This study evaluated the relationship between cholestatic biomarkers and pruritus severity, as well as the impact of pruritus on quality of life in patients with biliary obstruction. A cross-sectional observational study enrolled 110 patients: Group A, patients with calcular biliary obstruction, and Group B, patients with malignant biliary obstruction. Demographic, clinical, and laboratory data were collected, including cholestatic biomarkers, a visual analogue scale score, and a five-dimensional (5D) pruritus scale, which were used to assess pruritus severity, and the 36-item Short Form-36 health survey was used to evaluate the impact of pruritus on quality of life. Patients with malignant biliary obstruction (group B) presented with more advanced clinical manifestations than those with calcular biliary obstruction (group A), including greater weight loss, pruritus, hepatomegaly, higher bilirubin levels, more advanced imaging findings, and significantly higher pruritus severity scores. Pruritus severity correlated positively with bilirubin levels and negatively with health-related quality of life (HRQOL), particularly in group B. In contrast, higher GGT levels and GGT/direct bilirubin ratios were consistently observed in non-pruritic patients and showed a strong inverse correlation with pruritus severity. Overall, malignant obstruction and pruritus were linked to greater biochemical derangement and substantial impairment in physical and mental health-related quality of life. Pruritus was more frequent and severe in malignant biliary obstruction and was strongly associated with impaired quality of life. GGT and the GGT/direct bilirubin ratio showed a strong negative correlation with pruritus severity, highlighting a potential inverse association with the severity of pruritus.
Hepatocellular carcinoma (HCC) remains one of the leading causes of cancer-related mortality worldwide, largely due to delayed diagnosis and limited availability of reliable non-invasive biomarkers for early disease detection. Circulating microRNAs have emerged as promising minimally invasive molecular indicators because of their remarkable stability in serum and their involvement in liver tumor biology. This study aimed to evaluate the expression patterns and potential clinical relevance of circulating miRNA-122 and miRNA-223 across different TNM stages of HCC in Egyptian patients and to explore their association with molecular mediators of angiogenesis, apoptosis, and autophagy. A total of 200 participants were enrolled, including 50 healthy controls and 150 patients with stage I–III HCC. Serum expression of miRNA-122 and miRNA-223 was quantified using quantitative real-time PCR, while AFP-L3, MAPK14, AKT1, vascular endothelial growth factor (VEGF), caspase-8, and beclin-1 were determined by ELISA. Circulating miRNA-122 expression was significantly increased in all HCC groups compared with controls, with the highest levels observed in stage III disease, indicating a clear stage-dependent upregulation pattern. In contrast, miRNA-223 expression was significantly reduced across all HCC stages, with the lowest levels detected in advanced-stage tumors. These expression changes were accompanied by significant increases in MAPK14, AKT1, VEGF, AFP-L3, liver enzymes, and bilirubin levels, together with significant reductions in caspase-8 and beclin-1, reflecting progressive enhancement of proliferative, angiogenic, and anti-apoptotic signaling pathways during HCC progression. Histopathological findings further confirmed the progressive architectural and cytological deterioration across TNM stages. Circulating miRNA-122 and miRNA-223 exhibit distinct and stage-dependent expression signatures in Egyptian patients with HCC, supporting their potential utility as minimally invasive biomarkers associated with HCC and TNM stage. Their integration with AFP-L3 and key molecular mediators of tumor progression may provide a clinically relevant biomarker panel for improving HCC diagnosis and monitoring in hepatology practice.
Abstract Hepatocellular carcinoma is the most common primary liver cancer and the sixth leading cause of death worldwide. HCC incidence numbers are constantly increasing in Pakistan and are mainly caused by chronic HBV and HCV associated cirrhosis. Two Pakistani population-based studies reported that the frequency of HCV induced HCC was high compared to HBV and alcohol-induced HCC. In Pakistan, the reported incidence of alcohol-induced HCC is very low. Therefore, the number of alcohol-induced HCC cases is deficient. Literature was searched using ScienceDirect, PubMed, Google Scholar, Springer, and BMC. Pakistani population studies based on HBV induced HCC, HCV induced HCC, HBV + HCV co-infection induced HCC, and alcohol induced HCC were included. A total of 98 studies on HCC were included; among them, 32 were related to HCV induced HCC, 20 were related to HBV induced HCC, 20 were associated with HBV + HCV co-infection induced HCC, and 6 were related to alcohol induced HCC. We further investigated that surgery and radiotherapy are the primary treatments for HCC in Pakistan, with surgery being the most frequently applied treatment in 1820 cases. We conducted this systematic review to highlight the current status of HCC in Pakistan. We found that HCC is most commonly caused by HCV infection compared to HBV infection and alcoholism.
