Abstract Background Hepatitis B virus (HBV) infection is a primary global public health concern since it is commonly recognized as the primary risk factor for cirrhosis and liver cancer globally. This study aims to evaluate the level of knowledge and the prevailing attitudes of Jordanian nursing students toward hepatitis B, with a particular focus on identifying knowledge gaps and factors influencing their understanding and perceptions. Materials and methods A descriptive design was employed to collect data from December 1, 2023, to April 1, 2024. A self-administered questionnaire was used to conduct convenience sampling among senior Jordanian nurses. Result A total of 455 participants were analyzed, revealing a young cohort with a mean age of 22.5 years. The participants demonstrated moderate knowledge of hepatitis B, with specific misconceptions identified. Besides, participants demonstrated a moderately positive attitude toward hepatitis B. However, demographic characteristics showed significant differences in knowledge by sex, whereas certain factors did not. Still, attitudes significantly differed based on those infected with hepatitis B and family members infected with hepatitis B. Conclusion This study focused on training and awareness programs to enhance knowledge and foster a positive attitude towards hepatitis B amongst nursing students. Moreover, combining these training and awareness activities would help improve hospital safety protocols in Jordan and ensure that a hepatitis B virus outbreak is averted.

Abstract Gallstone disease is a widespread health issue driven by genetic, metabolic, and environmental factors. Among its types, pigment stones, primarily composed of bilirubin, arise due to disruptions in bilirubin metabolism. Heme degradation produces biliverdin, which is reduced to unconjugated bilirubin and transported to the liver. There, UGT1A1 conjugates bilirubin, making it water-soluble for excretion into bile. However, genetic variations, impaired hepatic processing, altered enterohepatic recycling, and gut microbiota imbalances can lead to bilirubin supersaturation, increasing the risk of gallstone formation. Conditions like haemolysis, liver dysfunction, and chronic biliary infections further promote bilirubin precipitation and stone development. This review examines the molecular and genetic regulation of bilirubin metabolism, the role of gut microbiota in bile metabolism, and their contributions to gallstone pathogenesis. Recent advancements in therapeutic strategies, including bile composition modulation, microbiome interventions, and nanoparticle-based drug delivery, present promising approaches for gallstone prevention and treatment. Understanding these mechanisms is crucial for developing novel diagnostic and therapeutic solutions for gallstone-related disorders.

Abstract Background Neonatal jaundice is one of the most prevalent illnesses in neonates, requiring care and treatment. Fenofibrate is a lipid-lowering drug that enhances the conjugation and excretion of bilirubin. Previous studies have suggested the usefulness of fenofibrate for the treatment of indirect hyperbilirubinemia in neonates. Objective To evaluate the role of fenofibrate in neonates with neonatal jaundice near the level of phototherapy. Patients and Methods seventy- five full-term infants with neonatal jaundice near the level of phototherapy were randomly divided into three groups: single-dose group: 25 neonates received a single oral dose of 10 mg/kg of non-micronized fenofibrate and an oral dose of an equivalent amount of distilled water as a placebo. Double-dose group: 25 neonates received two oral doses of 10 mg/kg non-micronized fenofibrate. The control group included 25 neonates who received two oral doses of an equivalent amount of distilled water as a placebo. Results The double-dose group had the highest significant drop in transcutaneous bilirubin (TCB) starting from 12 to 48 h after drug intake and the highest drop in total serum bilirubin (TSB) starting from 12 h to the 5th day in comparison to the single-dose group and the controls. The single-dose and double-dose groups had a significantly lower incidence of the need for admission and phototherapy than the control group ( P = 0.009). The double-dose group had a significantly higher incidence of drug side effects than the single-dose group ( P < 0.001), mainly in the form of abdominal distension (P = 0.008); however, only minor treatment was required. Conclusion Fenofibrate can significantly decrease bilirubin levels in full-term neonates with neonatal jaundice near the level of phototherapy, with no need for admission and phototherapy management. The drug was well-tolerated and safe. Double-dose treatment with fenofibrate significantly lowered TSB with no significant increase in side effects when compared to the single-dose group.

