Background/Objectives: Hepatic encephalopathy (HE) is characterized by hyperammonemia, neuroinflammation, oxidative stress, and blood–brain barrier (BBB) dysfunction, with brain endothelial cells being highly vulnerable to ammonia-induced damage. Adiponectin is a cytoprotective adipokine that may enhance endothelial resilience; however, its specific role under hyperammonemic conditions remains unclear. This study aims to investigate the protective effects of adiponectin on brain endothelial function and BBB integrity. Methods: In vivo, male C57BL/6J mice underwent bile duct ligation (BDL) surgery and received daily intraperitoneal adiponectin injections (10 μg/kg/day) for 6 days, starting 5 days post-surgery. On day 11, brain tissues and serum were collected for molecular and cytokine analyses. In vitro, mouse brain endothelial cells (bEnd.3) were pretreated with adiponectin before exposure to ammonia. Assays for tight junction preservation, mitochondrial membrane potential, reactive oxygen species (ROS) generation, and total RNA sequencing were performed. Results: In BDL mice, adiponectin increased the expression of the tight junction protein claudin-5 and synaptic marker PSD95 across the cortex, hippocampus, and striatum, while reducing pro-oxidant (Cyp2e1, Cyp4a1) and apoptotic (Caspase-9) markers. In vitro, adiponectin pretreatment maintained tight junction proteins, suppressed inflammatory markers, restored mitochondrial membrane potential, and decreased ROS generation in ammonia-exposed bEnd.3 cells. Transcriptomic profiling revealed that adiponectin modulates stress-related gene expression under hyperammonemic conditions. Conclusions: Adiponectin enhances cellular stress resistance and maintains BBB structural integrity under ammonia-induced toxicity. These findings suggest that adiponectin serves as a promising therapeutic target for mitigating neurovascular unit dysfunction in hepatic encephalopathy.

Background: Liver cirrhosis is a systemic disease characterized by progressive hepatic dysfunction and frequent decompensation events. Conventional prognostic models such as the Child–Turcotte–Pugh (CTP) and Model for End-stage Liver Disease (MELD) scores primarily reflect liver-specific severity and may not fully capture the multidimensional vulnerability of patients with cirrhosis. Frailty, a syndrome reflecting reduced physiological reserve, has emerged as a potential prognostic marker in this population. Methods: In this prospective single-center cohort study, 134 patients with liver cirrhosis were enrolled between March and October 2021 and followed at three-month intervals. Frailty was assessed at baseline using the Fried Frailty Index (FFI). Patients were categorized as fit/prefrail or frail. The primary endpoints were cirrhosis-related complications, unplanned hospitalizations, and all-cause mortality. Associations between frailty, its individual components, and clinical outcomes were evaluated. Results: Frailty was present in 41% of patients. Frail patients were older and had higher MELD and CTP scores. During follow-up, frailty was significantly associated with higher rates of ascites (p < 0.001), hepatic encephalopathy (p < 0.001), hepatorenal syndrome (p < 0.001), spontaneous bacterial peritonitis (p = 0.01), and unplanned hospitalizations (p < 0.001). Mortality occurred in 22% of frail patients compared with 3.8% in non-frail patients (p < 0.001). Each frailty component, including reduced grip strength, slow gait speed, low physical activity, exhaustion, and unintentional weight loss, was independently associated with adverse outcomes. Conclusions: Frailty, as assessed by the Fried Frailty Index, is a strong predictor of complications, hospitalization, and mortality in patients with liver cirrhosis. Incorporating frailty assessment into routine clinical practice may improve risk stratification and guide long-term management strategies.

