This study evaluates baseline characteristics associated with worsening ascites following TARE focusing on evaluation of the pre-existing ascites as a risk factor. A secondary objective was to examine survival among patients who developed ascites after TARE. A total of 288 TARE deliveries (237 patients) for primary liver tumors were retrospectively reviewed. Imaging before and six months after TARE was assessed for ascites. Tumor volume, treated area, delivered activity, and liver function tests and underlying etiology of liver disease were reviewed. Logistic regression was performed for risk factors of liver decompensation including pre-existing ascites as a risk factor. Survival curves were plotted for overall survival. Mean (SD) age was 66 (11). 204 were male (71%). Median follow-up was 12.3 months (IQR 5.5-23.5). Of 288 tumors, 266 (92%) were HCC, 11 (4%) IHC, and 11 (4%) biphenotypic. 60 (of 288, 21%) patients had pre-existing ascites. New/worsening ascites occurred in 121 (of 288, 42%) [93 (77%) new, 28 (23%) worsening]. Patients with new/worsening ascites had significantly greater increases in bilirubin (p = 0.01, p < 0.001). In multivariable regression analysis pre-existing ascites was not associated with increased risk of post-TARE ascites progression, but a higher ALBI grade (OR = 2.87, p < 0.001) and baseline liver cirrhosis (OR = 2.64, p = 0.007) were associated with ascites after TARE. Neither perfused volume nor activity delivered predicted new/worsening ascites. Child-Pugh class (HR = 2.3, p < 0.001), pre-existing ascites (HR = 2, p < 0.001), ALBI score (HR = 1.5, p < 0.011) and new/worsening ascites (HR = 2.1, p < 0.001) were associated with lower survival. Pre-existing ascites is associated with worse survival but should not preclude TARE. ALBI scoring can help distinguish patients at higher risk of post-TARE ascites.

Post-embolization syndrome (PES) is a frequent complication after hepatocellular carcinoma (HCC) treatment. This study compared dexamethasone (DEX) versus N-acetylcysteine (NAC) for efficacy and safety in preventing PES at 48 h after transcatheter arterial chemoembolization (TACE). This Phase 3, randomized (1:1), double-blind, double-dummy, parallel-group, non-inferiority study, included patients with early- to intermediate-stage HCC (BCLC Stages A-B) without macrovascular invasion who were candidates for TACE. Participants were randomly assigned to receive either an intravenous single dose of 8 mg DEX or NAC as part of the periprocedural TACE protocol. A total of 85 patients were included in the outcome analysis. PES incidence was non-inferior between groups (difference proportion DEX-NAC 0.02, [95% CI: -0.13 to 0.17]). However, subgroup symptoms' analysis showed significantly greater reduction in abdominal pain (87.5% vs. 55.3%, p = 0.002) and fever (52.5% vs. 28.9%, p = 0.035) in DEX group compared to NAC group. Liver decompensation was significantly greater reduction in the DEX group than the NAC group (90% vs. 52.6%, p < 0.001). Anaphylactoid reactions (18.4%) were observed exclusively in the NAC group. Multivariate analysis showed preexisting high serum ALT was associated with an increased risk of developing PES (OR: 1.05; 95% CI: 1.01-1.08), and a higher chemotherapy dosage emerged as an independent risk factor for post-TACE liver decompensation (OR: 1.00; 95% CI: 0.84-0.99). PES incidence was non-inferior between groups. However, at 48 h post-TACE, the DEX regimen was associated with a significant reduction in fever, pain, and liver decompensation.

Efficacy and safety of hepatectomy in hepatitis B-related hepatocellular carcinoma with compensated versus recompensated cirrhosis: A propensity score matching study.

