Search Results (2,861)

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is caused by excessive fat accumulation in the liver (steatosis) and affects approximately 38% of adults globally. MASLD may progress from simple steatosis to fibrosis and cirrhosis and is closely related to other cardio-metabolic conditions (e.g., obesity and type 2 diabetes), posing a risk factor for cardiovascular disease. Currently, lifestyle modification and weight reduction remain the main initial treatment options. Existing data suggest that there is low awareness among patients regarding MASLD diagnosis and its subsequent management. Therefore, this study aimed to develop a rich understanding of the lived experiences, concerns, and support needs of adults with MASLD. Methods: A qualitative design was applied, utilizing semi-structured interviews. Adults living with MASLD were invited to talk about their diagnosis and discuss their lived experiences. Participants were interviewed by telephone or video call, and each interview was transcribed and analyzed with a reflexive thematic analysis approach. Results: Twenty-five adults with MASLD (age range: 24–79 years; 40% men) were interviewed. The emergent key themes related to communication and emotions at diagnosis; independently seeking further information; lived experiences post-diagnosis; support needs; and future concerns. Many participants reported receiving the diagnosis incidentally, and a number of issues were raised regarding lack of clarity at the point of diagnosis. Additional concerns included information obtainable via the internet, symptoms, social relationships, stigma, and lifestyle modification. Future anxieties related mainly to fears of disease progression, while support needs were predominantly focused on information and follow-up. Conclusions: The concerns and support needs identified by this study highlight key issues/themes that should inform education and support initiatives by relevant healthcare services aiming to improve the lived experiences and holistic management of adults with MASLD. Full article

Background/Objectives: In cirrhotic patients, guidelines generally recommend maintaining mean arterial pressure (MAP) ≥ 65 mmHg, but the prognostic impact of MAP in transplant candidates is unclear. This study aimed to evaluate the association between MAP and waitlist mortality and cirrhosis-related complications in patients listed for liver transplantation. Methods: We conducted a retrospective cohort study of 103 adults (age ≥ 18 years) with cirrhosis listed for liver transplantation (MELD 20–24) at a single center (2019–2023). Patients with hepatocellular carcinoma were excluded. The primary outcome was death on the transplant waitlist (n = 9 events). Logistic regression was used to assess the association of MAP (per 1 mmHg) with mortality. Continuous variables were compared using the t-test, and categorical variables were compared using the chi-square test; p < 0.05 was considered significant. Results: Mean MAP at listing was significantly higher in survivors than non-survivors (83.2 ± 9.4 vs. 76.9 ± 8.7 mmHg; p = 0.04). In logistic regression, higher MAP was associated with lower odds of waitlist death (unadjusted odds ratio [OR] per 1 mmHg increase = 0.94; 95% confidence interval [CI] 0.89–0.99; p = 0.041). Subgroup analysis showed a significant inverse association between MAP and hepatorenal syndrome (HRS) (OR per 1 mmHg = 0.94; 95% CI 0.89–0.98; p = 0.011), whereas MAP was not significantly associated with hepatic encephalopathy, ascites, or variceal bleeding (all p > 0.2). Conclusions: Among the cirrhotic patients listed for transplantation, lower MAP at baseline is associated with waitlist mortality and hepatorenal syndrome. These findings should be interpreted cautiously given the small number of events and require validation in larger cohorts. Full article

Chronic hepatitis B (CHB) infection is a major risk factor for progressive cirrhosis and hepatocellular carcinoma. Persistent virus-induced inflammation alters liver function, leading to accelerated disease and increased mortality. Although lifelong treatment with nucleos(t)ide analogs (NAs) is highly effective at suppressing viral replication, covalently closed circular DNA (cccDNA) persists in hepatocytes to sustain chronic infection, underscoring the need for better interventions and combination therapies. The durable suppression of viral replication and restoration of immune responses through long-acting (LA) therapies offer a promising strategy for sustained HBV control. We transformed tizoxanide (TIZ), a broad-spectrum anti-infective and immunomodulatory agent, into a LA lipophilic prodrug formulation (NM2TIZ) for intramuscular or subcutaneous administration. NM2TIZ exhibited long-term stability during storage and was evaluated in AAV-HBV mice using monotherapy and combination therapy approaches with an LA tenofovir prodrug formulation (NM5TFV). NM5TFV reduced the HBV DNA levels by >2 log₁₀ fold. Furthermore, coadministration of NM5TFV with M2TIZ reduced the expression of liver inflammasomes and profibrotic markers. The NM5TFV and NM2TIZ combination reduced HBV replication, inflammation, and fibrogenesis in AAV-HBV-transduced mice. Full article