Abemaciclib, a cyclin-dependent kinase 4/6 inhibitor, is a standard treatment for hormone receptor-positive and HER2-negative breast cancer. However, liver dysfunction induced by abemaciclib is a significant clinical issue. We report three cases of drug induced liver injury caused by abemaciclib with characteristic liver atrophy. Case 1: A woman in her seventies developed acute liver failure 2months after initiation of letrozole and abemaciclib for breast cancer and bone metastases. A contrast-enhanced CT (CECT) scan revealed liver atrophy accompanied by Chilaiditi syndrome. Despite steroid pulse therapy, she progressed to coma. Her liver failure improved, but she died due to worsening of the underlying disease. Case 2: A woman in her seventies developed liver dysfunction 2months after initiation of anastrozole and abemaciclib to prevent recurrence. A CECT scan revealed liver atrophy and Chilaiditi syndrome. After admission, she progressed to acute liver failure and coma, and steroid pulse therapy was initiated. Hepatic encephalopathy improved with conservative treatment, and liver failure resolved with continued steroid administration. Case 3: A woman in her fifties. After breast cancer surgery, tamoxifen and abemaciclib were started as adjuvant therapy. Blood tests revealed liver dysfunction 2months later. A CECT scan revealed liver atrophy and Chilaiditi syndrome, which improved with liver support therapy alone without progressing to liver failure. This report is the first highlighting the imaging characteristics of rapid-onset hepatic atrophy associated with abemaciclib-induced liver injury. These findings may provide useful insights for distinguishing abemaciclib-induced liver injury from other etiologies.

Left versus Right Portal Vein Transjugular Intrahepatic Portosystemic Shunt (TIPS) Creation in Patients with Grade 1 Hepatic Encephalopathy.

Research progress of traditional Chinese medicine syndrome differentiation in prevention and treatment of hepatic encephalopathy

Validation of AMMON-OHE Model for Predicting Overt Hepatic Encephalopathy after Transjugular Intrahepatic Portosystemic Shunt.

This editorial provides commentary on the study by Wu et al , which investigates a novel intervention for a challenging clinical scenario: Transjugular intrahepatic portosystemic shunt (TIPS) placement with the assistance of surgery in patients with cavernous transformation of the portal vein. The authors compared surgically assisted TIPS (SATIPS) in 54 patients to endoscopic sclerotherapy in 53 patients. While 3-month survival rates were similar (94.4% vs 92.5%), a significant difference emerged at 6 months, with survival rates of 94.4% for SATIPS vs 73.6% for endoscope sclerotherapy. The SATIPS group also demonstrated significantly lower incidences of liver failure, esophagogastric bleeding, and hepatic encephalopathy at 6 months. However, the SATIPS procedure was not without risk, as four patients experienced major complications, including intraoperative hemorrhage. The study concludes that SATIPS is an effective alternative for cavernous transformation of the portal vein patients with esophagogastric bleeding, but its findings must be interpreted in light of its limitations. This research represents a significant contribution to the field.

Acute-on-chronic liver failure (ACLF) is a swiftly deteriorating condition characterized by profound systemic inflammation and failure of multiple organ systems, leading to high early mortality. There remains a critical need for more effective biomarkers to facilitate timely and accurate risk assessment. Recent findings by Zhu and Yan demonstrated that evaluating temporal changes in the C-reactive protein to albumin ratio (CAR), especially the 7-day variation, offers superior prediction of 28-day mortality compared with single baseline measurements. By integrating the 7-day variation of CAR with the model for end-stage liver disease sodium score and the grade of hepatic encephalopathy, the Chinese Group on Study of Severe Hepatitis B (COSSH)-CAR model was created, which surpassed traditional prognostic tools such as the Child-Pugh, model for end-stage liver disease, and COSSH-ACLF. This comment highlights the importance of using dynamic biomarker trajectories rather than static values for prognostic evaluation. CAR is biologically compelling because it captures both the inflammatory burden and the patient’s nutritional/physiological reserve. While the COSSH-CAR model is promising and based on routinely obtainable laboratory data, its widespread adoption will depend on validation in larger, diverse, and non-hepatitis B virus-related cohorts. Future work should examine CAR kinetics in prospective and interventional studies and consider how they may support individualized management strategies. Collectively, these observations suggest that the CAR could represent an important addition to current ACLF prognostic frameworks.

