Search Results (3,233)

Background: Cirrhosis is a progressive liver disease often associated with sarcopenia. Vitamin D and IGF-1 alterations may contribute to muscle loss and disease progression. This study evaluated their relationship in cirrhotic patients. Methods: A total of 90 patients with liver cirrhosis were included in this retrospective observational study. Clinical and laboratory data were collected, and disease severity was assessed using Child–Pugh and MELD-Na scores. Sarcopenia was evaluated using CT-based skeletal muscle index at the L3 level with sex-specific cut-offs. Patients with malignancy, acute liver failure, recent surgery, or muscle-affecting conditions were excluded. Vitamin D and IGF-1 levels were classified using standard and age-adjusted reference ranges. Results: A total of 90 patients were included, of whom 42 were alive, and 48 died during follow-up. Gender distribution was similar between groups (p = 0.388). Skeletal muscle area was significantly lower in non-survivors (110 vs. 140 cm², p = 0.002), while body mass index did not differ (p = 0.570). Vitamin D levels were significantly lower (10.0 vs. 17.9 ng/mL, p < 0.001), and hemoglobin levels were reduced in the non-survivor group (10.76 ± 2.13 vs. 12.87 ± 2.57 g/dL, p = 0.001). In multivariate analysis, age (OR 1.046, p = 0.032), MELD-Na score (OR 1.200, p = 0.001), and vitamin D level (OR 0.920, p = 0.024) were independently associated with mortality. Conclusions: CT-based sarcopenia assessment is a useful adjunct in cirrhosis when interpreted with disease severity. Radiological muscle depletion is common and associated with worse outcomes, while vitamin D deficiency independently associated with mortality, highlighting its potential as a biomarker and therapeutic target. Full article

Non-alcoholic fatty liver disease (NAFLD), now increasingly termed metabolic dysfunction-associated steatotic liver disease (MASLD), is a growing cause of chronic liver disease with limited treatment options. Glucagon-like peptide-1 (GLP-1) receptor agonists, approved for type 2 diabetes and obesity, possess metabolic effects that may render them suitable for treating NAFLD and metabolic dysfunction-associated steatohepatitis (MASH). To evaluate the therapeutic effects of GLP-1 receptor agonists in adults with NAFLD, non-alcoholic steatohepatitis (NASH), MASLD, or MASH. PubMed, Scopus, Embase, and the Cochrane Library were systematically searched using keywords related to NAFLD and GLP-1 receptor agonists. Given heterogeneity in populations, designs, and outcomes, findings were synthesized narratively. The review is registered with PROSPERO (CRD420261337353). Twelve studies met the inclusion criteria. The most consistent outcome was a reduction in hepatic fat, seen with semaglutide, liraglutide, dulaglutide, and beinaglutide. Improvements in liver enzymes, particularly alanine aminotransferase, were less consistent and best regarded as supportive rather than definitive evidence of histological improvement. Histological benefits were strongest for steatohepatitis resolution in non-cirrhotic MASH. Fibrosis findings were mixed, with the greatest benefit in F2–F3 MASH and limited improvement in established cirrhosis. GLP-1 receptor agonists were generally well tolerated, with gastrointestinal symptoms the most common adverse effects. GLP-1 receptor agonists show promising liver-related benefits in NAFLD and MASH, particularly in obesity, type 2 diabetes, or earlier-stage disease. Their effects on advanced fibrosis and long-term outcomes remain uncertain, warranting larger, longer-term studies. Full article

Metabolic dysfunction–associated steatotic liver disease (MASLD) is now the most common chronic liver disorder worldwide. Once started with hepatic steatosis, it can progress to metabolic dysfunction–associated steaohepatitis (MASH), cirrhosis, and even hepatocellular carcinoma. Insulin resistance is a major driver of hepatic lipogenesis in this disease context. Gut barrier dysfunction also contributes to the progression to MASH by allowing bacterial lipopolysaccharide (LPS) to breach into the hepatic tissues. Amphibian skin secretion peptides (ASSPs) are therefore of particular interest, given their combined metabolic and antimicrobial activities. Some ASSPs enhance glucose-stimulated insulin secretion and GLP-1 release, whereas others attenuate LPS-driven inflammatory signaling. This review introduces these ASSPs with a focus on their insulinotropic/incretinotropic and immunomodulatory activities. Also, in the latter part, pharmaceutical strategies to improve blood circulation time and structural stability would be discussed. Full article