Hepatocellular carcinoma (HCC) is the most common primary liver cancer. The most successful treatment for liver tumors is still hepatic resection; however hepatic resection hemorrhage remains a key factor determining outcome. Recent attempts have been made to perform bloodless hepatic resections. Our work included 96 participants with liver cirrhosis and HCC who were admitted to the department of hepato-pancreato-biliary surgery and the University Hospital. The mass with safety margin was determined by intraoperative ultrasound, and the resection line was marked preceding the application of Habib TM 4X. The mean time of operation was 113.4 min (ranging from 60 to 170), while the mean time of parenchymal transection was 40 (range 25–70 min). The mean amount of blood lost was 300 cc (range 50 to 1200 cc), while the average blood loss amount during parenchymal resection was found to be 150 cc (range 5 to 1100 cc). The mean amount of blood transfusion was 0.31 units of blood (range: 0–2), while prior to and following the procedure, the average hemoglobin levels were 13.1 and 12.23 mg/dl, respectively. This technique provides clear benefits by reducing anesthesia duration, operative time, and intraoperative blood loss, which are beneficial to both patients and surgical teams. As a result of the lessened physiological stress on the patient, liver resection becomes a safer treatment, requiring fewer critical care resources and resulting in lower postoperative morbidity and mortality.
Hepatocellular carcinoma (HCC) remains a major cause of cancer-related mortality worldwide. The limitations of alpha-fetoprotein (AFP) as a diagnostic biomarker have prompted the search for novel markers. Fibroblast growth factor-19 (FGF19) is involved in hepatocarcinogenesis and may also reflect tumor aggressiveness. Portal vein thrombosis (PVT) is a clinically important complication of HCC that is associated with advanced disease, limited therapeutic options, and poor prognosis. This study aimed to evaluate the diagnostic performance of serum FGF19 in HCC and to investigate its association with aggressive tumor features, particularly PVT. This comparative cross-sectional study was conducted between March 2023 and June 2024 and included 90 patients: 60 patients with newly diagnosed, treatment-naïve HCC and 30 patients with liver cirrhosis. Serum FGF19 and AFP levels were measured. Diagnostic performance was assessed using receiver operating characteristic (ROC) curve analysis. Factors associated with PVT were evaluated using univariate and multivariate logistic regression analyses. Serum FGF19 levels were significantly higher in the HCC group than in the cirrhosis group (median 133.4 pg/mL vs. 63.0 pg/mL, p < 0.001). FGF19 distinguished HCC from cirrhosis with excellent accuracy (AUC = 0.964; 95
Portal vein thrombosis (PVT) is an important cause of portal hypertension in the pediatric age group with high morbidity rates due to its main complication—the upper gastrointestinal varices and hypersplenism. No identifiable cause can be found in more than half of the cases of extrahepatic portal vein obstruction (EHPVO). Thrombophilia is incriminated in 35
Hepatocellular carcinoma (HCC) is a lethal malignancy with limited prognostic biomarkers. This study aimed to develop an RNA methylation-related long non-coding RNA (lncRNA) signature to predict survival and guide therapy in HCC. Transcriptomic and clinical data from 374 HCC tissues (TCGA) were analyzed. RNA methylation-related lncRNAs were identified (Pearson correlation, |cor|> 0.4, p < 0.001). A prognostic signature was constructed using univariate Cox and LASSO regression. Patients were stratified into high-/low-risk groups, validated for survival, immune infiltration, and drug response. A robust three-lncRNA signature (SNHG30, AL049840.5, NRAV) was established. High-risk patients showed significantly worse overall survival (p < 0.001) and progression-free survival (p < 0.001) compared to low-risk patients. The risk score emerged as an independent prognostic factor (multivariate Cox, p < 0.001) with strong predictive accuracy (1-/3-/5-year AUCs: 0.717/0.686/0.682). Functional analysis revealed distinct biological pathways between risk groups, with high-risk tumors associated with cell cycle dysregulation and immune suppression (higher TIDE scores), while low-risk tumors exhibited metabolic pathway activation. Drug sensitivity analysis suggested differential responses to chemotherapy and targeted therapies between risk groups. Our study developed and validated a clinically applicable RNA methylation-related lncRNAs signature that effectively predicts HCC prognosis and therapeutic response. This signature provides valuable insights for risk stratification and may guide personalized treatment decisions in HCC management.
