Search Results (3,332)

Hepatitis B virus (HBV) infection is a worldwide health concern that infects nearly 254 million people globally and causes more than 1 million deaths annually. The highest prevalence is seen in sub-Saharan Africa and the Western Pacific region. Cirrhosis, liver failure, and hepatocellular carcinoma (HCC) are reported as leading complications of chronic HBV. The route of transmission of this infection is mainly by exposure to infected blood and bodily fluids. Transmission from mother-to-child remains the predominant route in highly endemic areas. Vaccination has significantly reduced HBV seroprevalence and complications. However, incomplete vaccination of newborns continues to be a major obstacle to elimination of the disease. Current prevention strategies include universal vaccination, perinatal prophylaxis with hepatitis B immune globulin, and maternal antiviral therapy in pregnant women with high viral load. The management of chronic hepatitis B virus infection predominantly depends on nucleoside analogs, including entecavir, tenofovir disoproxil fumarate, and tenofovir alafenamide, as well as pegylated interferon alfa. These therapies effectively suppress viral replication and reduce the risks of cirrhosis, HCC, and liver-related mortality, but they rarely achieve functional cure characterized by hepatitis B surface antigen loss. The persistence of covalently closed circular DNA (cccDNA) remains a major hindrance in HBV eradication. Therefore, novel therapeutic strategies targeting different stages of the viral life cycle, including capsid assembly modulators, small interfering RNAs, nucleic acid polymers, and cccDNA-directed approaches, are under active investigation. This review summarizes the epidemiology, prevention, current therapies, clinical outcomes, and emerging therapeutic advances in HBV infection, highlighting ongoing efforts toward achieving a functional cure and global HBV elimination. Full article

The co-occurrence of liver cirrhosis (LC) and heart failure (HF) poses considerable clinical challenges, yet the cellular and molecular determinants of this comorbidity remain poorly characterized. To address this, we developed an integrative multi-omics pipeline encompassing GWAS meta-analysis, gsMap-based spatial transcriptomic projection, GeneEnrich functional annotation, single-cell atlas construction, seismicGWAS and ECLIPSER cell-type scoring, eCAVIAR and fastenloc colocalization, hdWGCNA network inference, scTenifoldKnk in silico gene perturbation, and GCTA-COJO fine-mapping. Quality-controlled meta-analysis yielded 12,347,758 and 9,256,862 variant-level associations for LC and HF, respectively. Spatial projection confirmed preferential enrichment of disease signals within embryonic hepatic and cardiac compartments. Pathway analyses disclosed that LC-linked loci were concentrated in lipid metabolic programs, whereas HF-linked loci implicated mitochondrial bioenergetics and lysosomal degradation. At the cellular level, endothelial cells emerged as the dominant HF-associated population. Convergent evidence from five orthogonal algorithms pinpointed CRIM1 as the sole robustly supported shared gene, selectively enriched in HF endothelial cells; virtual perturbation further identified LCP1 and PTPRC as downstream regulatory nodes. Fine-mapping of the chromosome 2 locus harboring rs12476437 revealed multiple statistically independent signals in the vicinity of CRIM1. Collectively, these findings computationally prioritize the endothelial–CRIM1 axis as a previously unappreciated candidate mechanistic bridge between LC and HF requiring experimental validation. Full article