Chronic hepatitis B (CHB) affects an estimated 254 million people globally. Historically, WHO and professional society guidelines have recommended treatment for individuals at high risk of disease progression, including those with hepatitis B virus (HBV) DNA concentrations >20 000 IU/mL. Whether individuals at lower risk, including those with HBV DNA <20 000 IU/mL and normal alanine aminotransferase concentrations, benefit from treatment remains uncertain. To inform 2024 WHO guidelines and the potential expansion of treatment threshold recommendations, we conducted two linked systematic reviews and meta-analyses; this analysis examines the incidence of clinical outcomes in untreated adults with non-cirrhotic CHB stratified by baseline HBV DNA and ALT concentrations. In this systematic review and meta-analysis, we searched PubMed, Embase, Web of Science, and the Cochrane Library for longitudinal prospective and retrospective cohort studies, randomised controlled trials, and non-randomised studies of interventions, published in any language, from Jan 1, 2000, to Feb 6, 2023. We also reviewed the reference lists of included studies and systematic reviews and consulted networks of experts to identify other data sources. Included studies followed up adults (≥18 years) with non-cirrhotic CHB who had no history of antiviral therapy at enrolment, had baseline HBV DNA quantification and ALT measurement, had a follow-up period of at least 48 weeks, and assessed one or more of six key clinical outcomes (hepatocellular carcinoma, cirrhosis, liver-related mortality, all-cause mortality, liver decompensation, and indication for liver transplantation) or six additional outcomes (advanced liver fibrosis, progression of liver fibrosis, becoming eligible for antiviral treatment, hepatitis flare, and HBsAg and HBeAg seroclearance). Outcomes were required to be stratified by HBV DNA concentrations (<200 IU/mL, <2000 IU/mL, 2000-19 999 IU/mL, 20 000-199 999 IU/mL, and ≥200 000 IU/mL) or ALT concentrations (less than the upper limit of normal [ULN], 1·0-1·9 × ULN, and ≥2·0 × ULN). We excluded studies that focused solely on individuals who were pregnant; were co-infected with HIV, hepatitis C virus, or hepatitis D virus; or had another underlying condition other than CHB. We extracted aggregate data and used random-effects meta-analysis to pool incidence rates per 100 person-years. This study was registered with PROSPERO (CRD42023431652). Of 13 231 studies screened, 71 met the inclusion criteria. A concentration-response relationship was observed between single baseline HBV DNA measurements and hepatocellular carcinoma incidence rates per 100 person-years: 0·131 (95% CI 0·097 to 0·177, I2=0%) for HBV DNA concentrations <200 IU/mL, 0·176 (0·117-0·266, I2=88%) for <2000 IU/mL, 0·311 (0·245-0·393, I2=13%) for 2000-19 999 IU/mL, 0·862 (0·725-1·026, I2=0%) for 20 000-199 999 IU/mL, and 0·941 (0·668-1·324, I2=58%) for ≥200 000 IU/mL (p<0·0001 for between-group difference). Similar concentration-response patterns were observed for development of cirrhosis (0·298 [95% CI 0·214-0·415], two studies, for <200 IU/mL; 0·300 [0·146-0·616], I2=88%, for <2000 IU/mL; 0·712 [0·624-0·814], I2=46%, for 2000-19 999 IU/mL; 1·436 [0·991-2·082], I2=76%, for 20 000-199 999 IU/mL; and 2·193 [1·690-2·846], I2=82%, for ≥200 000 IU/mL) and liver-related mortality (0·086 [95% CI 0·054-0·136], one study; 0·083 [0·015-0·451], I2=0%; 0·303 [0·228-0·402], I2=0%; 0·766 [0·591-0·993], one study; and 1·118 [0·951-1·314], two studies), but no concentration-response relationship was observed between a single baseline HBV DNA assessment and all-cause mortality or liver decompensation. Compared with ALT below the ULN, incidence rates of hepatocellular carcinoma, cirrhosis, and liver-related mortality were higher in individuals with baseline ALT concentrations 1·0-1·9 × ULN or ≥2·0 × ULN. A similar pattern was not found for all-cause mortality, and other outcomes were not meta-analysed due to small numbers. Within the HBV DNA strata of <2000 IU/mL, 2000-19 999 IU/mL, and ≥200 000 IU/mL, hepatocellular carcinoma incidence rates were 2-3 times higher in individuals with ALT 1·0-1·9 × ULN than in those with ALT concentrations less than the ULN. Individuals with persistently low HBV DNA concentrations (<2000 IU/mL) or persistently normal ALT concentrations across multiple assessments had slightly lower hepatocellular carcinoma incidence rates compared with those assessed by a single measurement. Our risk of bias assessment found 15 (21%) of 71 studies to be rated as good quality, 40 (56%) as fair quality, and 16 (23%) as poor quality. These findings, alongside the linked systematic review and meta-analysis of antiviral treatment efficacy, supported the 2024 WHO guidelines expansion of treatment criteria to include individuals with HBV DNA concentrations >2000 IU/mL and ALT concentrations above the ULN. For those with HBV DNA concentrations <2000 IU/mL and persistently normal ALT concentrations, treatment can be deferred. WHO.