Intentional or accidental intoxication is a common inciting cause of acute liver failure, which manifests as a severe clinical consequence of abrupt hepatocyte injury in the patient without any known underlying liver diseases (within 26weeks of illness duration). In addition, it often progresses to a lethal outcome. Thinner intoxication is a rare but non-negligible etiology of acute liver failure. Considering the potential neurotoxicity, myotoxicity, hepatotoxicity, nephrotoxicity, and cardiopulmonary toxicity of thinner, as well as the lack of effective specific reversal agents or antidotes, early and continuous supportive care by an artificial liver support system (Liu etal. in Artif Organs 49:762-777, 2025)-defined here as the integrated use of double plasma molecular adsorption system, plasma exchange, and continuous veno-venous hemofiltration-is conducive to remove thinner and ammonia from the blood, improve hepatic encephalopathy, replace lost liver function, alleviate thinner intoxication-induced multiorgan damage, restore hemodynamics and internal environment stability, modulate immune response, and maintain cytokine homeostasis. In this study, we presented the first reported case of acute liver failure induced by acute severe thinner intoxication in a Han Chinese adult, who was successfully rescued through the use of a double plasma molecular adsorption system, plasma exchange, and continuous veno-venous hemofiltration. A 46-year-old Asian man was admitted to the Department of Critical Care Medicine owing to nausea and vomiting for 4 days, abdominal pain and melena for 2 days, and disturbance of consciousness for 1 day after accidentally ingesting a mouthful of thinner (exact volume unknown) at a construction site. In the intensive care unit, the patient underwent orotracheal intubation, invasive mechanical ventilation, appropriate analgesia and sedation, infusion of blood products and hemostatic drugs, phlegm-removing, and correction of internal environment disorder. Subsequently, the patient received four double plasma molecular adsorption system treatments, two plasma exchanges (a total of 6000mL of fresh frozen plasma), and 79hours of continuous veno-venous hemofiltration during hospitalization. On the 8th day after admission, invasive mechanical ventilation was withdrawn, but the patient's consciousness remained unclear. On the 36th day after admission, the patient was in remission and discharged. However, his liver function and coagulation parameters did not revert to normal. Thinner intoxication is a rare but non-negligible etiology of acute liver failure. To the best of our knowledge, our case is the first attempt to combine double plasma molecular adsorption system treatment, plasma exchange, and continuous veno-venous hemofiltration for acute liver failure as a clinical manifestation of thinner intoxication. The combination of different therapeutic modalities of an artificial liver support system can compensate for the individual shortcomings and maximize their respective advantages, which requires a multidisciplinary team to determine their clinical application in suitable patients.

Malnutrition is common among patients with decompensated liver cirrhosis and linked to poor prognosis. Guidelines recommend intensified nutrition support e.g. parenteral nutrition, but evidence regarding safety and effectiveness is scarce. We aimed to investigate the impact of nutrition support, specifically parenteral nutrition, on mortality (primary end point) and on cirrhosis-specific complications (secondary end points) in patients with advanced liver cirrhosis. Consecutive malnourished patients with decompensated cirrhosis treated at our center between 2013 and 2018 were investigated. Fifty-three patients received specialized nutrition support; 33 received parenteral nutrition. The specialized nutrition support group (cohort 1) and the home parenteral nutrition group (cohort 2) were compared with patients without specific dietary support (standard-of-care group) after 1:1 and 1:2 propensity score matching, respectively. Mortality, hepatic encephalopathy, infections, and rehospitalization were investigated within 90 days. Median baseline Model for End-Stage Liver Disease score (possible range 6-40 points) was 18 in cohort 1 and 16 in cohort 2. No impact of specialized nutrition support on the clinical outcome was detected. Between cohort 2 and standard of care, no differences in mortality and rehospitalization were observed. Whereas parenteral nutrition was associated with increased risk for bloodstream infections (hazard ratio [HR] = 21.3; P = 0.004), overall incidence of bacterial infections was comparable between groups (HR = 0.82; P = 0.45). Of note, the likelihood for hepatic encephalopathy was significantly reduced in cohort 2 in the multivariable competing risk model (HR = 0.28; P = 0.03). Home parenteral nutrition seems safe overall and may ameliorate the risk for hepatic encephalopathy in candidates for liver transplant.