Non-cirrhotic portal hypertension (NCPHT) is defined as portal hypertension (PHT) occurring in the absence of cirrhosis. Major etiological causes of NCPHT include immunological disorders, chronic infections, exposure to medications or toxins, prothrombotic conditions, and several genetic syndromes, highlighting that NCPHT is not a single disease but a shared phenotype arising from diverse underlying pathways. NCPHT is frequently misdiagnosed, largely due to inconsistent nomenclature and limited scientific literature. The broader term non-cirrhotic portal fibrosis (NCPF) or porto-sinusoidal vascular disease (PSVD) includes patients in a preclinical stage who demonstrate histological features similar to NCPHT but lack clinical evidence of PHT. Early detection is linked to a favorable prognosis and improved clinical outcomes. Management strategies in pediatrics continue to rely on extrapolations from adult practice, with sparse evidence to guide pediatric care. Liver biopsy remains the cornerstone of diagnosis, demonstrating nodular regenerative hyperplasia, obliterative portal venopathy, or incomplete septal fibrosis. Management focuses on prophylactic and symptomatic care, with endoscopic therapy for controlling variceal bleeding. Porto-systemic shunts and, ultimately, liver transplantation therapies may be needed for advanced stages. A pressing need exists for standardized diagnostic criteria and multicenter studies to define natural history, refine risk stratification, and evaluate therapeutic approaches in the pediatric population. This review provides an overview of the pediatric causes of NCPHT, outlines the current understanding of pathophysiology, and discusses the clinical presentations and management strategies, while highlighting existing research gaps. Full article

Background/Objectives: The role of endoscopic ultrasonography (EUS) in surveillance after endoscopic variceal ligation (EVL) for primary prophylaxis of esophageal variceal hemorrhage remains uncertain. This study compared the predictive value of high-frequency intraluminal ultrasound (HFIUS) and esophagogastroduodenoscopy (EGD) for subsequent variceal hemorrhage after prophylactic EVL. Methods: In this retrospective study, follow-up EGD and HFIUS were performed in 40 patients with liver cirrhosis who underwent EVL as primary prophylaxis against variceal hemorrhage. EGD-based variceal grade and variceal cross-sectional area (CSA) measured by HFIUS were compared in all 40 patients. Among them, 31 who achieved variceal eradication or reduction to grade 0/1 on surveillance EGD were subsequently followed to evaluate subsequent variceal hemorrhage and clinical outcomes. Results: Spearman’s correlation analysis revealed a statistically significant yet weak positive correlation between EGD-based variceal grade and variceal CSA measured by HFIUS (ρ = 0.347, p = 0.028). Among the 31 patients with grade 0/1 varices on follow-up EGD, the mean follow-up duration was 32.4 ± 8.8 months, during which variceal hemorrhage occurred in seven patients and five patients died. In this exploratory analysis based on seven hemorrhagic events, a preliminary variceal CSA cutoff of 9.8 mm² predicted subsequent hemorrhage with an apparent sensitivity of 85.7% and specificity of 91.7% (optimism-corrected 75.3% and 90.0%; bootstrap-corrected AUC 0.945). Multivariate analysis showed that variceal CSA measured by HFIUS was independently associated with variceal hemorrhage (OR, 1.302; 95% CI, 1.040–2.020; p = 0.016), whereas EV grade assessed by surveillance EGD was not predictive of variceal hemorrhage. Conclusions: HFIUS-derived variceal CSA was associated with subsequent hemorrhage among patients with grade 0/1 varices after EVL and may provide prognostic information not captured by endoscopic grade alone. Incorporation of HFIUS-based EUS into post-EVL surveillance may help identify patients at persistent bleeding risk who may benefit from intensified prophylactic strategies, even when grade 0/1 eradication has been confirmed on surveillance EGD. Given the small number of events, the proposed cutoff is preliminary and requires external validation. Full article