Impact of Cardiometabolic Risk Factors and Steatotic Liver Disease on Liver-Related Outcomes in Patients With Chronic Hepatitis C After Curative Antiviral Therapy.

Cirrhosis favours infections that can lead to liver decompensation and death. Some of these infections can be prevented by vaccination. This study aimed to evaluate the immune response after HBV, pneumococcal, diphtheria, and tetanus vaccination in cirrhotic patients. Patients with cirrhosis were prescribed 3 doses of hepatitis B vaccine, a tetanus-diphtheria booster and/or a 13-valent pneumococcal conjugate vaccine followed by a 23-valent polysaccharide vaccine. HBs seroconversion was assessed 6 months after the last booster dose. Antibody concentrations for seven pneumococcal serotypes, tetanus and diphtheria were measured by ELISA before (V0) and 4 to 6 months after vaccination (V1). Of the 125 patients enrolled, 83 were analysed for HBs seroconversion, 119 for pneumococcal vaccine response and 117 for tetanus and diphtheria vaccine response. The anti-HBs seroconversion rate was 31%. A doubling of the antibody was observed in 19% of cases for tetanus and in 26% of cases for diphtheria. For the pneumococcal vaccine, the global protection (at least 5 antibodies with a concentration ≥ 1.3 mg/L against the 7 serotypes of pneumococcus tested) increased from 39% before vaccination to 80% after vaccination. However, only 48% of patients had a 2-fold increase in IgG antibody for at least five of the seven serotypes tested. Our study highlights a weak response to the hepatitis B, tetanus, and diphtheria vaccines and an acceptable immunological response to the pneumococcal vaccine, although lower than in healthy subjects. There is a real need to optimise vaccination in cirrhotics.

Impact of Hepatocellular Carcinoma on the risk of liver decompensation: a comparative analysis of patients with and without HCC: Role of HCC in liver decompensation.

Patients with cirrhosis have impaired immunity, predisposing them to severe infections. Streptococcus pneumoniae, a leading cause of community-acquired pneumonia, may worsen outcomes in this vulnerable patient population. This study aims to evaluate the burden and impact of pneumococcal pneumonia among patients with cirrhosis. The National Inpatient Sample database (2016-2022) was used to identify adult hospitalizations with cirrhosis. Patients were stratified by the presence or absence of pneumococcal pneumonia. Data were obtained on demographics, liver disease etiology and decompensations, comorbidities, and clinical outcomes. A multivariate logistic/linear regression analysis was used to assess the impact of pneumococcal pneumonia on clinical outcomes. Among 4,716,863 patients with cirrhosis, 90,680 (1.92%) developed pneumococcal pneumonia. Patients with pneumococcal pneumonia had higher odds of in-hospital mortality (adjusted odds ratio (aOR): 2.95, 95% confidence interval (CI): 2.84-3.09), acute kidney injury (aOR: 1.85, 95% CI: 1.79-1.91), shock (aOR: 4.75, 95% CI: 4.58-4.93), intensive care unit admissions (aOR: 7.55, 95% CI: 7.28-7.83), non-home discharges (aOR: 2.29, 95% CI: 2.21-2.38), longer length of stay (adjusted coefficient: 6.61 days, 95% CI: 6.38-6.83), and higher hospitalization charges (adjusted coefficient: $112,230.5, 95% CI: $106,802.3-$117,658.7) (all P < 0.001). We noted an increased in-hospital mortality and higher resource utilization among patients with pneumococcal pneumonia. These findings underscore the importance of targeted preventive strategies, including pneumococcal vaccination and early infection recognition, to reduce morbidity and healthcare burden in this vulnerable population.

Real-world outcomes in patients with cirrhosis undergoing cholecystectomy: a population-based study.