Background/Objectives: At-risk metabolic dysfunction-associated steatohepatitis (MASH) is associated with increased risks of cirrhosis, hepatocellular carcinoma, and liver-related mortality. Because impaired efferocytosis contributes to persistent hepatic inflammation and fibrotic remodeling in MASH, we investigated whether efferocytosis-associated molecular signatures could identify at-risk MASH. Methods: Bulk RNA-sequencing datasets from Gene Expression Omnibus (GSE135251 and GSE174478) were analyzed to identify differentially expressed efferocytosis-related genes and characterize associated pathways and immune infiltration patterns. Machine learning-based feature selection was used to identify hub genes, which were incorporated into a transcriptomic nomogram. Experimental validation involved reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blotting of liver tissues from a Western diet-induced murine metabolic dysfunction-associated steatotic liver disease (MASLD) model. Plasma proteomic data were analyzed to explore the discriminatory performance of hub gene products. Results: A total of 17 efferocytosis-related genes (ERGs) associated with at-risk MASH were identified and enriched in pathways related to efferocytosis, inflammation, and immune regulation. Five hub genes, CD24, CHI3L1, TREM2, PTGS2, and LGR6, were shared by all three feature-selection approaches and significantly upregulated in at-risk MASH. A transcriptomic nomogram yielded area under the curve (AUC) values of 0.866 and 0.805 in the training and external cohorts, respectively. In the murine MASLD model, all five hub genes showed increased mRNA and protein expression in advanced disease. Exploratory plasma proteomic analysis identified elevated circulating TREM2 and CHI3L1 levels in at-risk MASH, and a simplified plasma-based model achieved an AUC of 0.736. Conclusions: This study identified a five-gene efferocytosis-associated signature and developed models for identifying at-risk MASH, suggesting that these genes warrant further evaluation as candidate biomarkers. Full article

Background/Objectives: Cardiac comorbidities are increasingly common among liver transplant candidates, particularly those with metabolic dysfunction-associated steatohepatitis (MASH)-related cirrhosis. Although the Liver Transplant Comorbidity Index identifies coronary artery disease (CAD) as a predictor of post-transplant mortality, the impact of overall cardiac comorbidity burden on early outcomes after liver transplantation remains unclear. We evaluated the association between pre-transplant cardiac comorbidities and early post-transplant outcomes, with emphasis on MASH-related cirrhosis. Methods: We performed a retrospective cohort study using the TriNetX US Collaborative Research Network. Adults undergoing first-time isolated liver transplantation through May 2026 were included. Pre-transplant CAD, heart failure (HF), and atrial fibrillation (AF) documented within 12 months before transplantation were identified using ICD-10-CM codes. Patients were categorized by cardiac comorbidity burden (0–3 conditions). Recipients with any cardiac comorbidity underwent 1:1 propensity score matching to those without cardiac disease using 16 baseline demographic, clinical, and laboratory variables, including MELD-Na. The estimand was the average treatment effect in the treated patients. Primary outcomes comprised 30- and 90-day all-cause mortality. Secondary outcomes included a prespecified restricted major adverse cardiac event (MACE) composite, limited to hard endpoints (death, myocardial infarction, cardiac arrest, ischemic stroke), and a broader composite, i.e., acute kidney injury, prolonged mechanical ventilation, vasopressor requirement, renal replacement therapy, ICU and hospital length of stay, and 90-day readmission. Results: Among 5124 recipients, 986 (19.2%) exhibited at least one cardiac comorbidity. After matching, 974 patients remained in each group. Pre-transplant cardiac comorbidity was associated with higher 30- and 90-day mortality and increased risks of all secondary outcomes. The association with MACE persisted but was attenuated when restricted to hard endpoints (90-day RR 1.55; 95% CI 1.19–2.03) when compared with the broad composite (RR 1.75; 95% CI 1.40–2.18). MASH recipients with cardiac comorbidities experienced numerically higher event rates than did non-MASH recipients, but interaction estimates were imprecise and non-significant. In separate matched analyses, AF was most strongly associated with MACE, whereas CAD showed the strongest association with mortality. Conclusions: Pre-transplant cardiac comorbidity burden is associated with worse early post-transplant outcomes. Although MASH-cirrhosis recipients experienced numerically higher event rates, exploratory subgroup analyses did not demonstrate statistically significant differences from the non-MASH recipients. These findings may help refine cardiac risk prediction and perioperative planning, but they do not establish that intensified cardiac risk stratification or perioperative optimization improve outcomes. Prospective studies incorporating detailed cardiac, donor, operative, frailty, and medication data are needed to validate these associations and determine whether targeted risk-stratification and perioperative strategies can improve post-transplant outcomes. Full article