Liver fibrosis is the common pathway through which chronic liver injury progresses to cirrhosis, portal hypertension, liver failure, hepatocellular carcinoma, and systemic complications. Its burden is increasing worldwide, driven mainly by metabolic dysfunction-associated steatotic liver disease, alcohol-related liver disease, viral hepatitis, and cardiometabolic comorbidity. Current evidence supports a clinically practical approach centered on early risk recognition, non-invasive fibrosis assessment, etiologic treatment, lifestyle and metabolic risk reduction, and timely referral of patients with suspected advanced fibrosis. Although advanced cirrhosis may remain only partly reversible, fibrosis can regress when the injurious stimulus is controlled, making prevention of progression a realistic therapeutic goal. This review provides a clinically actionable framework for the assessment, management, and prevention of liver fibrosis, integrating current insights into epidemiological trends, etiopathogenesis, non-invasive and portal-hypertension assessment, sex-specific effects, hepatic and extrahepatic outcomes, and treatment strategies. It highlights the potential for fibrosis regression when the underlying etiologic factor is controlled and emphasizes the stages (F0–F2) at which reversibility is most achievable. Additionally, the paper outlines key research priorities to address current knowledge gaps in biomarker discovery, precision medicine, and artificial intelligence-assisted risk stratification, while defining priorities for personalized screening, multidisciplinary care, and combination antifibrotic research. Full article

Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as non-alcoholic fatty liver disease (NAFLD), has become one of the most common chronic liver diseases worldwide, representing a major global health challenge closely linked to metabolic syndrome, obesity, and type 2 diabetes mellitus (TD2M). The condition is characterized by a multisystem nature driven by complex multifactorial mechanisms, including insulin resistance, lipotoxicity, mitochondrial dysfunction, genetic predispositions, and gut-liver axis alterations. Although liver biopsy remains the gold standard, non-invasive markers and advanced imaging methods are of key importance for early risk stratification. Furthermore, while liver-related complications such as fibrosis, cirrhosis, and hepatocellular carcinoma (HCC) are significant, cardiovascular disease remains the leading cause of mortality in patients with MASLD. Current management relies primarily on lifestyle modifications, targeted pharmacotherapy (such as pioglitazone, GLP-1 receptor agonists, SGLT-2 inhibitors), and novel experimental therapies. Consequently, MASLD requires a multidisciplinary approach emphasizing early diagnosis, risk stratification, and comprehensive treatment of both hepatic and extrahepatic manifestations. Full article

Background/objectives: Liver cirrhosis is a life-limiting, non-malignant condition with a high symptom burden, psychosocial challenges, and unpredictable disease trajectory. As such, patients with cirrhosis and their caregivers might benefit from palliative care (PC) interventions. However, in most clinical settings, PC is not yet an integral part of basic hepatology care. This scoping review aimed to map how patients with cirrhosis are identified for palliative care, which interventions are delivered, and which factors influence implementation. Methods: The review was conducted in accordance with Joanna Briggs Institute methodology and reported following the PRISMA-ScR guidelines. PubMed, CINAHL, and Scopus were searched. The initial search was conducted in November 2024 and updated in December 2025, June and August 2026. Quantitative, qualitative, and mixed-method studies involving adults (≥18 years) with liver cirrhosis, informal caregivers, and healthcare professionals were included. Data were charted descriptively and organized according to identification approaches, interventions, barriers, and facilitators. Results: In total, 39 studies were included. Patients were identified using identification tools, screening tools, clinical criteria, and prognostic scores. Interventions across inpatient, outpatient, and home-based settings included symptom management, prognostic communication, advance care planning, goals-of-care discussions, psychosocial support, and multidisciplinary collaboration. Overall, studies reported improvements in symptom management, communication, healthcare utilization, and informal caregiver outcomes. However, palliative care integration remained inconsistent and often occurred late. Key barriers included prognostic uncertainty, fragmented care pathways, limited training, and misconceptions about palliative care. Facilitators included education, structured assessment tools, and integration of palliative care into hepatology services. Conclusions: This review identified diverse approaches to patient identification and palliative care delivery, alongside key barriers and facilitators to implementation. Earlier integration of palliative care based on care needs, supported by communication, education, and interdisciplinary collaboration, may improve care for patients with cirrhosis. Full article