There is an unmet need for simple tools to predict development of hepatic decompensation among patients with compensated cirrhosis. We applied machine learning to several international Data sets to develop and validate a straightforward predictive model of decompensation. We used routinely available clinical and laboratory data from 575 patients with compensated cirrhosis from the training cohorts in Nottingham (United Kingdom) and Modena (Italy), with a median follow-up of 4 years. Based on these data, we developed a predictive model using a random forest classifier and validated it across independent international populations involving over 2,100 patients from Dublin (Ireland), Menoufia (Egypt), Leeds (UK), and Ogaki (Japan). In the training cohorts, 22% of patients developed liver decompensation. Using machine learning, we developed risk of decompensation in cirrhosis (RODIC), a well-calibrated model based on albumin, bilirubin, and the Fib-4 value (area under the receiver operating characteristic curve = 0.86; weighted F1 score = 0.82) which predicts the risk of decompensation within 3 years (access free of charge at: https://antonkaly.pythonanywhere.com/predict ). RODIC showed strong performance across all validation sets, with area under the receiver operating characteristic curve scores ranging from 0.67 to 0.80 and weighted F1 scores from 0.70 to 0.81. Moreover, the model was effective regardless of cirrhosis etiology. For hepatitis C virus-positive patients, RODIC remained reliable irrespective of whether they achieved sustained virologic response. Our validated machine learning model based on readily available clinical, and laboratory features accurately quantitates the risk of liver decompensation in patients with compensated hepatic cirrhosis.

Abstract Aim Patients with chronic liver disease are predisposed to umbilical hernia due to ascites, sarcopenia, and abdominal wall weakness, with increased perioperative morbidity and mortality from the potential risk of liver decompensation. This study evaluates surgical outcomes of symptomatic umbilical hernia in chronic liver disease at a specialized liver transplant center. Materials and methods A retrospective observational study was conducted at Mahatma Gandhi Medical College and Hospital, Jaipur. Patients with symptomatic umbilical hernia and underlying chronic liver disease who underwent open umbilical herniorrhaphy after preoperative optimization from August 2021 to May 2024 were included. Severity of liver disease was assessed using Child–Turcotte–Pugh (CTP) and MELD-Na scores. Preoperatively, the risk of mortality was assessed using the Vocal-Penn score. Postoperative morbidity was graded by Clavien–Dindo classification (CDC) and outcomes included 90-day mortality and length of hospital stay. Results Thirteen patients (median age 55 years (IQR 41.5–62), 77% male) underwent surgery for symptomatic umbilical hernia. The most common etiology of chronic liver disease was alcohol-related (5 of 13 patients, 38.5%) and non-alcoholic steatohepatitis (NASH) (5 of 13 patients, 38.5%). Median preoperative CTP score was 9 (range 5–12) and MELD-Na score was 22 (range 8–29). All patients underwent open umbilical herniorrhaphy and two out of thirteen patients required bowel resection in view of bowel gangrene. Postoperative complications occurred in 8 of 13 patients (61.5%), and 5 of 13 patients (38.5%) experienced major complications (CD ≥ 3), including CD Grade IV ( n = 4) and Grade V ( n = 1). Postoperative MELD-Na score worsening was seen in 5 (38.4%) patients, of whom 4 patients recovered with appropriate care. The median hospital stay was 9 days (range 4–46), and 90-day mortality was 7.7%. Patients with preoperative Vocal Penn score with mortality risk of 32.6% had mortality. Median follow-up of these patients is 17.5 months. Conclusions Our study reaffirms that surgical repair of symptomatic umbilical hernia in decompensated liver cirrhosis patients can be performed with good outcomes when meticulous preoperative optimization and perioperative care is provided in a specialized liver transplant unit. This study with a small sample shows the feasibility of successful surgical outcomes for optimized, high-risk patients. Trial registration Clinical trial number is not taken because it is an observational study and a retrospective collection of data and approval was taken from the university institutional ethics committee (No: MGMC&amp;H/IEC/JPR/2025/4994).

Long-term outcomes of atezolizumab-bevacizumab in unresectable hepatocellular carcinoma: A real-world study.