Cirrhosis is a chronic illness with high morbidity, marked by persistent physical and psychological symptoms that impact patients and their caregivers. Longitudinal data on symptom trajectories and their determinants, particularly hepatic encephalopathy (HE), are limited. We conducted a secondary analysis of PAL-LIVER, a 19-site cluster-randomized trial comparing hepatologist-led and consultative palliative care for patients with decompensated cirrhosis and/or hepatocellular carcinoma. Patients and caregivers completed assessments at baseline and multiple intervals up to 12 months (patients: modified ESAS-13, PHQ-9, Distress Thermometer; caregivers: Zarit Burden Interview-12). Latent class growth analysis identified subgroups with persistently high or low burden for each symptom. Multivariable models evaluated associations between HE and symptom/caregiver burden, adjusting for demographics, disease severity, and comorbidities. 935 patients were enrolled, 823 with HE information, 368 of whom had HE at baseline. Symptom burden trajectories remained stable over 12 months. HE was the primary independent predictor of high overall symptom burden (ESAS OR 1.83, 95%CI 1.38-2.41), depression (PHQ-9 OR 1.93, 95%CI 1.44-2.60), and greater caregiver burden (ZBI-12 OR 1.53, 95%CI 1.02-2.30). Alcohol-related liver disease and female sex were also associated with higher symptom burden. Caregiver burden remained generally low and stable. Symptom burden in cirrhosis is generally stable but remain high among certain subgroups, especially those with HE. HE is the strongest and most consistent determinant of physical, psychological, and caregiver burden in cirrhosis. These findings highlight the urgent need for novel, HE-targeted interventions and comprehensive symptom management strategies particularly for women and those with alcohol-related liver disease.

Minimal hepatic encephalopathy (MHE) represents a reversible, early-stage form of hepatic encephalopathy (HE). Although probiotics have been extensively studied for MHE management, direct comparative evidence against standard lactulose therapy remains limited. This meta-analysis aimed to quantitatively evaluate the relative efficacy and safety of probiotics versus lactulose in cirrhotic patients with MHE. PubMed, the Cochrane Library, Embase, Web of Science, and the Chinese Biomedical Literature Database (CBM) were systematically searched from inception to August 2025 to identify randomized controlled trials (RCTs) comparing probiotics with lactulose for the treatment of MHE in patients with cirrhosis. Extracted outcomes included MHE reversal, overt hepatic encephalopathy (OHE) development, serum ammonia reduction, and adverse events (AEs). Five studies involving 345 cirrhotic patients were included. Pooled analyses showed no statistically significant differences between probiotics and lactulose in reversing MHE (RR: 0.98, 95% CI: 0.79-1.20; p = 0.822), preventing OHE development (RR: 1.40, 95% CI: 0.75-2.61; p = 0.289), and reducing serum ammonia levels (SMD: -0.05, 95% CI: -0.29 to 0.19; p = 0.678). In contrast, probiotics were associated with a significantly lower incidence of AEs compared with lactulose (RR: 0.17, 95% CI: 0.05-0.60; p = 0.005). This meta-analysis found no evidence that probiotics are superior or inferior to lactulose in terms of MHE reversal, prevention of OHE, and reduction of serum ammonia levels. Probiotics were associated with fewer AEs, suggesting a potential safety advantage. Further large-scale, high-quality RCTs are warranted to confirm these findings.