Pancreato-hepatobiliary (HPB) malignancies—pancreatic ductal adenocarcinoma (PDAC), hepatocellular carcinoma (HCC), and the biliary tract cancers (BTC) comprising intrahepatic, perihilar and distal cholangiocarcinoma, gallbladder carcinoma, and ampullary adenocarcinoma—together constitute one of the heaviest and fastest-growing burdens in global oncology. Liver cancer is the third leading cause of cancer death worldwide, and pancreatic cancer, with a mortality-to-incidence ratio approaching unity, is projected to become the second leading cause of cancer death in high-income countries. This narrative review synthesises PubMed-indexed evidence across the full clinical arc of all three disease families, organised around epidemiology and risk; diagnosis, staging and biomarkers; surgical and multimodal management; and the rapidly evolving systemic therapy landscape, with survival and prognosis integrated throughout. Three cross-cutting narratives emerge. First, HPB cancers are united by late presentation, biological aggressiveness, and dependence on a background of organ dysfunction (cirrhosis in HCC, biliary obstruction in BTC and PDAC, and chronic pancreatitis as a major predisposing background in PDAC) that constrains therapy. Second, their trajectories are diverging: HCC has achieved the largest proportional survival gain of any solid tumour, driven by surveillance and immunotherapy in the subset of patients who reach specialist care; BTC has entered a nascent precision-oncology era in which FGFR2, IDH1, HER2, and BRAF alterations are druggable and immune-chemotherapy is first-line standard, although absolute survival gains remain modest and access to comprehensive molecular profiling is uneven; whereas PDAC has improved only incrementally, its immunosuppressive stroma and near-universal KRAS driver remaining formidable barriers. Third, molecular profiling, multidisciplinary care, and surgical centralisation are now non-negotiable structural determinants of outcome. We conclude that HPB oncology has entered a phase of real but unevenly distributed progress: long-term survival remains poor for most patients globally, and translating these advances into population-level gains will require earlier detection, broader access to molecular profiling and novel therapies, and biology-driven innovation. Full article

Background: Adolescent and adult citrin deficiency (AACD), formerly known as adult-onset citrullinemia type II, is a rare autosomal recessive disorder caused by biallelic pathogenic variants in SLC25A13. It is an underrecognized cause of recurrent hyperammonemic encephalopathy, particularly when hepatic function is relatively preserved. Methods: We report two unrelated Vietnamese young men, aged 21 and 18 years, who presented with recurrent neuropsychiatric episodes. Clinical, biochemical, imaging, electrophysiological, and genetic findings were evaluated; whole-exome sequencing findings were confirmed by Sanger sequencing. Results: Both patients had long-standing preferences for protein- and fat-rich foods and avoidance of carbohydrate-rich foods, together with episodic hyperammonemia (345.21 and 103.07 µmol/L during symptomatic episodes). The first patient had a history of neonatal jaundice, mild cirrhosis, and severe behavioral disturbances, whereas the second was markedly lean and had no structural liver disease. Acquired causes of hyperammonemia and portosystemic shunting were excluded. Both patients harbored the homozygous pathogenic SLC25A13 variant NM_014251.3.852_855del (p.Met285ProfsTer2). Ammonia-lowering therapy and a low-carbohydrate, protein- and fat-enriched diet supplemented with medium-chain triglycerides resulted in clinical improvement, with no recurrent encephalopathic episodes during 6 months of follow-up in either patient. Conclusions: AACD should be considered in adolescents and adults with otherwise unexplained recurrent hyperammonemic encephalopathy, especially when ammonia elevation is disproportionate to liver disease. Characteristic dietary preferences provide an important diagnostic clue, and molecular testing enables definitive diagnosis and timely management. Full article