Hepatitis D virus (HDV) is a satellite RNA virus of the hepatitis B virus (HBV) infecting an estimated 12 million people worldwide. Chronic HDV infection is causing the most severe form of chronic viral hepatitis, leading to a rapid progression of chronic inflammation to fibrosis, cirrhosis, liver decompensation and cancer. The detailed mechanisms responsible for HDV pathogenicity and its contribution to the development of hepatocellular carcinoma (HCC) are not clearly understood. This review aims to summarize the current knowledge of HDV-induced injuries, which gradually accumulate and increase the oncogenic pressure in the liver. Here, we provide a comprehensive yet concise overview of the following topics: (1) virus sensing and innate responses, (2) molecular basis of HDV pathogenesis, and (3) pathogenesis of chronic HDV infection in patients. We summarize the compelling evidence of the direct and indirect contributions of HDV to the development of HCC, which is driven by the rapid progression to liver cirrhosis. These results led to the classification of HDV as a group 1 carcinogenic agent in 2025 and emphasize the urgent need for improved antiviral and chemopreventive treatments. In addition, it highlights the necessity of routine HDV screening in patients with chronic hepatitis B and intensified HCC surveillance in patients with chronic hepatitis D.

Transarterial chemo-embolisation (TACE) is an established treatment for patients with hepatocellular carcinoma (HCC). As the majority have pre-existing liver disease, only patients with adequate liver function undergo TACE. Liver maximum capacity (LiMAx), using C13-Methacetin, is a novel method to assess liver function prior to major oncologic resections. We evaluated the safety and feasibility of using LiMAx to assess the changes in liver function with TACE and whether it could predict post-intervention complications. The prospective study was conducted between November 2021 and March 2023 on patients undergoing TACE for HCC at the University Hospitals Birmingham NHS Foundation Trust, UK. Patients underwent LiMAx assessment on three occasions: 1-2 weeks before, 4-6 weeks after, and 12-14 weeks following TACE. This was compared with well-established biochemical analyses. Thirty non-consecutive patients were included, with a median LiMAx value of 278[Formula: see text]g/kg/h (range 44-688) on visit 1, 30% had a LiMAx value < 140 [Formula: see text]g/kg/h. There was no significant difference in the pre- and post-TACE LiMAX values (median difference - 6%). One patient presented with symptoms consistent with post-intervention liver decompensation with a pre-TACE LiMAx value of 95 [Formula: see text]g/kg/h. LiMAx correlated with established biochemical scoring systems of liver functions such as Child-Pugh (r=-0.4055, p = 0.0262) and UKELD (r=-0.4166, p = 0.0220). LiMAx assessment is a safe, feasible and non-invasive measurement of liver function. Despite low LiMAx values in some patients, there was no incidence of post-procedural liver decompensation. Future research should aim at identifying patients with Child-Pugh B disease with adequate liver function, based on LiMAx assessments, who may benefit from TACE.

Objective: To look for a possible association between the use of proton pump inhibitors and the development of spontaneous bacterial peritonitis in patients with decompensated chronic liver disease and to draw a comparison between decompensated chronic liver disease patients who are using PPIs and those who are not using them.Study Design: Analytical cross-sectional study.Place and Duration of Study: This study was conducted at the Department of Gastroenterology, Combined Military Hospital (CMH), Lahore, Pakistan, from 5th June 2023 to 4th December 2023.Methods: Patients were divided into two groups. The first group included all patients with decompensated chronic liver disease who were taking PPIs, and the second group included all decompensated chronic liver disease patients who were not taking PPIs at the time of development of Spontaneous bacterial peritonitis. Written informed consent was obtained from all patients in both groups. Inclusion Criteria included patients of the age group ranging from 30 to 80 years having confirmed liver cirrhosis along with splenomegaly and ascites on abdominal ultrasound. Exclusion Criteria included all patients with a history of Child Pugh Class A chronic liver disease, patients with alcohol intake, and patients with gastrointestinal malignancy.Results: Among diagnosed cases of decompensated chronic liver cirrhosis, the rate of development of spontaneous bacterial peritonitis was 7.58 % in patients using proton pump inhibitors as compared to 1.7 % among patients with chronic liver disease who were not using proton pump inhibitors, with a significant P-value of 0.01.Conclusion: Use of proton pump inhibitors significantly increased the likelihood of developing spontaneous bacterial peritonitis in decompensated chronic liver patients. How to cite this: Habib A, Uddin R, Khan R, Manzar MA, Malik A, Ashraf S. Association of Proton Pump Inhibitors with Increased Risk ofSpontaneous Bacterial Peritonitis in Patients with Decompensated Chronic Liver Disease: Analytical Cross-Sectional Study. Life andScience. 2026; 7(1): 106-111. doi: http://doi.org/10.37185/LnS.1.1.599

Laparoscopic liver resection is superior to open liver resection for hepatocellular carcinoma patients with BCLC stage 0-A hepatocellular carcinoma and portal hypertension.