Early detection of hepatocellular carcinoma (HCC) is crucial for curative treatment, yet current screening strategies for high-risk liver cirrhosis (LC) patients lack sufficient sensitivity. This study evaluates plasma cell-free DNA(cfDNA) concentration and fragmentomics as biomarkers to improve HCC diagnosis and prognosis. Plasma samples from 39 HCC and 46 LC patients were analyzed for cfDNA concentration and fragment patterns. A multivariate logistic regression model (CMAC), integrating cfDNA concentration, mononucleosome proportion (%MN), alpha-fetoprotein (AFP), and c-reactive protein (CRP), was developed and validated using Leave-One-Out Cross-Validation and bootstrapping. HCC patients exhibited significantly higher cfDNA concentrations (p < 0.0001) and longer fragment lengths (p < 0.05) compared to LC patients. The CMAC model demonstrated superior diagnostic performance (AUROC = 0.946) compared to AFP alone (AUROC = 0.777, p < 0.001). Notably, in early-stage HCC, the CMAC model remained highly accurate (AUROC = 0.941), whereas AFP failed to reach statistical significance. Higher CMAC scores were significantly associated with advanced BCLC stages (p = 0.009), lymphovascular invasion (p = 0.0063) and reduced overall survival (p = 0.0037). Integration of cfDNA analysis with established clinical markers in the CMAC model shows promise as a complementary tool for the early detection of HCC in LC patients. Validation in larger, multicenter cohorts will be necessary to confirm these findings and their clinical applicability. Full article

Background/Objectives: Variceal bleeding (VB) is a major complication of cirrhosis, marking a progression from a compensated to a decompensated stage of the disease. Previous research has suggested that HMG-CoA reductase inhibitors, commonly called statins, may have therapeutic benefits for those living with cirrhosis, though their exact benefits and role have yet to be elucidated. This scoping review evaluates the potential role of statins in the primary prevention of variceal bleeding in patients with cirrhosis, and if there exists a difference between hydrophilic and lipophilic statins for this indication. Methods: Publications from the last 10 years with primary or secondary outcomes reporting variceal bleeding among statin users and non-users were included. A search via PubMed, the Cumulative Index to Nursing and Allied Health Literature (CINAHL), and the Cochrane Library was conducted, identifying nine studies. Results: Findings related to the benefit of statin use for the prevention of variceal bleeding were inconsistent among study designs. Retrospective studies suggest a lower incidence of VB among statin users compared to non-users. However, this finding has not been borne out in prospective studies. Conclusions: Given the conflicting findings, there is insufficient evidence at present to suggest the routine use of statins for the prevention of variceal bleeding in patients with cirrhosis. Full article

Oxidative stress biomarkers are elevated in liver cirrhosis, but their clinical utility for severity staging and complication prediction remains uncertain. This retrospective single-centre study enrolled 90 patients with decompensated cirrhosis (Child–Pugh classes B and C) to evaluate serum malondialdehyde (MDA) and 8-isoprostane (8-isoPGF2α) as predictors of Child–Pugh severity, severe ascites, and severe hepatic encephalopathy, and to quantify their incremental value within supervised machine learning models. Four algorithms—logistic regression, Random Forest, Gradient Boosting, and Support Vector Machine—were evaluated using stratified 10-fold cross-validation; logistic regression models with and without oxidative stress biomarkers were compared for the prediction of ascites and encephalopathy. Routine biochemical parameters effectively discriminated Child–Pugh class B from C, with machine learning models achieving AUC-ROC values of 0.921–0.972. Neither MDA nor 8-isoPGF2α differed between Child–Pugh classes or across ascites categories, and both failed to improve ascites prediction (ΔAUC = −0.015). For severe hepatic encephalopathy, the extended model showed modest but consistent improvements in accuracy (+3.4 percentage points), sensitivity (+6.4%), and model fit, suggesting an outcome-specific complementary role consistent with the established involvement of lipid peroxidation in ammonia neurotoxicity. These findings support the use of machine learning for automated cirrhosis severity classification and indicate that oxidative stress biomarkers hold selective relevance for hepatic encephalopathy rather than global disease staging. Full article