Mitochondria and peroxisomes are critical for hepatic energy metabolism, lipid homeostasis, and reactive oxygen species (ROS) detoxification. In chronic hepatitis C virus (HCV) infection, continuous injury leads to cirrhosis; however, the spatial arrangement and reversibility of organelle dysfunction remain poorly understood. This study aimed to examine the zonal distribution of mitochondrial and peroxisomal injury in liver biopsies and elucidate the role of circulating cell-free mitochondrial DNA (ccfDNA) in patients with chronic HCV and cirrhosis following antiviral therapy. We employed advanced microscopy imaging and transcriptomic analysis of liver biopsies and quantified ccf-mtDNA as a noninvasive marker of mitochondrial injury in the peripheral blood of these patients. Transcriptomic data revealed alterations in mitochondrial and peroxisomal pathway alterations in HCV-infected patients. The imaging data displayed distinct zone-specific patterns of organelle damage. Following viral removal, significant improvement in mitochondrial and peroxisomal protein expression were noted, indicating partial recovery of organelle integrity following viral clearance; whether this reflects true subcellular regeneration or an early stage of a longer recovery process remains to be determined. Additionally, we showed that ccf-mtDNA quantitatively reflects intrahepatic mitochondrial dysfunction, indicating its potential as a diagnostic biomarker in therapeutic approaches. These findings indicate that organelle injury in chronic HCV is spatially patterned, disease severity-dependent, and partially reversible following antiviral therapy. Full article

Background: Acute kidney injury (AKI) is associated with poor outcomes in patients with cirrhosis. However, most studies evaluate AKI as a single clinical entity, whereas predictors of mortality and renal recovery, specifically in non-hepatorenal syndrome AKI (non-HRS-AKI), remain poorly defined. Methods: We performed a retrospective cohort study including consecutive patients with liver cirrhosis admitted with non-HRS-AKI to a multidisciplinary emergency hospital between 1 January 2024 and 31 December 2025. Only variables available at hospital admission were included in the multivariable analyses. Independent predictors of in-hospital mortality and factors associated with incomplete renal recovery in survivors at hospital discharge were identified using multivariable logistic regression. Results: A total of 139 patients were included. Overall, 57 patients (41.0%) died during hospitalization. Among the 82 survivors, complete renal recovery occurred in 35 cases (42.7%), whereas 47 patients (57.3%) had incomplete renal recovery at discharge. Independent predictors of in-hospital mortality were a higher MELD-Na score (adjusted OR 1.16 per 1-point increase, 95% CI 1.07–1.26; p < 0.001), an advanced AKI stage (KDIGO stage 3 vs. stage 1, adjusted OR 6.71, 95% CI 1.73–26.04; p = 0.006), the absence of pre-existing chronic kidney disease (adjusted OR 0.233, 95% CI 0.085–0.644; p = 0.005), and higher admission C-reactive protein (adjusted OR 1.12 per 10 mg/L increase, 95% CI 1.01–1.23; p = 0.029). Factors independently associated with incomplete renal recovery among hospital survivors at hospital discharge were pre-existing heart failure (adjusted OR 3.07, 95% CI 1.10–8.62; p = 0.033) and higher admission C-reactive protein (adjusted OR 1.17 per 10 mg/L increase, 95% CI 1.00–1.34; p = 0.047). Conclusions: In patients with cirrhosis-associated non-HRS-AKI, in-hospital mortality was primarily associated with the severity of liver disease and AKI, whereas incomplete renal recovery at hospital discharge was independently associated with pre-existing heart failure. Admission C-reactive protein was independently associated with both outcomes, supporting the role of systemic inflammation in determining short-term prognosis and suggesting that C-reactive protein may serve as a simple, readily available biomarker for early risk stratification. Full article