Chronic liver diseases impose a considerable global public health burden, yet available treatment options remain largely inadequate. The gut microbiota exerts a key modulatory effect on liver disease pathogenesis via the gut-liver axis. Among them, Lachnospiraceae, a dominant bacterial family in the healthy adult gut, has drawn growing interest in recent years. Lachnospiraceae exert protective functions by producing short-chain fatty acids, participating in secondary bile acid conversion, and synthesizing active metabolites such as N-acetyl-glutamic acid, thereby maintaining intestinal barrier integrity and regulating host metabolic and immune homeostasis. Extensive evidence indicates that in cirrhosis, alcohol-associated liver disease, and metabolic dysfunction-associated steatotic liver disease, Lachnospiraceae abundance is consistently and significantly reduced, and this decrease is closely correlated with disease severity and adverse prognosis. In hepatocellular carcinoma, however, different members of Lachnospiraceae exhibit functional divergence, with some butyrate-producing genera decreasing while other subgroups may become enriched and influence the tumor immune microenvironment. Live biotherapeutic products based on Lachnospiraceae have achieved clinical breakthroughs in recurrent Clostridioides difficile infection and metabolic syndrome, providing important references for their translational application in liver diseases. This review systematically synthesizes the abundance changes and mechanisms of Lachnospiraceae across major liver diseases, evaluates their biomarker and therapeutic target potential, and seeks to provide fresh perspectives for precision microbiome-modulating strategies in chronic liver disease management. Full article

Chronic hepatitis B and C are major causes of cirrhosis, hepatocellular carcinoma, and liver-related mortality worldwide. The genetic diversity of hepatitis B virus (HBV) and hepatitis C virus (HCV) influences disease progression, diagnosis, vaccine response, and antiviral treatment. Periods of healthcare disruption, such as the COVID-19 pandemic, reinforce the importance of molecular surveillance to monitor viral genotypes and clinically relevant mutations. This study described the distribution of HBV and HCV genotypes and mutations in Rio de Janeiro, Brazil, during the COVID-19 pandemic. A cross-sectional study included 25 patients (15 HBV and 10 HCV) recruited between 2020 and 2022. Viral nucleic acids were amplified and sequenced by Sanger methodology, and mutations were analyzed using the Geno2pheno platform. HBV genotype A predominated (67%), comprising subgenotypes A1 (40%) and A2 (27%), followed by the rare genotypes B1 (13%), F2 (13%), and G (7%). Among HCV-infected individuals, genotypes 1a (40%) and 1b (30%) predominated, followed by genotypes 4 (20%) and 2 (10%). HBV immune escape mutations (Y100C and T126S) and unusual insertions in the S and RT domains were identified. In HCV, the substitutions C316Y, C316N, and S282R were detected. These findings highlight the importance of molecular surveillance for detecting clinically relevant viral variants. Full article

