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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

Background and Objectives: Patients with cirrhosis and acute kidney injury (AKI) frequently receive albumin, although plasma volume expansion may contribute to pulmonary or venous congestion. Point-of-care ultrasound (POCUS) may complement bedside assessment when formal echocardiography or advanced hemodynamic monitoring is not immediately available. This study evaluated baseline pulmonary and venous congestion using POCUS in patients with cirrhosis and AKI receiving albumin therapy. Materials and Methods: This exploratory prospective cohort included adults with cirrhosis, ascites, and ICA-AKI stage 1B or higher who were managed under an institutional protocol prescribing intravenous 20% or 25% albumin at 1 g/kg/day for two consecutive days, capped at 100 g/day. Before albumin administration, B-line-defined pulmonary congestion was assessed using a 28-site lung protocol, and IVC-defined venous congestion was assessed using inferior vena cava (IVC) diameter and collapsibility. Serum creatinine was recorded within 12 h before treatment and 48 h after initiation. Complete renal response was defined as serum creatinine within 0.3 mg/dL of the pre-AKI baseline; partial response was defined as regression by at least one ICA-AKI stage without complete response. Results: Twenty-two patients were included. B-line-defined pulmonary congestion was present in 18/22 (81.8%). IVC assessment was technically evaluable in 20 patients, of whom 6/20 (30.0%) met the criteria for IVC-defined venous congestion. The Hodges–Lehmann estimate of the median paired creatinine difference was +0.03 mg/dL (95% CI, −0.52 to 1.31) without pulmonary congestion and −0.33 mg/dL (95% CI, −0.67 to −0.20) with pulmonary congestion. Renal response occurred in 1/4 (25.0%) and 12/18 (66.7%), respectively (two-sided Fisher exact p = 0.264). Among patients with evaluable IVC examinations, renal response occurred in 8/14 (57.1%) without and 3/6 (50.0%) with IVC-defined venous congestion (p = 1.000). Conclusions: Baseline POCUS frequently identified ultrasound-defined congestion, but congestion status did not clearly distinguish short-term renal response. These exploratory findings support the feasibility of bedside POCUS phenotyping but do not establish that congestion modifies albumin response or clinical outcomes. Full article

Background/Objectives: Nonselective beta-blockers (NSBBs) are foundational for variceal bleeding prophylaxis in cirrhosis. After transjugular intrahepatic portosystemic shunt (TIPS) placement, portal pressure is mechanically decompressed, and practice guidance generally supports discontinuing NSBBs when shunt function is adequate and no other indication exists; however, real-world adoption and outcomes associated with post-TIPS NSBB strategies remain incompletely characterized in large, multicenter populations. Methods: We performed a real-world, target-trial emulation in the TriNetX U.S. Collaborative Network using a prespecified 90-day landmark. Adults (≥18 years) with cirrhosis undergoing first TIPS who had NSBB prescribed in the prior year and who survived to post-TIPS day 90 were included. Strategy was classified during days 0–90 (continuation: ≥1 NSBB prescription; discontinuation: none). Propensity score matching (1:1) balanced demographics, comorbidities, portal hypertension complications, and laboratory values (including the components of the Freiburg Index of Post-TIPS Survival [FIPS], Model for End-stage Liver Disease–Sodium [MELD-Na], and Child–Pugh scores). Follow-up began at day 90 and continued through day 365. Primary outcomes were overall survival and transplant-free survival; secondary outcomes were hepatic encephalopathy (HE), esophageal variceal bleeding (EVB), and ICU admission. Results: Among 5111 patients (continuation: n = 2558; discontinuation: n = 2553), 2180 matched pairs were analyzed. One-year survival was similar (89.3% vs. 89.6%; HR: 1.03; 95% CI: 0.84–1.27), as was transplant-free survival (78.8% vs. 77.9%; HR: 0.95; 95% CI: 0.82–1.10). The cause-specific hazard of HE was higher with continuation (HR; 1.29; 95% CI: 1.14–1.46), while those of EVB (HR: 1.08; 95% CI: 0.90–1.29) and ICU admission (HR: 1.02; 95% CI: 0.86–1.22) were similar. Results were consistent in both strict discontinuation and adherence-based sensitivity analyses. Conclusions: In stabilized post-TIPS patients with prior NSBB use, continuation was not associated with improved 1-year survival or transplant-free survival and was associated with a higher cause-specific hazard of HE. Full article