Background: Early detection of hepatocellular carcinoma (HCC) is critical for improving patient outcomes; however, ultrasound-based surveillance has limited sensitivity and variable performance across patient populations. We evaluated the performance of a multitarget HCC blood test (mt-HBT), incorporating methylated DNA markers, alpha-fetoprotein (AFP), and patient sex, across clinically relevant subgroups. Methods: We performed a subgroup analysis of a multicenter, prospective case-control study that included 159 patients with early-stage HCC (Barcelona Clinic Liver Cancer Stage 0/A) and 649 control patients with cirrhosis or chronic hepatitis B without HCC. The mt-HBT combined methylated HOXA1, TSPYL5, and B3GALT6 markers with AFP and sex. Sensitivity and specificity were evaluated overall and according to age, sex, obesity, liver disease etiology, Child Pugh class, and tumor size. Performance was compared with AFP and GALAD. Results: Overall sensitivity and specificity of mt-HBT for early-stage HCC detection were 76.7% (95% CI, 69.6–82.6) and 87.5% (95% CI, 84.8–89.8), respectively. Sensitivity was significantly higher than that of AFP (35.2%, p < 0.001) and comparable to that of GALAD (78.6%, p = 0.56), whereas specificity was lower than that of AFP (98.5%, p < 0.001) but higher than that of GALAD (76.9%, p < 0.001). Sensitivity was maintained across key subgroups, including patients with obesity (68.9%), Child Pugh B cirrhosis (75.0%), hepatitis C (80.0%), hepatitis B (72.2%), alcohol-associated liver disease (80.5%), and metabolic dysfunction-associated steatotic disease (69.0%) (all p > 0.05 between subgroups). Specificity exceeded 80% in all examined populations and was significantly higher in women than in men (92.5% vs. 83.9%, p < 0.001). Sensitivity increased with tumor size, ranging from 60.0% for tumors < 2 cm to 100% for tumors > 5 cm. Conclusions: The mt-HBT demonstrated robust, consistent performance for early-stage HCC detection across diverse patient populations, including subgroups in which ultrasound surveillance commonly underperforms. These findings support the prospective validation of mt-HBT as a blood-based surveillance strategy for HCC. Full article

Background/Objectives: Esophageal variceal bleeding (EVB) is a life-threatening complication of portal hypertension, yet many patients experience their first bleeding episode without prior diagnosis or adequate prophylaxis. This study aimed to describe the clinical, laboratory, and radiological findings present one year before the first EVB episode and to examine whether these findings were recognized and acted upon in clinical practice. Methods: We retrospectively reviewed 48 patients admitted with a first episode of EVB between January 2020 and January 2025. Demographic data, laboratory values, abdominal ultrasonography findings, and liver fibrosis scores were recorded both at the time of bleeding and during a baseline period of 12 ± 3 months prior to bleeding. Results: Of 48 patients, 22.9% (n = 11) had not been diagnosed with cirrhosis prior to bleeding, and 33.3% (n = 16) remained without primary prophylaxis despite a known diagnosis—meaning that 56.2% experienced their first EVB without effective preventive management. At baseline, splenomegaly was present in 90% of patients with available ultrasonography data, and 72.9% had platelet counts below 150 × 10³/µL. Annual changes in clinical scores (expressed as delta values) demonstrated progressive hepatic deterioration during the unmonitored period, as evidenced by worsening Child–Pugh and MELD scores. Conclusions: In the majority of patients who experienced a first EVB episode, simple and routinely available findings—namely splenomegaly and thrombocytopenia—were already present one year before the bleeding event. Furthermore, delta values indicate that disease severity progressively worsened during this unrecognized at-risk period. These findings represent missed clinical opportunities for earlier diagnosis and initiation of prophylaxis. Full article