Several metabolic disorders have been linked to chronic hepatitis C virus (HCV) infection, especially HCV related hepatic steatosis, insulin resistance, and lipid dysregulation. We aimed at comparing the effects of treatment of HCV direct-acting antivirals (DAAs) alone versus DAAs combined with metformin or lifestyle modifications on improving glycemic control and reducing hepatic steatosis in prediabetic patients chronically infected with HCV. We enrolled 150 chronic HCV-infected patients with confirmed diagnosis of prediabetes [glycosylated hemoglobin (HbA1c) = 5.7–6.4
Abstract Background Metabolic dysfunction-associated steatotic liver disease has emerged as the most prevalent liver disease with a rapidly increasing incidence worldwide. Targeting mitochondria in this condition opens up innovative avenues for the development of new therapeutic molecules. Mitochondrial dysfunction potentially influences the pathways of this disease and facilitates lipid accumulation and inflammation in hepatocytes, which can be targeted and reversed in the liver. Main body Mitochondria are crucial in signalling pathways that regulates oxidative stress and fatty acid are essential for maintaining the integrity of hepatocyte. Mitochondrial dysfunction significantly influences the onset and progression of metabolic dysfunction-associated steatotic liver disease, revitalising the research of steatotic liver therapy. The limited availability of treatment strategies arises from the heterogeneity of the disease pathology, and for a considerable time, insights into the aetiology of the disease remained unclear. Until very recently, treatment options for managing the condition were limited to antidiabetic, anti-inflammatory, and miscellaneous drugs. However, Resmetirom has emerged as the only FDA-approved drug, that specifically targets the thyroid hormone receptor-β receptor in the liver. More direct and targeted therapies are essential for this condition. Conclusion Targeting the mitochondrial dysfunction significantly expands the landscape of therapeutic potential, facilitating the introduction of additional therapies aimed at preventing, managing, or curing the condition, alongside the traditional therapies currently available.
Primary subcutaneous hydatid disease is an exceptional presentation of echinococcosis, bypassing the liver and lungs—its usual organs of involvement. This case presents a co-occurrence of hepatic and parietal wall hydatid cysts, emphasizing the importance of considering echinococcosis in differential diagnoses of long-standing cysts even in atypical locations, and highlights the effectiveness of minimally invasive surgical techniques to avoid spillage of cyst contents combined with antiparasitic therapy in prevention of recurrence.