Background/Objectives: Cirrhosis is characterized by a fragile and unstable hemostatic balance, predisposing patients to both hemorrhagic and thrombotic complications, particularly in the context of chronic liver disease (CLD). This dual risk presents significant challenges for clinical management and complicates therapeutic decisions. The objective of this study was to evaluate coagulation profiles in cirrhotic patients and their association with bleeding and thrombotic events, with the aim of identifying predictors of hemostatic complications. Methods: A retrospective study was conducted on patients with cirrhosis admitted to a tertiary liver transplant center between February 2022 and March 2024. Inclusion criteria required the availability of extended coagulation data in medical records. Demographic, clinical, and laboratory parameters were collected and analyzed to assess associations with thrombotic events and upper gastrointestinal bleeding (UGIB). Results: Fifty-nine patients met the inclusion criteria (mean age 53.4 ± 10.3 years), of whom 62.7% were male. UGIB occurred in 18.6% of patients, thrombotic events in 20.3%, and portal vein thrombosis in 16.9%. Routine coagulation parameters, including international normalized ratio (INR) and activated partial thromboplastin time (APTT), did not demonstrate significant predictive value for either bleeding or thrombotic events. Conclusions: Patients with cirrhosis are simultaneously at risk for both bleeding and thrombosis, reflecting the fragile and complex nature of hemostatic regulation in advanced liver disease (ALD). Standard laboratory coagulation tests are inadequate for accurate risk stratification in this setting. These findings highlight the limitations of conventional coagulation tests and support the need for further studies evaluating advanced hemostatic assessment tools in patients with cirrhosis. Full article

Background: Clostridioides difficile infection (CDI) remains a leading cause of hospital-acquired infection. Metabolic-dysfunction-associated steatotic liver disease (MASLD) is the most common chronic liver disease worldwide and has been associated with increased infectious susceptibility. However, whether non-cirrhotic MASLD independently worsens inpatient CDI outcomes and whether this differs across the MASLD spectrum remain unclear. Methods: We conducted a retrospective cohort study using the National Inpatient Sample (NIS) 2017–2023, identifying adult hospitalizations with a principal diagnosis of CDI. Patients with cirrhosis and alcoholic liver disease were excluded. Propensity score matching (1:1) was performed for the primary MASLD vs. non-MASLD comparison in the principal-diagnosis CDI cohort. To evaluate whether outcomes differ across the MASLD spectrum, survey-weighted multivariable logistic regression was used to compare K76.0-coded (MASLD without steatohepatitis) and K75.81-coded (MASH) hospitalizations against non-MASLD/MASH hospitalizations within the principal-diagnosis CDI cohort. The primary outcome was in-hospital mortality; secondary outcomes included complications, healthcare utilization, and discharge disposition. Results: The principal-diagnosis CDI cohort comprised 76,103 discharges (weighted ~380,515). MASLD prevalence among non-cirrhotic CDI hospitalizations nearly doubled from 1.98% in 2017 to 3.74% in 2023 (OR per year 1.089; p < 0.001). After propensity score matching (1756 pairs), MASLD was not associated with significantly higher in-hospital mortality (OR 1.252; p = 0.574) or most adverse outcomes, but was associated with lower odds of non-routine discharge (OR 0.794; p = 0.003). In the matched utilization analysis, length of stay and total charges were not significantly different, although the adjusted pre-match analysis showed higher charges among MASLD hospitalizations (+$4431; p = 0.001). Within the same principal-diagnosis cohort, K76.0-coded MASLD (n = 1988) was associated with lower odds of acute kidney injury (aOR 0.821; p = 0.004) and non-routine discharge (aOR 0.805; p = 0.001). K75.81-coded MASH (n = 197) was independently associated with higher in-hospital mortality (aOR 2.840, 95% CI 1.154–6.985; p = 0.023) and peritonitis (aOR 4.136, 95% CI 1.543–11.082; p = 0.005), although confidence intervals were wide and the number of MASH-coded hospitalizations was modest. Conclusions: The prevalence of MASLD among CDI hospitalizations is rising. Non-cirrhotic MASLD without steatohepatitis does not independently worsen inpatient CDI outcomes after adjustment, whereas K75.81-coded MASH may identify a higher-risk subgroup with increased mortality and peritonitis, pending confirmation in larger cohorts. These findings suggest that hepatic inflammatory activity, rather than steatosis alone, may drive adverse CDI outcomes and support further investigation of MASLD phenotyping in CDI risk stratification. Full article