Background: Chronic hepatitis B virus (HBV) and hepatitis C virus (HCV) infection remain leading causes of cirrhosis and hepatocellular carcinoma (HCC) worldwide, and continue to represent a major challenge despite the growing contribution of alcohol-related and metabolic dysfunction-associated steatotic liver disease. Direct-acting antivirals now cure most patients with chronic HCV infection, while nucleos(t)ide analogues durably suppress HBV replication, producing a rapidly expanding population of treated and cured patients. Many nonetheless retain residual fibrosis, portal hypertension and long-term cancer risk, creating a need for non-invasive long-term liver assessment. Multiparametric ultrasound (MPUS) integrates the evaluation of morphology, fibrosis, steatosis, haemodynamics and perfusion within a single examination. Methods: Publications indexed in PubMed/MEDLINE, Scopus and Google Scholar between January 2000 and April 2026 were reviewed narratively, with priority given to international guidelines and consensus documents, meta-analyses, and prospective studies using histological, haemodynamic or clinical reference standards. Results: This narrative review summarises the evidence supporting MPUS in chronic viral hepatitis, covering elastographic fibrosis assessment, Baveno VII liver and spleen stiffness criteria for clinically significant portal hypertension, contrast-enhanced ultrasound characterisation of focal liver lesions, and emerging techniques such as microvascular and viscosity-sensitive imaging. Particular attention is given to the confounding effect of inflammatory activity on liver stiffness. MPUS is presented here as a proposed evaluation framework for organising complementary measurements within a single examination, and not as an approach of demonstrated clinical superiority: no comparative or outcome-based study has yet shown that acquiring these parameters together improves clinical decisions relative to the individual techniques applied according to current guidelines. Conclusions: Within this framework, the most plausible role of MPUS in the elimination era is longitudinal assessment of the treated liver, a proposition that requires prospective validation against clinical endpoints. Full article

Hepatitis C virus (HCV) infection is a major cause of chronic hepatitis, affecting approximately 50 million people worldwide. An estimated 15–30% of individuals with chronic HCV infection progress to cirrhosis, which may subsequently develop into hepatocellular carcinoma. Beyond liver disease, HCV is associated with a broad spectrum of extrahepatic manifestations, particularly mixed cryoglobulinemia (MC) and B-cell non-Hodgkin lymphoma (B-NHL). Persistent viral infection induces chronic antigenic stimulation of B lymphocytes, a key pathogenic mechanism underlying the progression from MC to overt B-NHL. These observations have important therapeutic implications and support the use of antiviral therapy as a cornerstone of treatment. The efficacy of direct-acting antivirals (DAAs) has been well established in patients with HCV-related MC and cryoglobulinemic vasculitis. Several studies have shown that DAAs achieve sustained virologic response rates exceeding 90%, often approaching 100% in contemporary cohorts. Viral eradication is frequently associated with clinical and immunological improvement, as well as regression of cryoglobulinemia. Encouraging outcomes have also been reported in patients with HCV-associated indolent B-NHL, particularly marginal zone lymphoma, although confirmation in larger studies with longer follow-up is needed. In patients with HCV-positive aggressive lymphomas, DAAs have been safely administered in combination with immunochemotherapy, yielding promising results. This review summarizes the current evidence on HCV-associated MC and B-NHL and discusses the impact of DAA therapy on the clinical course and management of these disorders. Full article

Metabolic dysfunction-associated steatotic liver disease (MASLD) encompasses a spectrum of liver injury ranging from simple steatosis to metabolic dysfunction-associated steatohepatitis (MASH), a progressive inflammatory state associated with hepatocyte injury, fibrosis, cirrhosis, and hepatocellular carcinoma. Increasing evidence suggests that progression to MASH is not spatially uniform across the liver. Instead, it reflects region-specific metabolic stress, inflammatory signaling, and fibrogenic remodeling along the porto-central axis of the hepatic lobule. Recent advances in spatial transcriptomics, lipidomics, proteomics, and multiplex imaging have provided new insight into how hepatocytes, immune cells, endothelial cells, and hepatic stellate cells interact within distinct hepatic microenvironments during disease progression. In this review, we discuss emerging concepts linking hepatic zonation to steatosis, inflammation, fibrosis, and extracellular matrix remodeling in MASLD and MASH. We highlight how disruption of normal lobular organization contributes to a progressive loss of metabolic compartmentalization and to the amplification of inflammatory and fibrogenic signaling. We additionally examine how spatial disease programs differ between adult and pediatric MASLD, particularly given the periportal-predominant injury patterns frequently observed in children and the current lack of pediatric-focused mechanistic studies. Finally, we discuss recently approved therapies and emerging therapeutic strategies within the context of hepatic microenvironment remodeling and disease heterogeneity. Collectively, these findings support a framework in which MASLD and MASH are spatially organized diseases driven by dynamic multicellular interactions, emphasizing the importance of incorporating zonation and tissue context into future mechanistic studies and therapeutic development. Full article