Abstract Background Liver cancer, primarily hepatocellular carcinoma (HCC), is a significant global health concern, responsible for over 800,000 deaths annually. Its primary causes include chronic viral hepatitis, heavy alcohol consumption, and nonalcoholic fatty liver disease. Recent research has identified additional risk factors, such as exposure to heavy metals and endocrine disruptors, contributing to regional variations in incidence and mortality rates. Liver cancer stem cells (LCSCs) play a crucial role in disease development, contributing to high recurrence rates and drug resistance. Main body Understanding the genetic landscape of liver cancer is essential for developing personalized treatment strategies. Next-generation sequencing technologies allow comprehensive genomic profiling, revealing mutations, copy number variations, and gene expression patterns associated with LCSCs and HBV-induced liver cancer. Integration of multi-omics data enhances our understanding of liver cancer biology and aids in the development of precision medicine approaches. Therapeutic targeting of clonal evolution pathways such as Wnt/β-catenin and Notch signaling shows promise for inhibiting tumor growth and overcoming therapeutic resistance. Immunotherapy, particularly immune checkpoint inhibitors, demonstrates effectiveness in certain instances, offering hope for improved patient outcomes. However, challenges remain in developing T cell-based immunotherapies for HBV-related liver cancer, highlighting the need for innovative strategies to enhance treatment efficacy and safety. Additionally, genetic variations such as single nucleotide polymorphisms (SNPs) influence individual susceptibility to HBV-mediated HCC, emphasizing the importance of personalized risk assessment models. Disparities in mutation frequencies among different ethnic groups underscore the need for tailored approaches to liver cancer management. Conclusion Insights into the genetic landscape of liver cancer pave the way for more effective and individualized treatment strategies, addressing the pressing need to combat this deadly disease. By understanding the essential genes and pathways associated with LCSCs and HBV-induced liver cancer, researchers can develop targeted therapies and personalized risk assessment models, ultimately improving patient outcomes and reducing the global burden of liver cancer.
Abstract Background Hepatocellular carcinoma (HCC) remains a major global health burden, particularly among individuals with chronic hepatitis C virus (HCV) infection. Genetic factors, including single-nucleotide polymorphisms (SNPs), play an important role in susceptibility to HCC and its progression. This study aimed to investigate the association of MICA (rs2596542) and COMT (rs4680) polymorphisms with HCC risk in Egyptian patients infected with HCV. Methods A case-control study was conducted with 200 participants, including 100 HCC patients infected with HCV and 100 healthy controls. Genotyping of MICA and COMT polymorphisms was performed using real-time PCR. Clinical and biochemical parameters, such as AFP, ALT, AST, and albumin levels, were assessed. Statistical analyses were carried out to investigate genotype distributions and their association with the risk of HCC. Results The MICA TT genotype was significantly more prevalent in HCC patients compared to controls (35.0% vs. 11.0%, p < 0.0001), indicating a significant association with increased HCC risk. In contrast, the COMT AA genotype was more prevalent in controls (62.0% vs. 40.0%, p = 0.007), suggesting a potential protective effect. Analysis of genotype distribution across HCC histological grades showed no statistically significant differences for either MICA or COMT polymorphisms (all p > 0.05), although non-significant trends toward higher frequencies of mutant genotypes in advanced grades were observed. Increased levels of AFP and liver enzymes were associated with advanced grades of HCC. Multivariate analysis revealed that AST, independent of genetic variants, is a significant risk factor (OR = 4.46, p = 0.005), while higher albumin levels were protective (OR = 0.31, p = 0.012). Conclusions This study suggests that the MICA rs2596542 polymorphism is significantly associated with susceptibility to HCC, while the COMT rs4680 may have a modest role. However, neither polymorphism showed a significant association with histological grade. The integration of genetic variants with clinical biomarkers may improve risk stratification in HCC. Further large-scale studies are warranted to validate these findings.
Abstract Background Liver fibrosis represents a critical stage in the progression of chronic liver diseases and remains a major global health concern due to its potential to advance to cirrhosis and hepatic failure. Epigallocatechin-3-gallate (EGCG), the principal catechin in green tea, has demonstrated potent antioxidant and antifibrotic properties. However, its dose-dependent hepatoprotective efficacy and mechanism of action against chemically induced liver fibrosis remain insufficiently elucidated. This study aimed to evaluate the hepatoprotective effects and underlying mechanisms of EGCG at varying doses against thioacetamide (TAA)-induced hepatic fibrosis in rats. Methods Forty-two adult male rats were randomly divided into six groups (n = 7 per group): control, TAA, TAA + EGCG (50, 100, or 200 mg/kg/day), and TAA + silibinin (100 mg/kg/day). Liver fibrosis was induced by intraperitoneal injection of TAA (200 mg/kg) three times per week for three weeks. EGCG and Silibinin were administered orally for the same duration. At experiment end, blood samples were collected for hematological and biochemical analysis, while liver tissues were examined histopathologically and assessed for oxidative stress biomarkers including malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH). Results TAA administration caused marked hepatic injury characterized by significant increases in serum liver enzymes, bilirubin, white blood cells, and platelets, along with decreases in red blood cell indices, total protein, and albumin. Oxidative stress markers showed elevated MDA and reduced SOD and GSH levels. EGCG treatment significantly ameliorated these alterations in a dose-dependent manner, with the 200 mg/kg dose producing effects comparable to Silibinin. Histopathological findings confirmed that EGCG mitigated fibrotic changes and preserved hepatic architecture. Conclusion EGCG exerts potent hepatoprotective and antifibrotic effects against TAA-induced hepatic fibrosis by enhancing antioxidant defense mechanisms and improving liver function. These findings highlight EGCG as a promising natural therapeutic candidate for preventing and managing liver fibrosis.