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD), a leading cause of chronic liver disease, encompasses a continuum from steatosis to metabolic dysfunction-associated steatohepatitis (MASH), fibrosis, cirrhosis, and hepatocellular carcinoma. This review aimed to synthesize current evidence on how metabolomic, lipidomic, and spatial multi-omic approaches illuminate MASLD pathogenesis and support precision hepatology. Methods: A structured narrative review was conducted through searches of PubMed, Scopus, and Web of Science, complemented by manual screening of key references. Studies were prioritized when they addressed MASLD biology, metabolic rewiring, lipid remodeling, mitochondrial dysfunction, inflammatory and fibrogenic pathways, gut–liver–adipose crosstalk, biomarker development, or therapeutic monitoring. Results: The reviewed evidence identifies MASLD as a systemic metabolic disorder shaped by excess lipid flux, enhanced de novo lipogenesis, impaired mitochondrial adaptation, oxidative and endoplasmic reticulum stress, sterile inflammation, and hepatic stellate-cell activation. Recurrent metabolomic signatures include altered amino acid, fatty acids, bile acid, and microbial co-metabolite pathways. Lipidomic studies consistently implicate depletion of protective polyunsaturated fatty acids, lysophosphatidylcholines, and phosphatidylcholines, in association with accumulation of diacylglycerols and ceramides, in the transition from steatosis to MASH and fibrosis. Emerging spatial and multi-omic analyses further resolve cell-specific metabolic niches involving hepatocytes, macrophages, endothelial cells, and stellate cells. Conclusions: Metabolomics provides a mechanistic and translational bridge between molecular injury, histological progression, and non-invasive risk stratification in MASLD. Future progress requires standardized analytical workflows, longitudinal validation, causal pathway interrogation, and integration with imaging, genetics, microbiome profiling, and treatment-response phenotyping. Clinical implementation will require standardized platforms, transparent metabolite identification, external validation across diverse populations, cost-effectiveness analyses, and regulatory-grade evidence of clinical utility. Full article

Hepatic fibrosis is a pathological process involving the systemic reconfiguration of the liver microenvironment under chronic liver injury. It is a pathological wound healing response characterized by the excessive deposition of extracellular matrix (ECM) driven by the activation of hepatic stellate cells (HSCs), starting with the capillarization of liver sinusoidal endothelial cells (LSECs). This process can lead to liver structure destruction, portal hypertension, and even liver dysfunction, and is a major driving factor for death related to liver diseases. During this process, hypoxia initiates the transcriptional upregulation of effector molecules such as vascular endothelial growth factor (VEGF) and Lysyl oxidase (LOX) by stabilizing hypoxia-inducible factors (HIFs), inducing changes in LSEC phenotype and activation of HSCs, thus becoming a core driving factor. Activated HSCs not only exacerbate the capillarization of LSECs and tissue hypoxia but also strengthen the transcriptional activity of HIFs through autocrine/paracrine signaling, establishing a positive feedback loop linking hypoxia to HIFs and HSC activation, continuously driving the progression of liver fibrosis and significantly increasing the probability of chronic liver diseases evolving into cirrhosis and the risk of death. This review will analyze the mechanism of liver fibrosis driven by hypoxia, integrate the current treatment landscape, focus on exploring the therapeutic targets related to hypoxia-induced activation of hepatic stellate cells leading to liver fibrosis, and evaluate their translational potential. It is expected to provide information for future effective anti-fibrotic intervention strategies. Full article

Background/Objectives: Hepatitis B virus (HBV) infection remains a major global health challenge because of its association with cirrhosis, hepatic failure, and hepatocellular carcinoma. Patients receiving rituximab-containing regimens are at particularly high risk for HBV reactivation due to profound B-cell depletion and prolonged immunosuppression. This study aimed to evaluate HBV serologic testing practices before rituximab initiation and to assess the incidence and outcomes of HBV reactivation among patients treated with rituximab at a tertiary care center in Jeddah, Saudi Arabia. Methods: A retrospective observational study was conducted on patients who received rituximab between 2010 and 2020 at a tertiary university hospital in Jeddah, Saudi Arabia. Demographic, clinical, laboratory, and treatment-related data were collected from electronic medical records. HBV reactivation was defined according to the American Association for the Study of Liver Diseases (AASLD) criteria. Results: A total of 611 patients were included. HBV serologic testing prior to rituximab initiation was documented in 60.8% of patients with hematological malignancies and 71.7% of those with non-hematological diseases. HBV reactivation occurred in 7 patients (3.4%) in the hematological malignancy cohort, all with lymphoma. Nine patients received antiviral prophylaxis. HBV reactivation was associated with significant morbidity, and liver-related mortality occurred in 28% of reactivation cases. Conclusions: HBV serologic testing was not universally documented prior to rituximab initiation, and antiviral prophylaxis was received by few patients. HBV reactivation was associated with significant morbidity and mortality. These findings support the need for systematic HBV evaluation and prophylaxis protocols in patients receiving rituximab. Full article