Cirrhotic patients receiving trans-jugular intrahepatic portosystemic shunt (TIPS) for preventing re-bleeding may benefit from a shunt diameter of ≤ 8mm. This study aimed to emulate a target trial comparing decompensation-free survival in patients receiving coaxial stent versus fully- or under-dilated 8mm TIPS for preventing variceal re-bleeding. Participants were recruited from a single-center, prospective, non-randomized cohort after excluding patients impossible to be assigned to the coaxial stent group. The coaxial stent consisted of a pre-implanted 5-/6mm balloon-expandable stent with an internal 8mm Viatorr stent. Causal inference framework was designed based on a directed acyclic graph, incorporating inverse probability weighting (IPW), doubly robust estimation by augmented IPW, mediation analysis, and E value analysis. 200 patients entered into target trial emulation, with 47 (23.5%), 101 (50.5%), and 52 (26.0%) in coaxial stent, under-dilated, and fully dilated groups. Coaxial stent feasibility was demonstrated by portacaval pressure gradient adjustability (33 pairs before/after dilation: 22.8 ± 3.0 to 17.9 ± 3.1mmHg, p < 0.001) and stability (76 pairs without intervention: 17.7 ± 4.2 to 18.5 ± 4.5mmHg, p = 0.035, r = 0.712, ICC = 0.710). Crude (IPW-weighted) 1-year decompensation-free survival incidences were 57.7% (52.6%), 60.1% (60.0%), and 76.6% (78.9%) for fully dilated, under-dilated, and coaxial stent groups, with doubly robust analysis revealing improved prognosis in coaxial stent versus fully dilated (HR 0.54 [0.25-0.93], p = 0.026, E value = 3.108, direct effect 66.3%) and under-dilated (HR 0.63 [0.34-1.05], p = 0.070, E value = 2.553, direct effect 60.7%) groups. Coaxial stent group demonstrated significantly reduced hepatic encephalopathy risk compared with other groups (p = 0.045/0.026), while other outcomes were comparable. The coaxial stent TIPS strategy could effectively achieve controlled expansion of 5-8mm and may improve overall prognosis in cirrhotic patients with previous variceal bleeding.

The optimal nutritional management strategy after transjugular intrahepatic portosystemic shunt (TIPS) procedure in cirrhotic patients remained controversial. A quantitative dietary intervention approach was developed for patients in the post-TIPS period, and its impact on clinical outcomes was evaluated in this study. This study was a retrospective, non-randomized controlled cohort study. A total of 92 cirrhotic patients who underwent TIPS were enrolled. Following TIPS, patients were categorized into two groups according to whether they received TIPS-oriented quantitative dietary intervention during hospitalization. The quantitative dietary guidance group received individualized and quantitative dietary instructions after TIPS, and the usual care group served as control. The primary endpoint was death, and the secondary endpoint was overt hepatic encephalopathy (OHE) occurrence. Kaplan-Meier survival analysis and Cox proportional hazards regression models were used to evaluate the association between quantitative dietary intervention and outcomes. The quantitative dietary guidance group (n=54) showed significantly lower mortality rates (5.56% vs. 21.05%, p=0.05) and OHE occurrence (12.96% vs. 36.84%, p=0.01) during follow-up than the usual care group (n=38). Liver-related mortality was also significantly lower in the quantitative dietary guidance group (1.85% vs. 15.79%, p=0.04). Multivariate Cox regression analysis demonstrated that the dietary intervention was independently associated with lower liver-related mortality risk (HR 0.09, 95% CI 0.01-0.75, p=0.03) and OHE risk (HR 0.34, 95% CI 0.14-0.85, p=0.02). Survival analysis demonstrated that the OHE probability was significantly lower in the quantitative dietary guidance group compared to the usual care group (HR 0.32, 95% CI 0.13-0.77, p=0.01), as was liver-related survival (HR 0.13, 95% CI 0.02-0.66, p=0.03). A structured quantitative dietary intake protocol following the TIPS procedure could improve survival rates and reduce the incidence of HE. These findings highlighted the importance of TIPS-oriented nutritional management for cirrhotic patients.

Detection of Esophageal Varices and Prediction of Hepatic Decompensation in Unresectable Hepatocellular Carcinoma using AI: AI Detection of Varices and Decompensation.

Statins, originally developed as lipid-lowering agents, have effects that extend well beyond cholesterol. By altering inflammatory signaling, vascular tone, fibrogenesis, and immune regulation, they engage pathways that shape a wide range of gastrointestinal diseases. Human data now suggest that these biological actions carry clinical weight. In metabolic dysfunction-associated steatotic liver disease and its progressive form, metabolic dysfunction-associated steatohepatitis, alcohol-associated liver disease, and chronic viral hepatitis (HBV and HCV), statin exposure is safe and associated with slower disease progression, fewer episodes of decompensation, and lower incidence of hepatocellular carcinoma. Randomized studies in cirrhosis show reductions in portal pressure, with cohort data linking use to fewer variceal bleeds, ascites, and hepatic encephalopathy. In inflammatory bowel disease, large registries and pilot trials indicate reduced flares, lower corticosteroid requirements, and decreased need for surgery, with early biomarker evidence supporting an anti-inflammatory effect. Smaller studies hint at benefits in other gastrointestinal contexts, though the evidence remains fragmented. Across these populations, true hepatotoxicity is rare; risk of myopathy is modest and largely confined to advanced cirrhosis or drug-drug interactions. Collectively, these findings support cautious repurposing of statins in gastroenterology and underline the need for definitive randomized trials to resolve class effects, optimize dose and duration, and identify reliable biomarkers of response.