Abstract Background Liver cirrhosis represents a significant global health burden, affecting over 160 million individuals worldwide in 2017. The aim of this study was to describe the different clinical presentations and outcomes of patients with decompensated liver cirrhosis admitted to Suez Canal University Hospital due to complications of decompensated cirrhosis. This may help determine the magnitude of each complication in terms of morbidity and mortality and identify factors that may be associated with poor outcomes. Methods A prospective observational analytical study was conducted to evaluate outcomes in patients with decompensated cirrhosis. Adult male and female patients with decompensated cirrhosis admitted to Suez Canal University Teaching Hospital due to complications of liver decompensation were included. Results A total of 75 patients were enrolled, of whom six died during follow-up. The ROC curve evaluating caffeine clearance demonstrated that at a cutoff value of 0.0055, with an AUC of 0.79 (95% CI: 0.67–0.92), the test achieved 89.9% sensitivity and 66.7% specificity, with a PPV of 94% and NPV of 22% for predicting survival in chronic liver disease patients. Caffeine clearance showed a significant positive correlation with hemoglobin, platelets, albumin, and sodium, and a significant negative correlation with age, INR, AST, ALT, total and direct bilirubin, creatinine, AFP, and MELD score. No other significant correlations were observed. Conclusions Caffeine clearance is a valuable indicator of liver function and can serve as a useful predictor of prognosis and mortality in patients with chronic liver disease, especially when interpreted alongside other laboratory parameters.
Abstract Background The liver’s role in human immunodeficiency virus (HIV) infection has been historically undervalued, often viewed through the lens of co-infections or drug toxicity. Emerging evidence now positions the liver as a critical immune organ, actively shaping HIV pathogenesis through its unique cellular composition and immunological functions. Objective This review synthesizes current knowledge to argue that the liver is a central site of HIV persistence and chronic inflammation. It aims to detail the mechanisms of hepatic immune subversion and their direct clinical consequences in the antiretroviral therapy (ART) era. Methods We conducted a systematic analysis of contemporary literature, focusing on studies investigating hepatic reservoirs, immune cell dysfunction, microbial translocation, and the resulting inflammatory and fibrotic pathways in both HIV-mono-infected and co-infected individuals. Results The liver constitutes a significant sanctuary for HIV, harboring latently infected Kupffer cells and T-cells. HIV subverts the liver’s tolerogenic state, driving chronic inflammation through mechanisms including persistent microbial translocation and direct activation of hepatic stellate cells. This pathological remodeling accelerates liver fibrosis in mono-infected individuals and contributes to systemic non-AIDS comorbidities, including cardiovascular and metabolic disease. The efficacy of cure strategies and drug metabolism are further complicated by this altered hepatic immune environment. Conclusion The liver is a significant actor in HIV immunopathogenesis, not a passive bystander. Its dysfunction underpins key clinical challenges in managing people living with HIV. Future research must prioritize liver-targeted therapeutic interventions and the development of non-invasive biomarkers to improve long-term patient outcomes.