Background: Liver diseases are an increasing public health concern in Morocco; reliable national population-based estimates of liver fibrosis and cirrhosis in Morocco are currently unavailable. Existing evidence is largely limited to selected high-risk groups and hospital-based cohorts. Generating reliable prevalence data is crucial for designing evidence-based screening pathways, targeting high-risk groups and informing prevention and treatment policies. Objectives: Our aim was to comprehensively review studies on the prevalence of liver fibrosis and cirrhosis in Morocco, focusing on characterizing study populations, specifically high-risk populations and hospital-based cohorts, diagnostic methods and thresholds used. The review also summarizes hospital-based cirrhosis cohorts without merging them with prevalence estimates, and identifies gaps in the literature, particularly the absence of population-based prevalence studies and national epidemiological data in Morocco. Methods: The study systematically reviewed literature up to 26 October 2025, including studies conducted in Morocco among high-risk populations or hospital-based cirrhosis cohorts, using multiple databases. Two reviewers independently screened and extracted data, assessing bias with the Joanna Briggs Institute (JBI) checklist. Due to heterogeneity in study populations and diagnostic approaches, a narrative synthesis was performed. Hospital-based cohorts were analyzed separately to provide contextual information and were not included in prevalence estimates. Results: From 1198 records, four Moroccan studies providing prevalence data on liver fibrosis and cirrhosis were included, primarily involving patients with hepatitis C, HIV, or rheumatoid arthritis. Additionally, three hospital-based cirrhosis cohorts were incorporated for a contextual analysis of disease severity and complications. In total, seven studies were included, with prevalence and hospital-based data analyzed separately to ensure clarity. Conclusions: Current evidence on liver disease in Morocco is limited but suggests a significant burden among high-risk groups. The findings highlight major gaps in national epidemiological data and underscore the urgent need for comprehensive nationwide data and improved diagnostic tools to guide effective screening, prevention, and resource allocation. Full article

Background and Objectives: Acute or severe limb ischemic events are limb- and life-threatening complications of peripheral artery disease (PAD). Although cirrhosis is increasingly recognized as a systemic disorder associated with endothelial dysfunction, inflammation, and altered hemostatic balance, its relationship with coding-defined limb ischemic events among individuals with PAD remains poorly defined. We investigated whether cirrhosis is independently associated with coding-defined acute or severe limb ischemic events among hospitalized adults with PAD. Materials and Methods: We performed a retrospective discharge-level analysis of the National Inpatient Sample from 2016 to 2018. Adult hospitalizations with PAD were identified using ICD-10-CM diagnosis codes and stratified according to the presence or absence of cirrhosis. The primary outcome was coding-defined acute or severe limb ischemic events. Multivariable logistic regression was used to evaluate the association between cirrhosis and acute or severe limb ischemic events after adjustment for demographic and cardiovascular comorbidities. Propensity-score matching was additionally performed to balance baseline characteristics between hospitalizations with and without cirrhosis. Results: Among 276,702 hospitalizations with PAD, 5942 had cirrhosis. Before matching, cirrhosis was independently associated with higher odds of acute or severe limb ischemic events after multivariable adjustment (odds ratio [OR] 1.47, 95% confidence interval [CI] 1.35–1.60; p < 0.001). After 1:1 propensity-score matching, 5883 matched pairs were analyzed. The association between cirrhosis and acute or severe limb ischemic events persisted in the matched cohort, with cirrhosis remaining significantly associated with increased odds of these events (OR 1.41, 95% CI 1.24–1.60; p < 0.001). Conclusions: In this large discharge-level analysis of hospitalizations with PAD, cirrhosis was independently associated with higher odds of coding-defined acute or severe limb ischemic events. These findings suggest that cirrhosis may represent an underrecognized vascular risk amplifier in PAD. Further prospective studies are needed to validate this association, clarify underlying mechanisms, and determine whether cirrhosis may improve PAD risk stratification. Full article