BACKGROUNDThe health challenges of partial hepatectomy in patients with clinically significant portal hypertension (CSPH) have been a subject of study for decades. No meta-analysis has systematically evaluated the relationship between CSPH and posthepatectomy liver failure (PHLF), despite its potential role as a critical factor in surgical decision-making. This systematic review and meta-analysis investigated the incidence of PHLF in patients with and without CSPH.AIMTo include more recent studies and focus on short-term postoperative outcomes, particularly the association between CSPH and PHLF. Additionally, stratified analyses were also performed according to CSPH and PHLF assessment methods, study design, study period, surgical technique, and underlying liver diseases.METHODSA comprehensive literature search was conducted in EMBASE, PubMed, MEDLINE, ScienceDirect, Elsevier, and Cochrane databases using combinations of the following terms: (“portal hypertension” OR “hypertension, portal” OR “portal hypertensions”) AND (“hepatectomy” OR “hepatectomies” OR “liver resection”) AND (“liver failure” OR “hepatic failure” OR “liver decompensation”). Studies published from January 1996 to April 2025, 21 published studies were finally included in the systematic review and meta-analysis. The quality assessment was performed independently by using the Newcastle-Ottawa Scale. Odds ratios (OR) and 95% confidence intervals (CI) were calculated and compared using a random-effects model. Heterogeneity was assessed with the χ2 test, and the degree of inconsistency was measured using I2. A P value < 0.05 or I2 > 50% indicated substantial heterogeneity. Sensitivity analysis was conducted to test the robustness of the findings and to identify potential sources of bias.RESULTSA total of 6981 patients (1453 patients with CSPH and 5529 patients without CSPH) were finally included in this study. Compared with patients without CSPH, the incidences of PHLF increased in patients with CSPH (OR = 3.14; 95%CI: 2.45-4.02; P < 0.001). Subsequent subgroup analysis suggested that the diagnostic methods for CSPH is a potential interfering factor in PHLF, the OR was maximal in hepatic venous pressure gradient measurement groups (OR = 15.61; 95%CI: 2.11-115.35; P = 0.007).CONCLUSIONThe presence of CSPH should be considered as a significant risk factor, it still should be taken into account seriously prior to surgery and needs strict perioperative management. Meanwhile, different methods of diagnosing CSPH could influence PHLF.

Mounting evidence indicates that the p53 Pro72Arg single-nucleotide polymorphisms (SNPs) may play a role in modulating hepatocarcinogenesis in the setting of chronic HBV infection. However, there is currently a lack of studies focusing on this genetic variant in Indonesia, a country characterized by its diverse genetic landscape comprising over 1300 distinct ethnic groups. We aimed to investigate the association between the p53 Pro72Arg polymorphism and the risk of hepatocellular carcinoma (HCC) among Indonesian patients with chronic HBV infection. A total of 140 patients with chronic hepatitis B (CHB) were recruited, including 79 with HCC and 61 without HCC serving as controls. We used direct sequencing of DNA extracted from peripheral blood to analyze the SNPs of p53 codon 72. The distribution of p53 Pro72Arg genotypes among Indonesian CHB patients was 12.9% for proline homozygotes (Pro/Pro), 31.4% for arginine homozygotes (Arg/Arg), and 55.7% for proline/arginine heterozygotes (Pro/Arg). Despite the lack of association between the SNPs and HCC risk in the overall population, both the Pro/Arg and Arg/Arg genotypes demonstrate an increased susceptibility to HCC compared to Pro/Pro genotypes exclusively in the Madurese ethnic group. Additionally, we discovered that in those with decompensated cirrhosis, the heterozygote Pro/Arg was more likely to develop HCC than the homozygous Pro/Pro. No significant association was found between the SNPs of p53 Pro72Arg and the clinicopathological characteristics of HCC. The p53 Pro72Arg polymorphism might contribute to hepatocarcinogenesis in Indonesian chronic hepatitis B patients, particularly Madurese and those with liver decompensation.