Introduction: Upper gastrointestinal bleeding is a frequent medical and surgical emergency, associated with significant morbidity and mortality. The etiologies of upper gastrointestinal bleeding are dominated by gastroduodenal lesions, particularly peptic ulcers, followed by esophageal varices. Upper gastrointestinal endoscopy remains the first-line examination for etiological investigation. The study has for aim to evaluate the epidemiological, etiological, therapeutic, and prognostic profile of upper gastrointestinal bleeding in adults at the Hepatogastroenterology Department of the Ibn Rochd University Hospital in Casablanca. Materials and methods: It was a retrospective study conducted on the medical records of adult patients hospitalized for upper gastrointestinal bleeding, from January 1, 2023 to December 31, 2024, who underwent endoscopic gastrointestinal exploration. Data were entered into an Excel file and analyzed using Jamovi software. Results: Out of 1,565 admissions for all conditions, 362 cases involved upper gastrointestinal bleeding (23%), of which 20.8% (n = 327) met the inclusion criteria. The mean age was 55 years (range: 16–97 years), with a male-to-female ratio of 1.59. The majority of patients, 77% (n = 252), required hospitalization for more than 72 hours. Concomitant hematemesis and melena was the most frequent reason for hospitalization, observed in 41% (n = 134) of cases. Risk factors for esophageal variceal rupture were the most common, present in 29.4% (n = 96) of patients, including cirrhosis in 23.5% (n = 77) and portal hypertension in 5.8% (n = 19). Toxic habits were reported in 22.9% (n = 75) of patients. A hemorrhagic-risk iatrogenic drug interaction was identified in 16.8% (n = 55), including the use of gastrotoxic drugs in 12.2% (n = 40) and anticoagulants in 4.6% (n = 15). Esophageal and/or gastric variceal rupture accounted for 38.5% (n = 126) of cases, and gastroduodenal ulcers for 30.3% (n = 99), making them the main etiologies. Regarding management, 61.5% (n = 201) of patients received blood transfusions, among whom 30.6% (n = 100) received more than two units of packed red blood cells. Esophageal variceal ligation was performed in 32.4% (n = 106) of patients. Outcomes were marked by cessation of bleeding in 75.2% (n = 246) of cases. Early rebleeding and in-hospital mortality rates were 9.8% (n = 32) and 5.8% (n = 19), respectively. The causes of death were mainly hepatic encephalopathy in eight cases (2.4%), hemorrhagic shock in four cases (1.2%), respiratory distress in three cases (0.9%), and underlying malignant disease in four cases (1.2%). At discharge, 73.1% (n = 239) of patients had a hemoglobin level between 7 and 10 g/Dl and Two patients were transferred to the hematology department. Furthermore, chronic kidney disease, although present in only 1.8% (n=6) of cases, is recognized as an independent risk factor for gastrointestinal bleeding. Conclusion: Upper gastrointestinal bleeding remains a frequent and severe medical–endoscopic emergency. In Casablanca, the main causes are esophageal variceal rupture and gastroduodenal ulcers, often associated with cirrhosis and the use of gastrotoxic medications, reflecting the significant burden of chronic liver diseases and drug-induced complications in our population. These findings highlight the importance of screening for liver diseases, monitoring high-risk treatments, and improving access to specialized care in order to reduce morbidity and mortality.