Abstract Background The introduction of direct-acting antiviral drugs (DAAs) could safely eliminate the hepatitis C virus (HCV). Steatosis and fibrosis regression after HCV treatment could occur with subsequent improvement in the portal pressure. However, a subgroup of patients is still at risk of variceal bleeding from persistent clinically significant portal hypertension (CSPHT). Recognition of these patients, hence continuous screening, is clinically relevant. In resource-limited areas, the availability of noninvasive, simple markers to identify at-risk patients will help avoid gastroscopy. We aimed to investigate the utility of liver stiffness measurement (LSM) and the portal vein congestion index (PVCI) as noninvasive markers to identify subgroups of patients who need follow-up after HCV elimination. Patients and methods Retrospectively, we included 181 patients who received DAAs for HCV and achieved sustained virologic response. After 5 years of follow-up, we evaluated baseline parameters that could predict variceal bleeding. Baseline clinical and laboratory data, including baseline LSM and PVCI, were included. Patients were followed for 5 years for the occurrence of variceal bleeding. Results The ROC analysis revealed that at a cutoff level ≥ 0.563, PVCI could identify patients who experienced variceal bleeding with a 91.8% sensitivity, 90.9% specificity, and 79% PPV. Patients with PVCI ≥ 0.563 and LSM ≥ 21.2 kPa had a shorter interval before variceal bleeding. Cox regression analysis identified baseline CTP, PVCI, and LSM as the only significant independent predictors of variceal bleeding in the study population. Conclusions Although HCV treatment ameliorates liver pathology and may regress PHT, it may give “false assurance” to a subset of patients who are still at risk of variceal bleeding and require close follow-up to avoid devastating variceal rupture. Noninvasive identification and stratification of these patients can be achieved by integrating PVCI and LSM into the management strategy.

Abstract Background Liver cirrhosis (LC) represents the terminal stage of diverse chronic hepatic disorders and is characterized by substantial morbidity and mortality. Early identification of hepatic dysfunction is critical, especially during the compensated phase when clinical signs are often absent. Kallistatin (KAL), a liver-derived serine proteinase inhibitor, has demonstrated anti-inflammatory and anti-fibrotic properties and may serve as a biomarker of hepatic functional reserve. This investigation aims to evaluate serum KAL level as a biomarker for assessment of liver function status in cirrhotic cases. Results Serum KAL levels were significantly lower in cases (13.81 ± 4.56 ng/mL) compared to controls (57.93 ± 7.47 ng/mL, P < 0.001). KAL negatively correlated with spleen size ( r = –0.230, P = 0.029), ascites grade ( r = –0.235, P = 0.042), and varices grade ( r = –0.301, P = 0.009), and positively correlated with Hemoglobin (Hb) ( r = 0.623, P < 0.001), platelets ( r = 0.640, P < 0.001), and albumin ( r = 0.651, P < 0.001). Multivariate regression showed KAL as an independent predictor of albumin (β = 0.028, P = 0.03), total bilirubin (β = –0.13, P < 0.001), Alanine Aminotransferase (ALT) (β = –8.059, P = 0.004), and Aspartate Aminotransferase (AST) (β = –10.551, P = 0.005). Conclusions Serum KAL levels are substantially reduced in LC cases and show strong associations with both clinical and biochemical indicators of liver function.

Abstract Background Liver fibrosis and cirrhosis require accurate, noninvasive diagnostic methods. Deep learning-enhanced magnetic resonance imaging (MRI) modalities, including T2-weighted imaging, gadoxetic acid-enhanced MRI, and magnetic resonance elastography (MRE), have shown promise in improving diagnostic accuracy. Objective To systematically review and evaluate the diagnostic accuracy of deep learning-enhanced MRI modalities for liver fibrosis and cirrhosis detection, using liver biopsy as the reference standard, and to perform a meta-analysis of the diagnostic accuracy. Methods A systematic search was conducted across multiple databases (PubMed, Cochrane Library, Embase, Scopus, Google Scholar, and IEEE Xplore). Studies reporting diagnostic accuracy metrics (sensitivity, specificity, area under the receiver operating characteristic (AUROC)) for deep learning-based MRI modalities in adults with chronic liver disease were included. A meta-analysis was performed for the studies providing sufficient data. Results Seven studies with 6,547 participants were included. MRE-based approaches exhibited the highest diagnostic accuracy (AUROC: 0.759–0.93). A meta-analysis of three studies with liver biopsy as the reference standard showed high sensitivity (0.80–0.91) and specificity (0.79–0.90), but model non-convergence prevented pooled estimates. Conclusion Deep learning-enhanced MRI, particularly MRE, shows promise for noninvasive detection of liver fibrosis and cirrhosis. Despite promising individual results, further validation, standardized protocols, and larger studies are needed to confirm its clinical utility.