Patients with chronic liver disease are systematically excluded from acute myocardial infarction (AMI) trials, and prior real-world data rely on administrative coding alone. Whether ICD-coded liver disease and laboratory-defined liver fibrosis identify the same patients, and whether they predict the same outcomes, is unknown. We conducted a single-center retrospective cohort study of 1037 consecutive adults admitted with AMI (ICD-10 I21.x) to a tertiary New York center between November 2022 and December 2024. The primary exposure was ICD-defined advanced liver disease (cirrhosis, hepatic failure, or portal hypertension/decompensation; n = 102). The secondary, lab-based exposure was the Fibrosis-4 (FIB-4) index calculated from earliest admission AST, ALT, and platelet count (computable in 1031 patients, 99.4%), stratified as low (<1.45), indeterminate (1.45–3.25), or advanced (>3.25). Co-primary outcomes were invasive management (diagnostic angiography, percutaneous coronary intervention, or coronary artery bypass grafting) and in-hospital mortality. Multivariable logistic regression adjusted for age, sex, diabetes, chronic kidney disease, heart failure, and ST-elevation; the trend across FIB-4 tiers was assessed with the Cochran–Armitage test. Denominators throughout (including the 168/909 occult-fibrosis estimate) use the full exposure group as denominator under a missing-as-not-exposed convention; the four no-LD and two advanced-LD patients with missing FIB-4 are counted as non-advanced fibrosis for this calculation. Patients with ICD-defined advanced liver disease received invasive management less often (12.7% vs. 50.4%; adjusted odds ratio [aOR] 0.17, 95% CI 0.09–0.32) and died in hospital more often (43.1% vs. 7.9%; aOR 8.22, 95% CI 5.02–13.46) than patients without coded liver disease. Outcomes worsened monotonically across FIB-4 tiers (mortality 4.4% → 9.2% → 27.5%; invasive management 55.2% → 45.6% → 33.5%; both p < 0.001 by Cochran–Armitage trend test). Critically, 168 of 909 patients with no coded liver disease (18.5%) had FIB-4 > 3.25, representing a substantial population of unrecognized advanced fibrosis missed by clinical coding. Coded liver disease identifies a small, severely affected subgroup with markedly lower rates of invasive management and 6- to 8-fold higher mortality after AMI. Routine FIB-4 calculation, a free, three-variable lab score, identifies a much larger population with occult advanced fibrosis and graded excess risk that ICD codes miss entirely. Pending prospective validation, FIB-4 may serve as a low-cost adjunct to bedside risk stratification in AMI care. Full article

Liver fibrosis staging plays a key role in the prognosis and management of chronic liver disease. Liver biopsy remains the reference standard for fibrosis assessment but is limited by its invasiveness and risk of complications, while magnetic resonance elastography, though also considered a gold standard, is constrained by cost and limited availability. Ultrasound-based elastography techniques—vibration-controlled transient elastography (VCTE), point shear wave elastography (pSWE), and two-dimensional shear wave elastography (2D SWE)—have emerged as accessible non-invasive alternatives. This narrative review aimed to summarize the principles, diagnostic performance, advantages, and limitations of these three techniques across a range of etiologies. A comprehensive literature search was conducted across Scopus, PubMed, Embase, CINAHL, the Cochrane Library, Informit, and the JBI Database of Systematic Reviews and Implementation Reports, covering January 2015 to February 2026. Search terms included “vibration-controlled transient elastography”, “point shear wave elastography”, “two-dimensional shear wave elastography”, “liver stiffness measurement”, “non-invasive assessment” and “chronic liver disease”. International guidelines, systematic reviews and meta-analyses, large observational cohort studies, and narrative reviews were included in the synthesis. VCTE, pSWE, and 2D SWE all demonstrated good diagnostic performance for detecting advanced fibrosis and cirrhosis across multiple etiologies. VCTE was the most extensively validated technique, with standardized cut-offs endorsed by major international guidelines. pSWE and 2D SWE showed comparable diagnostic accuracy and can be integrated into conventional ultrasound systems, enabling simultaneous structural and stiffness assessment, although validated cut-off values for these two techniques are not yet established in current guidelines, and absolute stiffness values are not directly interchangeable across techniques, manufacturers, or software versions. Obesity, inflammation, steatosis and recent food intake were identified as factors affecting measurement accuracy across all three techniques. Ultrasound-based elastography techniques offer effective, non-invasive alternatives to liver biopsy for fibrosis assessment. VCTE remains the most validated option despite cost and availability constraints, while pSWE and 2D SWE offer comparable accuracy with practical integration advantages. Future research should focus on standardizing cut-off values, addressing confounding factors, and combining elastography with biomarkers and AI-driven models. Full article