Biliary atresia (BA) is the leading indication for pediatric liver transplantation. In the absence of surgical treatment, BA progresses rapidly toward hepatic fibrosis and cirrhosis. Although liver biopsy remains the gold standard for histological evaluation, its utility is limited by invasiveness, associated risks, and sampling variability. These limitations have spurred the development and validation of noninvasive tools to evaluate liver fibrosis in this patient population. Multiple imaging techniques have been developed to assess liver fibrosis and cirrhosis. In recent years, additional BA-related biomarkers have been identified, showing significant potential for diagnosis, assessment of fibrosis severity, and prediction of native liver survival outcomes. This article reviews the roles and potential clinical applications of the following biomarkers: matrix metalloproteinase-7 (MMP-7), fibroblast growth factor 19 (FGF-19), interleukin-33 (IL-33), clusterin, and osteopontin. Further research is needed to confirm the utility of these prognostic biomarkers in predicting and improving outcomes in BA. Full article

Small intestinal bacterial overgrowth (SIBO) refers to an abnormal increase in the number of bacteria in the small intestine and is observed in various diseases. SIBO can also develop after long-term use of proton pump inhibitors (drug-induced SIBO), bariatric surgery, gastrectomy, and other surgeries (postoperative SIBO). The aim of this narrative review is to summarize all of the published information on the treatment of SIBO in as much detail as possible and present it separately for each specific disease and intervention associated with SIBO. The most extensively studied drug for the treatment of SIBO is rifaximin. It eliminates SIBO in 63% of cases; however, most studies lack a control group. Small RCTs assessing the effects of this antibiotic on SIBO have reported conflicting results, and a meta-analysis showed no effect. A large RCT is required to verify the results of uncontrolled studies. Neomycin and norfloxacin showed efficacy in the treatment of SIBO in single RCTs, with elimination rates of 20 and 100%, respectively. Ciprofloxacin, rifamycin, metronidazole, and other antibiotics, as well as ursodeoxycholic acid, showed positive effects for the treatment of SIBO, but only in uncontrolled studies or in comparison with rifaximin or other drugs. The reported elimination rates were 54%, 67%, 79%, and 75%, respectively. Eradication therapy for Helicobacter pylori infection eliminated SIBO at a rate of approximately 70%. Probiotics have been tested for treatment of SIBO in various diseases. VSL#3 and Saccharomyces boulardii CNCM I-745 were effective in RCTs, with elimination rates of 58% and 80%, respectively. In conclusion, when selecting SIBO treatment regimens, those that have demonstrated the greatest efficacy for a specific concomitant disease should be preferred, despite the generally low level of evidence supporting these approaches in most cases. Full article

