pressure (PP). Htr1a -knockout (Htr1a –/–) rats and vascular smooth muscle cell (VSMC)–specific Htr1a -knockout (Htr1a ΔVSMC) mice were used to confirm the regulatory role of HTR1A on PP. HTR1A expression was significantly increased in the hypertensive PV of PH model rats and cirrhotic patients. Additionally, 8-OH-DPAT increased, but WAY-100635 decreased, the PP in rats without affecting liver fibrosis and systemic hemodynamics. Furthermore, 5-HT or 8-OH-DPAT directly induced the contraction of isolated PVs. Genetic deletion of Htr1a in rats and VSMC-specific Htr1a knockout in mice prevented the development of PH. Moreover, 5-HT triggered adenosine 3′,5′-cyclic monophosphate pathway–mediated PV smooth muscle cell contraction via HTR1A in the PV. We also confirmed alverine as an HTR1A antagonist and demonstrated its capacity to decrease PP in rats with thioacetamide-, bile duct ligation–, and partial PV ligation–induced PH. Our findings reveal that 5-HT promotes PH by inducing the contraction of the PV and identify HTR1A as a promising therapeutic target for attenuating PH. As an HTR1A antagonist, alverine is expected to become a candidate for clinical PH treatment. HTR1A antagonist, such as alverine, decreases portal hypertension in preclinical animals by targeting the portal vein and is expected to become a candidate for the clinical treatment of portal hypertension. [ABSTRACT FROM AUTHOR]

Oxaliplatin (OX) has been described as a potential etiologic agent for porto-sinusoidal vascular disorder (PSVD). Our aim was to describe the natural history of PSVD due to OX in colon cancer (CRC) and identify risk factors for its development. We made a multicenter retrospective case-control (ratio 1:3) study with patients diagnosed of PSVD-OX. Baseline data, end of treatment, years of follow-up and diagnosis of PSVD were collected and compared to controls (without PSVD). Besides, 16 different SNPs were selected from bibliography and analyzed by genotyping in the case group to identify potential genetic risk factors. 41 cases were identified, with a median time to PSVD diagnosis after the end of OX of 34 months. Spleen diameter was the strongest predictor of PSVD during treatment (OR 43.94 (14.48–133.336); p < 0.0001). Additionally, thrombocytopenia (<150 × 10^9) at one year was a significant disease risk marker (OR 9.35; 95% CI: 3.71–23.58; p = 0.001). We could not establish any significant association between the selected SNPs and PSVD diagnosis. The increase of spleen diameter is the strongest predictor of PSVD in patients treated with OX for CRC. These patients could be candidates for a specific follow-up of portal hypertension-related complications. [ABSTRACT FROM AUTHOR]

Although upper gastrointestinal endoscopy (EGD) remains the gold standard for detecting varices in cirrhosis, the Baveno VI criteria proposed a combination of transient elastography and platelet count that could rule out high-risk varices, therefore sparing the need for an endoscopy, with significant potential cost savings. We performed a cost-effectiveness analysis of the Baveno VI criteria compared with EGD in the diagnosis of high-risk varices in cirrhosis. We built an analytical decision model to estimate the cost and benefits of using the Baveno VI criteria compared with EGD in patients with Child-Pugh A cirrhosis. The analysis was performed from the UK National Health Service perspective, over 1, 5, and 20 years. A Markov model was populated with data from published evidence. Outcomes were measured in terms of quality-adjusted life years (QALYs) and avoided deaths. The analyses were repeated for Canada and Spain, using relevant cost inputs. The Baveno VI criteria were cost effective compared with endoscopy in all analyses. For 1000 patients, they produced 0.16 additional QALYs at an incremental cost of £326 ($443.41) over 5 years, resulting in an incremental cost of £2081 ($2830) per additional QALY gained. The incremental net monetary benefit of Baveno VI compared with EGD was £2808 ($3819) over 5 years per patient. Baveno VI criteria also were cost effective in Canada and Spain. Deterministic and probabilistic sensitivity analysis supported these findings. The findings demonstrate that the Baveno VI criteria are cost effective, suggesting that they should be considered for widespread implementation on the basis of safety, appropriateness, and economic grounds. [Display omitted] [ABSTRACT FROM AUTHOR]

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Objective: This study aims to evaluate the differences between The balloon catheter method and End-hole Catheter Method in measuring hepatic venous pressure gradient (HVPG) among cirrhosis patients. Methods: From October 2017 to January 2024, patients who underwent HVPG measurements using both methods were consecutively included. HVPGs obtained from both methods were compared with the portal vein pressure gradient (PPG) obtained via transjugular intrahepatic portosystemic shunt (TIPS) using paired comparisons. Additionally, the consistency and predictive ability for bleeding risk of the two methods, as well as the impact of intrahepatic veno-venous shunt (IHVS), were analyzed. Results: The study enrolled 145 patients, each of whom had HVPG measured by both methods. PPG was measured in 61 patients. There was a statistically significant difference between the PPGs and HVPGs measured by both the balloon catheter method and the end-hole catheter method (P < 0.001), with the HVPG mean values obtained by the end-hole catheter method being closer to the PPGs. In the non-IHVS group, no significant statistical difference was found between the two methods (P = 0.071). In contrast, the IHVS group showed a significant difference (P < 0.001), with a mean difference of 2.98 ± 4.03 mmHg. When IHVS was absent, the measurement results from the end-hole catheter method and the balloon catheter method were found to be highly correlated. The end-hole catheter method has a higher screening capability for patients at risk of bleeding compared to the balloon catheter method (75.90% vs. 72.86%). Conclusion: HVPG measurements using either the balloon catheter method or end-hole catheter method showed significant difference with the PPG. The end-hole catheter method has a higher screening capability for patients at risk of bleeding, and IHVS could lead to lower HVPG measurements with The balloon catheter method. [ABSTRACT FROM AUTHOR]

Background: The accuracy of administrative codes to capture patients with both primary biliary cholangitis (PBC) and cirrhosis could be challenging because of the potential for incorrect coding due to the old nomenclature "Primary Biliary Cirrhosis." Therefore, the aim of this study was to examine the positive predictive value (PPV) of International Classification of Diseases (ICD) codes for PBC and cirrhosis. Methods: This was a retrospective cohort study using data from the VA Corporate Data Warehouse. Eligibility criteria included adult patients diagnosed to have PBC and cirrhosis based on one inpatient or two outpatient ICD 9 or 10 codes, and were validated against chart review of each participant. Results: We identified 1408 patients who were found to have ICD codes for both cirrhosis and PBC. The ICD 9/10 codes for PBC and cirrhosis had a PPV of 0.75 (95% CI 0.73–0.75) for cirrhosis, 0.75 for PBC (95% CI 0.73–0.78), and 0.52 (0.50–0.55) for PBC and cirrhosis. When portal hypertension was combined with ICD 9/10 codes, the PPV of cirrhosis improved to 0.92 (0.90–0.94), and that of PBC cirrhosis improved to 0.64 (0.60–0.67). By combining ICD 9/10 codes for portal hypertension and receipt of ursodeoxycholic acid (UDCA), the PPV for cirrhosis improved to 0.91 (0.88–0.94), PBC increased to 0.78 (0.74–0.82), and that for PBC cirrhosis to 0.69 (0.65–0.74). Conclusions: In a large national cohort, the use of ICD 9/10 codes had modest reliability for identifying participants with PBC and cirrhosis. The PPV for cirrhosis can be improved by incorporating ICD 9/10 codes for portal hypertension with receipt of UDCA. [ABSTRACT FROM AUTHOR]