Abstract Background Non-alcoholic fatty liver disease (NAFLD) has been frequently reported as a relatively common comorbidity in patients with inflammatory bowel disease (IBD). We aimed to calculate the prevalence of NAFLD and related terms like MAFLD (metabolic dysfunction-associated fatty liver disease) and MASLD (metabolic dysfunction-associated steatotic liver disease) in IBD (inflammatory bowel disease) patients by reviewing and analyzing the most recent evidence. Main body We systematically searched PubMed, Web of Science, Scopus, EMBASE, and ProQuest databases for studies published between January 01, 2001 and December 31, 2024. Eligible studies included cohort and cross-sectional designs that reported the prevalence of NAFLD in IBD patients. Studies were screened according to inclusion and exclusion criteria and subsequently evaluated. A total of 34 studies were included in our systematic review, of which 32 studies were eligible for meta-analysis. The overall pooled prevalence of NAFLD in IBD patients was 32.3% CI95% (27.3 to 37.3%), (I 2 = 98.97%), with a prevalence of 31.3% CI95% (22.7 to 39.8%) (I 2 = 98.78%) in Crohn’s disease (CD) and 27.1% CI95% (20.3 to 33.9%) (I 2 = 96.69%) in ulcerative colitis (UC). NAFLD was found to be more common in male IBD compared to females. Diagnostic modality influenced prevalence rates, with controlled attenuation parameter (CAP) reporting a higher prevalence (36.6% CI95% (32.4 to 40.9%) (I 2 = 70.54%)) compared to other methods. Liver fibrosis was also examined as an important comorbidity and complication among IBD patients. Based on the included studies, the overall prevalence of fibrosis in IBD was 7.3% (5.5 to 9.1%) (I 2 = 80.99%). Conclusion About one-third of IBD patients are likely to present with NAFLD. Evolving definitions of NAFLD such as MAFLD highlight the urgent need for international standardization and much more studies in this area. Trial registration PROSPERO CRD420250651182
Abstract This review finds the genetic interaction between fatty acid-binding protein (FABP) polymorphisms and the role of these polymorphisms in the association between type 2 diabetes mellitus (T2DM) and non-alcoholic fatty liver disease (NAFLD)—two closely related metabolic diseases sharing common pathophysiological mechanisms. Whereas the previous research has independently documented the association of FABP variants with metabolic diseases, this review gives an integrative picture and the combined effect of multiple FABP isoforms (FABP1, FABP2, FABP4, and FABP5) across various metabolic tissues; these include liver, adipose tissue as well as intestine. In particular, this paper integrates the current evidence on the role of FABP polymorphisms in the combined effect on lipid trafficking, insulin resistance, and inflammatory signaling, and thus leads to an overlapping phenotype of T2DM and NAFLD. Also, the review identifies some emerging evidence that supports the connections between the circulating FABP levels and genetic variants, which provides insight into their potential role as biomarkers of metabolic dysfunction. Instead of establishing causality, this work presents a hypothesis-generating framework, which highlights the significance of FABP-mediated pathways in convergence of metabolic diseases. These results justify the necessity of additional multi-marker, multi-omics, and longitudinal studies to confirm the value of FABPs as possible targets in the scope of risk stratification and treatment intervention.