Background: Chronic hepatitis B virus (HBV) infection remains a major global health challenge and a leading cause of liver cirrhosis and hepatocellular carcinoma. Interleukin-6 (IL-6), a key pro-inflammatory cytokine, plays an important role in immune regulation and hepatic inflammation. However, its relationship with HBV viral load and disease severity remains incompletely understood. Methods: A hospital-based cross-sectional study was conducted among 293 HBsAg-positive patients. Serum IL-6 levels were measured using ELISA, and HBV DNA was quantified using real-time quantitative PCR. Patients were stratified according to viral load. Statistical analyses included non-parametric tests, Spearman correlation, principal component analysis (PCA), and multiple linear regression. Results: The median age was 45 years (IQR: 34–57), among which 54.6% were male. The median HBV DNA was 3.37 log₁₀ IU/mL (IQR: 2.45–3.75), and IL-6 concentration was 2.38 log₁₀ pg/mL (IQR: 2.21–2.49). IL-6 levels increased significantly across viral load categories (p < 0.001) and were higher in HBeAg-positive patients (p = 0.002), with no significant differences across age, sex, or cirrhosis. IL-6 levels correlated with HBV DNA (r = 0.40, p < 0.001). PCA identified distinct viral-inflammatory and biochemical axes. Regression analysis confirmed HBV DNA as the significant independent predictor (β = 0.461, p < 0.001; adjusted R² = 0.206). Conclusion: IL-6 was closely associated with HBV DNA levels, while the association with conventional biochemical markers of hepatocellular injury was significantly less in this cohort, suggesting that IL-6 may serve as an adjunct biomarker of disease activity in patients with chronic hepatitis B. Full article

Background/Objectives: Recompensation in patients with decompensated cirrhosis has significant prognostic implications. In this study, we aimed to evaluate the incidence and predictors of recompensation in cirrhotic patients, specifically focusing on elucidating the influence of sarcopenia and visceral obesity on achieving recompensation in a cohort of decompensated individuals. Methods: We conducted a retrospective analysis of 195 patients with decompensated cirrhosis from 2021 to 2024. Body composition abnormalities were determined by the skeletal muscle index (SMI) and visceral-to-subcutaneous adipose tissue ratio (VSR) on computed tomography (CT), respectively. Factors related to recompensation, defined using the modified Baveno VII criteria, were identified using multivariate regression. Results: Patients who achieved recompensation exhibited a lower age (62 vs. 67, p < 0.05), a higher body mass index (22.8 vs. 21, p < 0.01), a lower aspartate aminotransferase level (32 vs. 39, p < 0.01), a higher albumin level (35.2 vs. 32.3, p < 0.01), a lower ascites prevalence (60% vs. 74.07%, p < 0.05), a lower Child–Pugh score (6 vs. 7, p < 0.01), and a lower End-Stage Liver Disease score (9 vs. 10, p < 0.05) compared to those with non-recompensated cirrhosis. Body composition abnormalities were significantly more prevalent in non-recompensated patients than in recompensated patients (77.04% vs. 63.33%, p < 0.05), mainly because of a significantly higher prevalence of combined sarcopenia and visceral obesity in non-recompensated individuals (28.29% vs. 6.67%, p < 0.01). Multivariate analysis indicated that combined sarcopenia and visceral obesity was the sole independent risk factor for non-recompensation in this population. Furthermore, in the subgroup of patients aged < 70 years, with normal weight and preserved liver function, differences in recompensation rates among various states of body composition abnormalities were more pronounced. Conclusions: Sarcopenic visceral obesity is an independent risk factor for non-recompensation in patients with decompensated cirrhosis, highlighting the need for targeted interventions to mitigate body composition abnormalities in this vulnerable population. Full article

Chronic infection with the hepatitis C virus (HCV) is the most significant risk factor for the development of hepatocellular carcinoma (HCC). It has been shown that the progression of HCV-related liver disease is mediated by both viral and host-specific factors. The HCV replication cycle is a host-dependent process that relies on intracellular signalling pathways within target cells. Thus, intracellular signal transduction plays a pivotal role in the modification of interactions between the host and HCV. These pathways are key regulators of liver diseases, including cirrhosis and HCC. In addition, HCV induces epigenetic modifications in the host genome that inhibit the expression of various tumour-suppressor genes. Some of these changes persist even after successful antiviral treatment and represent a continued risk for HCC development. Despite significant progress in the management of chronic HCV infection, this challenge remains unresolved. In this narrative review, we summarise the mechanisms of HCV-induced disease progression, focusing on the host immune response, the regulatory roles of viral and cellular proteins, and viral survival strategies during chronic infection. We also discuss HCV-induced epigenetic alterations that contribute to hepatocarcinogenesis both during infection and after viral clearance. These insights are important for identifying novel, reliable molecular biomarkers for patient surveillance and for designing new therapeutic approaches. Full article