491 Background: Hepatocellular carcinoma (HCC) is the sixth most common cancer worldwide and the third leading cause of cancer related mortality. Outcomes are often shaped not only by the cancer itself but also by the burden of underlying cirrhosis and treatment related complications. Hospitalizations are common and carry substantial costs, driven by both disease progression and liver decompensation. This study examines resource use and the leading causes of 90-day readmissions after HCC admissions. Methods: We conducted a retrospective study using the 2022 Nationwide Readmissions Database (NRD), part of the Healthcare Cost and Utilization Project. We identified patients with Hepatocellular carcinoma who were hospitalized between January and October. The first unplanned readmission within 90 days of discharge was used to define the readmission cohort. Survey-weighted logistic, linear, and Cox regression models were used to assess clinical and hospital-level factors associated with readmission. Results: In multivariable analysis, younger age (aHR 0.99, p&lt;0.001) and thrombocytopenia (aHR 0.92, p=0.035) were associated with lower readmission risk, while longer length of stay during index admission (aHR 1.00, p=0.005), diabetes (aHR 1.08, p=0.007), hyperlipidemia (aHR 1.09, p=0.004), ascites (aHR 1.23, p&lt;0.001), varices (aHR 1.10, p=0.027), renal impairment (aHR 1.07, p=0.023), and treatment under 'other’ insurance payers was associated with lower risk compared with Medicare (aHR 0.79, p=0.030). Alcohol-related liver disease was protective (aHR 0.84, p&lt;0.001). Top 90-day readmission causes were sepsis (2,181), cancer progression (1,822), cirrhosis (1,157), hepatic failure (965), acute kidney failure (504), cholangitis/biliary disorders (305), chronic pain (166), COVID-19 (145), hypertensive heart and kidney disease with heart failure (145), and pneumonia (137). Conclusions: In patients with hepatocellular carcinoma, 90-day readmissions are driven not only by tumor progression but also by sepsis and complications of portal hypertension, including ascites and varices. Metabolic comorbidities such as diabetes and hyperlipidemia further increased risk, Targeting infection prevention and better management of cirrhosis related decompensation may reduce readmissions and improve outcomes in this high-risk population. Comparative resource utilization between index hospitalizations and 90-day readmissions in patients with hepatocellular carcinoma. Category Index Admission 90-Day Readmission Weighted admissions 36,143.38 11,576.02 In-hospital deaths 3267.847 N/A Mean length of stay (days) 7.25 7.29 Mean charges (USD) $113,925 $111,415.6 Mean costs (USD) $27,787.15 $27,179.18 Cumulative hospital days 262,174.8 84,459.19 Cumulative charges (USD) $4.08 billion $1.28 billion Cumulative costs (USD) $996 million $312 million

Introduction: Liver cirrhosis is the terminal phase of a vast number of chronic hepatic diseases. It is classified into compensated and decompensated stages according to occurrence of complications. Portal hypertension is a severe consequence of cirrhosis. It results from increased vascular resistance and release of endotoxins and cytokines which trigger splanchnic arterial vasodilation which activates the RAAS. This ends in the release of arginine vasopressin (AVP) which is difficult to be measured because of its small size and short half-life. Copeptin, the C-terminal part of the AVP precursor, is produced from the posterior pituitary along with AVP in equimolar levels. Being stable makes it a sensitive surrogate marker for AVP release.Aim of the work: This study aimed to evaluate copeptin’s level as a marker predicting decompensated liver cirrhosis and its use as a prognostic marker.Patients and Methods: The study was conducted on 90 subjects admitted to Alexandria main university hospital who were divided into three groups: Group I (n=35) compensated cirrhotic patients, Group II (n=35) decompensated cirrhotic patients and Group III (n=20) apparently healthy individuals. Serum copeptin was measured by ELISA. Candidates underwent detailed clinical evaluation and laboratory investigations which included CBC, renal function tests and liver profile; alanine transaminase (ALT), aspartate transaminase (AST), prothrombin time, INR, serum albumin, total serum protein, serum bilirubin (total and direct). Liver disease severity was assessed by Child-Pugh, MELD and MELD-Na scores.