Cirrhosis, accounting for 2.4% of global mortality in 2019, represents a leading cause of death in chronic liver disease. Hepatic encephalopathy (HE), a decompensated complication of cirrhosis, is associated with a median survival of only 0.92 years post-diagnosis. Current screening methods relying on neuropsychological tests (e.g., Psychometric Hepatic Encephalopathy Score, PHES) have limitations such as time-consuming procedures and subjective interpretation, potentially delaying diagnosis. To address this, we integrated four cirrhotic transcriptomic cohorts (GSE41919, GSE57193, GSE139602, and GSE15654) and employed an integrated algorithm (LASSO [Least Absolute Shrinkage and Selection Operator]–RFE [Recursive Feature Elimination]–random forest) to identify HE-specific biomarker genes. Ultimately, we developed an HE risk-prediction system centered on eight HE-specific marker genes, namely, PRB2, TUBA1C, NPC2, LRRC32, TLN1, SOX9, SERPINA3 and RNASE4. Based on these genes, an XGBoost (eXtreme Gradient Boosting)-based HE risk stratification model was constructed, and SHAP (SHapley Additive exPlanations) analysis was further introduced to address the “black-box” limitation of conventional machine learning models and to improve the interpretability. The finalized eight-gene system enables accurate, efficient, and interpretable HE risk assessment in patients with cirrhosis. Functional characterization through gene set enrichment analysis and structural equation modeling further revealed that these marker genes converge on four interconnected biological processes, namely, metabolic homeostasis, synaptic and neural transmission, immune inflammatory signaling, and hepatic detoxification, which collectively reflect the gut–liver–brain axis disruption central to HE pathogenesis. This dual-model system, incorporating both cirrhosis progression and survival prognosis, provides a reliable and clinically applicable tool for early HE risk warning and stratification, reducing the limitations of traditional neuropsychological screening and offering a translational foundation for timely intervention and prognostic optimization in high-risk cirrhotic patients. Full article

Circulating lipoprotein concentrations decrease in critical illness, suggesting that plasma phosphatidylcholine (PC) levels may also decline. However, published data on individual PC species in critical illness are conflicting, and underlying liver cirrhosis may substantially influence systemic lipid profiles. We therefore examined the impact of systemic inflammatory response syndrome (SIRS)/sepsis, with and without liver cirrhosis, on circulating PC species. We quantified 21 plasma PC species in 160 patients with SIRS, sepsis, or septic shock, including 31 patients with liver cirrhosis. PC profiles were compared with those of healthy controls and across clinically relevant subgroups. In patients with SIRS/sepsis without liver cirrhosis, 15 PC species were reduced compared with healthy controls, whereas PC 32:0 was increased. In patients with SIRS/sepsis and concomitant liver cirrhosis, 12 PC species were lower than in septic patients without cirrhosis, while PC 32:0 was again increased. Because a proportion of circulating PC is derived from phosphatidylethanolamine (PE), we explored whether altered PE-to-PC conversion could account for these changes; however, the observed pattern did not support this mechanism. No significant differences in PC species were observed between survivors and non-survivors. In summary, critical illness is associated with a broad reduction in circulating PC species, and this decrease is accentuated by coexisting liver cirrhosis. In contrast, PC 32:0 is consistently increased in both SIRS/sepsis and SIRS/sepsis with cirrhosis, suggesting a distinct biological role that warrants further investigation. Full article

Background and Objectives: In Taiwan, hepatitis B virus (HBV) or hepatitis C virus (HCV) infections are the most common causes of hepatocellular carcinoma (HCC). However, an increasing number of non-HBV and non-HCV (NBNC) patients developing HCC has been noted in recent years. The pathogenic connection between NBNC status and HCC development remains largely elusive. This study aims to explore the differences in clinical manifestations and pathological findings among HCC patients with HBV, HCV, and NBNC etiologies. Methods: This retrospective study analyzed 521 HCC patients with complete hepatic viral profiles at a single medical center in Taiwan between 2016 and 2020. Differentially expressed gene (DEG) analysis, xCell stromal cell estimation, and Gene Set Enrichment Analysis (GSEA) were employed to explore the distinct oncogenic mechanisms between the viral and NBNC groups. Results: The final cohort included 38 NBNC-HCC patients. Clinically, the NBNC-HCC patients exhibited a significantly lower FIB-4 index than the HCV-HCC patients (3.191 vs. 6.077, p = 0.0019). Furthermore, fewer NBNC-HCC patients presented with imaging-defined cirrhosis compared to HBV-HCC patients (44.4% vs. 68.1%, p = 0.0057), and a lower proportion had high Ishak scores (5–6) compared to HCV-HCC patients (31.3% vs. 75.6%, p = 0.0025). DEG analysis revealed differential expression in oncogenes (OIT3, AKR1B10) and liver fibrosis-related genes (COLEC10, CXCL14, and LINC01093). Subsequent GSEA and stromal cell analyses highlighted significant differential enrichment in hepatic stellate cells and vascular endothelial cells. Conclusions: NBNC-HCC patients present with significantly lower rates of cirrhosis and fibrosis compared to their viral counterparts. The distinct gene expression profiles and cell-type enrichment features observed between the viral and NBNC groups indicate a divergent, etiology-specific pathogenesis driving NBNC-HCC. Full article