Primary sclerosing cholangitis (PSC) is a chronic cholestatic liver disease with inflammatory bowel disease (IBD) present in 60-80% of affected individuals. We aimed to investigate whether concurrent IBD worsens outcomes in PSC patients. We conducted a retrospective cohort study using the TriNetX database to identify patients (≥ 18years) with PSC. Patients were then divided into two groups: PSC with IBD (PSC-IBD cohort) and PSC without IBD (isolated PSC cohort). Propensity score matching (PSM) was used to control for covariates between both cohorts. The primary outcome was the risk of developing liver-related decompensation (combined ascites, hepatic encephalopathy, and variceal hemorrhage). Secondary outcomes included colorectal cancer (CRC), hepatobiliary malignancy, liver transplantation, and overall mortality. Cox proportional hazards models were used to calculate hazard ratios (HR) with 95% confidence intervals (CIs). We identified 6,690 patients with PSC, including 3,012 patients (45%) with isolated PSC and 3,678 patients (55%) with PSC-IBD. After PSM, 1,714 pairs were well-balanced. Over an average of 5-year follow-up, PSC-IBD patients had a higher risk of liver-related decompensation (HR 1.26, 95% CI 1.09-1.46, p = 0.001), cholangiocarcinoma (HR 1.38, 95%CI 1.08-1.76, p = 0.008), and liver transplantation (HR 1.50, 95%CI 1.28-1.78, p < 0.001) compared to those with isolated PSC, with no difference in overall mortality. CRC was more common in IBD-PSC patients (HR 3.91, 95%CI 2.46-5.21, p < 0.001). Subgroup analysis revealed that patients with ulcerative colitis had more severe liver disease than Crohn's disease patients. Concurrent IBD was associated with adverse clinical outcomes in patients with PSC, including an increased risk of liver-related decompensation and cholangiocarcinoma.

Aminoglycosides, vancomycin, and metronidazole for people with cirrhosis and hepatic encephalopathy.

Hepatic veno-occlusive disease (HVOD), or sinusoidal obstruction syndrome (SOS), is a potentially liefe-threatening complication following allogeneic stem cell transplantation (allo-SCT). Historically, HVOD has affected up to 60% of allo-SCT recipients, with reported mortality rates exceeding 75% in severe cases. The approval of defibrotide in 2016 represented a major therapeutic milestone, significantly improving outcomes in high-risk patients. Despite this advancement, large-scale data on HVOD epidemiology & outcomes in allo-SCT recipients remain limited. This study aims to address these gaps & offer updated insights into its clinical impact. We utilized National Inpatient Sample (2016-2020) to examine factors associated with HVOD in allo-SCT recipients. Admissions for allo-SCT & HVOD were identified using International Classification of Diseases, Tenth Revision. Baseline characteristics, including patient demographics, hospital characteristics, comorbidities, complications & outcomes were compared between allo-SCT admissions with & without HVOD. Categorical variables were analyzed by χ² test (%), & continuous variables by adjusted Wald's test (mean±SD). During the study period, 200 allo-SCT admissions with HVOD were identified. HVOD admissions were younger (45.05 vs. 52.42 years; P=0.0045) & were more likely to be female (43.72% vs. 25%; P=0.0191). They had higher rates of acute graft-versus-host disease (GVHD) (17.5% vs. 6.47%; P=0.0043), acute respiratory failure (32.5% vs. 8.37%; P<0.001), & acute kidney injury (50% vs. 20.66%; P<0.001). Hepatic complications, including portal hypertension (7.5% vs. 0.52%; P<0.001), hepatic encephalopathy (12.5% vs. 0.28%; P<0.001), cirrhosis (7.5% vs. 0.07%; P<0.001), ascites (37.5% vs. 1.97%; P<0.001) & spontaneous bacterial peritonitis (2.5% vs. 0.06%; P<0.001) were also more common in this cohort. HVOD was associated with worse outcomes, including longer hospital stays (45.5 vs. 29.51 days; P<0.001) & over 6 times higher in-hospital mortality (30% vs. 4.72%; P<0.001). HVOD also imposed a greater economic burden, with more than double mean total hospitalization charges ($1,321,650 vs. $541,391.1; P<0.001) & nearly triple hospitalization costs ($358,463.2 vs. $141,464.1; P<0.001). This study describes HVOD-specific characteristics in allo-SCT admissions. Patients with HVOD were younger, had higher comorbidity burden, & showed increased rates of acute GVHD, multiorgan dysfunction, & hepatic complications. They also faced high in-hospital mortality, longer hospital stays, & greater healthcare costs.