Abstract Introduction Hyperuricemia is frequently reported to be associated with metabolic dysfunction-associated steatotic liver disease (MASLD). This study aimed to assess the effect of xanthine oxidase (XO) inhibitors on metabolic parameters in MASLD. Methods A systematic search of databases including MEDLINE, ProQuest, Google Scholar, ScienceDirect, and Cochrane Library was conducted, focusing on preclinical and clinical studies relevant to XO inhibitors in MASLD. The Joanna Briggs Institute (JBI) critical appraisal tools were used for quality assessment in clinical studies, while the Systematic Review Centre for Laboratory Animal Experimentation (SYRCLE)’s risk-of-bias tool was used in preclinical studies. The meta-analysis was performed using Review Manager 5.4 to compute summary estimates for standardized mean differences (SMDs). Results A total of eight studies were included in the review and seven in the meta-analysis. Significant differences in alanine aminotransferase (ALT), aspartate aminotransferase (AST), and triglycerides (TG) were found in preclinical settings of MASLD animal models treated with XO inhibitors compared to controls. Meanwhile, in clinical settings, the serum uric acid (SUA) decreased significantly after treatment with febuxostat (SMD = 2.28, 95% CI: 0.76, 3.8, p = 0.003); however, there were no significant differences in liver enzymes, including AST and ALT (SMD = 0.05, 95% CI: −0.23, 0.32, p = 0.73). Both XO inhibitors had similar effects on liver enzymes and SUA in MASLD patients (SMD = 0.01, 95% CI: −0.40, 0.42, p = 0.96; SMD = −0.03, 95% CI: −0.39, 0.33, p = 0.87, respectively). Conclusions While XO inhibitors have shown efficacy in preclinical models, clinical evidence is limited. Febuxostat and allopurinol have produced comparable effects on liver enzymes and serum uric acid (SUA), but differences in patient selection criteria reduce the comparability of findings.

Abstract Background Malnutrition is a common and serious complication in patients with liver cirrhosis, contributing to increased morbidity and mortality. Despite the high prevalence of nutritional deficits in this population, dietary guidance remains inconsistent across clinical practice. Objective This review aims to synthesize current evidence and nutritional society guidelines to clarify optimal dietary practices for patients with cirrhosis and translate these findings into actionable, patient-centered dietary recommendations. Methods We reviewed and integrated data from over 50 primary studies and position statements from ESPEN, AASLD, and INASL. Each macronutrient category was examined with respect to its impact on outcomes such as hepatic encephalopathy, sarcopenia, hospitalization risk, and survival. Where guidelines lacked clarity, primary literature was used to fill critical gaps. Practical recommendations were consolidated into a summary table and accompanying educational infographic for patients. Results Optimal protein intake for cirrhotic patients is 1.2–1.5 g/kg/day, including animal protein if plant-based options are poorly tolerated. Long-term BCAA supplementation improves nitrogen balance and may reduce cirrhosis-related complications. Carbohydrates should comprise 50–60% of total caloric intake, with late-evening snacks providing 50–100 g of carbohydrates shown to reduce overnight catabolism, preserve muscle mass, and improve quality of life. Whole grains, fruits, vegetables, and fermented dairy products enhance gut microbial diversity, which is associated with reduced hospitalization rates. Sodium should only be restricted in patients with ascites; routine restriction in stable patients may lead to malnutrition. Micronutrient supplementation, including thiamine, zinc, and vitamin D, should be targeted based on clinical risk factors and lab parameters. Conclusion This review translates current evidence and clinical guidelines into a practical, food-based framework to support nutritional counseling for patients with liver cirrhosis. The findings are summarized in a visual patient handout to help bridge the gap between evidence-based nutrition and real-world dietary behavior.

Abstract Chronic liver disease (CLD) remains a major global health concern, necessitating robust experimental models for advancing research and therapy development. This review highlights the crucial role of both animal and in vitro models in elucidating disease mechanisms and identifying therapeutic targets. Key findings highlight that while chemically and drug-induced animal models effectively replicate aspects of human liver pathology, their translational relevance varies depending on the disease context. In vitro models, particularly 3D cultures and microfluidic systems, are rapidly evolving to mimic the liver’s complex microenvironment better, improving drug screening and mechanistic studies. The review highlights that an integrative approach—combining suitable animal models and advanced in vitro models—offers the greatest potential for understanding CLD progression and accelerating the development of effective, targeted treatments. This comprehensive review covers animal and in vitro models of chronic liver diseases.