Background/Objectives: The 2026 Barcelona Clinic Liver Cancer (BCLC) update recommends surgical resection for a single hepatocellular carcinoma larger than 2 cm with preserved liver function and states that age alone should not preclude surgery. How often eligible older patients undergo resection, and how they fare, remains unquantified. Methods: Using the Korean Primary Liver Cancer Registry (2008–2021), we identified 3374 patients meeting all registry-based eligibility criteria of the 2026 BCLC update. Survival was measured from the date of radiological diagnosis in every patient, with vital status and cause of death obtained by linkage to national death records. We compared use of resection and survival among patients younger than 75 years and those 75 years or older, and across resection, ablation, other treatment, and no treatment, using Cox regression, restricted mean survival time (RMST), and competing-risk models. Results: Resection was performed in 60.6% of patients younger than 75 years versus 28.9% of those 75 years or older (p < 0.001); among older patients not undergoing resection, 21.5% received none. Older age was independently associated with lower odds of resection (adjusted odds ratio 0.36, 95% CI 0.28–0.46; p < 0.001). In this age group, 5-year survival was 61.3%, 62.1%, 32.9%, and 6.5% across the four treatment categories; the adjusted hazard ratio for no treatment versus resection was 4.97 (95% CI 3.26–7.57; p < 0.001). In unadjusted analysis, mean survival within the first 5 years was 13.3 months longer after resection (RMST difference, 95% CI 9.7–16.9; p < 0.001). Findings were consistent in competing-risk, weighted, cirrhosis-adjusted, and multiply imputed analyses. Conclusions: Older patients meeting eligibility criteria underwent resection far less often than younger patients, and a substantial minority received none, a pattern associated with markedly shorter survival. Full article

Liver involvement is frequent in rheumatoid arthritis (RA) and may progress from steatosis to fibrosis, cirrhosis, or hepatocellular carcinoma. Liver fibrosis (LF) in RA is multifactorial, but the available data are limited and the impact of methotrexate (MTX) remains controversial. In this cross-sectional study, 51 RA patients (46 females; mean age of 48.8 ± 8.2 years; and a median disease duration of 12 years) were enrolled. LF was assessed using non-invasive indices (the aspartate aminotransferase-to-platelet ratio index [APRI] and fibrosis-4 index [FIB-4]) and liver stiffness measurement (LSM) using shear wave elastography. Serum endothelin-1 (ET-1) and selected organokines (namely myostatin, resistin, and osteoprotegerin) were quantified by the ELISA. Associations of the APRI, FIB-4, and LSM with organokines and endothelin-1 were analyzed using univariable and multivariable linear regression, whereas correlations with the RA-specific cardiovascular (CV) risk score (ERS-RA) and echocardiographic parameters of left ventricular diastolic dysfunction (LVDD) were assessed using Spearman’s rank correlation. Myostatin and resistin showed a significant positive and significant negative association with LSM, respectively, while FIB-4 was negatively correlated with lateral and medial e’ velocities and positively with the ERS-RA. MTX use, mean weekly dose, cumulative dose, and endothelin-1 were not associated with the APRI, FIB-4, LSM, or LVDD. These exploratory findings support the potential role of myostatin and resistin in LF-related phenotypes and suggest that FIB-4 may capture aspects of both hepatic and cardiovascular risk in RA. RA patients with elevated FIB-4 values may require echocardiographic assessment and comprehensive CV risk evaluation. In this cohort, MTX exposure and endothelin-1 were not associated with LF or LVDD. Full article