Abstract Background Esophageal varices (EV) are a major complication of pediatric portal hypertension. Data on the diagnostic accuracy of noninvasive indices for identifying EV in Egyptian children remain scarce. This exploratory study aimed to evaluate the association between readily available clinical, laboratory, and sonographic parameters and the presence of EV in children with portal hypertension at a tertiary referral center. Patients and methods In this cross-sectional diagnostic accuracy study, 41 children with chronic liver disease, extrahepatic portal vein obstruction (EHPVO), or cirrhosis were consecutively enrolled at Assiut University Children Hospital between January 2022 and January 2023. All participants underwent clinical evaluation, laboratory testing, abdominal and Doppler ultrasonography, and calculation of noninvasive indices including platelet count, spleen-size z-score, platelet/spleen ratio, and Aspartate Aminotransferase-to-Platelet Ratio Index (APRI). Esophagogastroduodenoscopy (EGD) served as the reference standard for diagnosis and grading of varices. Results Esophageal varices were detected in 31 children (75.6%). Compared with those without varices, affected children had significantly lower hemoglobin (9.4 ± 1.8 vs. 11.9 ± 1.3 g/dL, p = 0.027), platelet counts (139.7 ± 87.6 vs. 245.7 ± 61.0 × 10⁹/L, p = 0.001), and albumin (2.9 ± 0.6 vs. 3.9 ± 0.3 g/dL, p < 0.001), with prolonged prothrombin time (14.9 ± 2.9 vs. 12.6 ± 1.1 s, p = 0.021). Sonographic findings showed smaller liver size (9.8 ± 1.4 vs. 12.0 ± 1.9 cm, p = 0.002), larger spleen size (128.2 ± 3.7 vs. 88.1 ± 1.6 mm, p = 0.002), and higher APRI scores (1.69 ± 1.65 vs. 0.28 ± 0.16, p = 0.011). On multivariate analysis, splenomegaly (aOR 8.45, 95% CI 3.21–22.28), elevated APRI (aOR 5.10, 95% CI 2.30–11.30), and thrombocytopenia (aOR 4.82, 95% CI 1.95–11.92) were associated with EV in the exploratory multivariate model, though confidence intervals were wide, reflecting the small sample size. Spleen length ≥ 120 mm demonstrated the highest area under the receiver operating characteristic curve (AUC 0.88; bootstrap-corrected 0.86). In an exploratory etiology-stratified analysis, APRI was significantly associated with EV in the cirrhosis subgroup (n = 25) but not in the EHPVO subgroup (n = 16). Conclusion In this single-center exploratory study, splenomegaly, thrombocytopenia, and elevated APRI showed significant associations with the presence of EV in children with portal hypertension. These findings suggest that readily available clinical and laboratory parameters may have potential utility for risk stratification; however, the small sample size, high disease prevalence, and absence of external validation preclude definitive conclusions. Prospective multicenter studies with larger, etiology-stratified cohorts are needed to confirm these observations and establish reliable diagnostic thresholds.
Abstract Background Refractory hepatic encephalopathy (HE) in decompensated chronic liver disease may result from large spontaneous portosystemic shunts, including ectopic pathways that are often overlooked on routine imaging. Case A 51-year-old man with alcohol-related decompensated chronic liver disease presented with recurrent low-grade HE despite optimal medical therapy. Imaging demonstrated a large spontaneous ectopic portosystemic shunt arising from an epiploic tributary of the splenic vein, forming a retroperitoneal variceal complex draining via the left testicular vein into the left renal vein. Retrograde transvenous embolization was performed through the left gonadal vein using an Amplatzer Vascular Plug II at the shunt–testicular vein junction, followed by n-butyl-cyanoacrylate embolization of distal varices. Serum ammonia decreased from 118 to 49 µmol/L with rapid clinical improvement and no immediate complications. Conclusion Selective embolization of ectopic portosystemic shunts is a safe and effective treatment for refractory HE in appropriately selected patients.
Abstract Background Esophageal varices can lead to morbidity and mortality in patients with chronic liver diseases. There is a debate about the frequency of endoscopic variceal band ligation sessions needed for the eradication of esophageal varices. We aimed to explore the optimal interval for endoscopic variceal band ligation sessions needed to obliterate esophageal varices. Methods This study enrolled 374 patients with liver cirrhosis indicated for endoscopic variceal band ligation. After the first variceal band ligation, patients were randomly assigned to one of four groups regarding the interval of subsequent band ligation sessions: group 1 (subsequent band ligation every week), group 2 (subsequent band ligation every 2 weeks), group 3 (subsequent band ligation every 3 weeks), and group 4 (subsequent band ligation every 4 weeks). Patients were followed until esophageal varices were eradicated, with complications reported as bleeding or post-banding ulcers. Results The studied groups showed insignificant differences in the mean number of sessions required to eradicate varices completely and the mean number of subsequent band ligation sessions. Post-banding ulcers were highly incident in group 1 (52.9%), followed by group 2 (22.8%), group 3 (8.0%), and group 4 (2.7%), with a statistically significant difference between the studied groups (p < 0.001). Bleeding after the first band ligation session was reported in only group 2 (1.3%). Conclusion A 4-week interval of elective variceal band ligation sessions achieved complete eradication with a lower rate of complications, particularly post-banding ulcers.
