The concept of recompensation has emerged as an important milestone in cirrhosis management, shifting attention beyond symptom control toward sustained recovery of liver function. At EASL Congress 2026, the EUROTIPS-German Cirrhosis Study Group presented multicenter data demonstrating that recompensation following transjugular intrahepatic portosystemic shunt (TIPS) is achievable and associated with excellent long-term outcomes. Baveno VII defines recompensation as durable clinical recovery after control or removal of the underlying liver disease cause. This requires sustained absence of decompensating events, withdrawal of therapies previously needed for complications, and stable restoration of liver function. The concept reflects meaningful disease stabilization rather than temporary symptomatic improvement. The EuroTIPS study focused on patients with decompensated cirrhosis undergoing TIPS for recurrent variceal bleeding or refractory and recurrent ascites. Investigators specifically examined whether portal decompression through TIPS could facilitate recompensation in patients with potentially controllable etiologies such as alcohol-related liver disease, viral hepatitis, and autoimmune hepatitis. The findings were encouraging. Approximately one-tenth of eligible patients achieved recompensation following TIPS. More importantly, most individuals who reached this state maintained durable clinical stability during follow-up, while only a small minority developed renewed decompensation. These observations suggest that meaningful hepatic recovery can occur after successful portal pressure reduction in appropriately selected patients. Recompensation carried substantial prognostic significance. Patients who achieved recovery demonstrated markedly superior transplant-free survival compared with those who remained decompensated. The survival benefit persisted throughout long-term follow-up, supporting the view that recompensation reflects genuine disease modification rather than transient clinical improvement. Clinical recovery was also accompanied by reduced treatment burden. Many recompensated patients were able to discontinue medications previously required for ascites or hepatic encephalopathy management, further supporting the durability of improvement after TIPS. Investigators identified several factors associated with successful recompensation. Patients generally had better preserved liver function at the time of TIPS placement, and lower MELD scores emerged as an independent predictor of recovery. Alcohol-related liver disease also showed a greater likelihood of recompensation, suggesting that disease etiology remains an important determinant of reversibility. Although re-decompensation occurred in a minority of cases, outcomes remained favorable overall. The study reinforces the concept that TIPS may offer more than portal decompression alone and supports recompensation as an important therapeutic endpoint in advanced cirrhosis management.

Cirrhosis represents more than progressive fibrosis; it reflects a state of regenerative failure in which the liver gradually loses its ability to repair and restore functional tissue. At EASL Congress 2026, investigators presented early clinical findings evaluating hepatocyte-derived liver progenitor-like cells (HepLPCs) as a regenerative treatment strategy for advanced cirrhosis. In advanced disease, extensive fibrosis, portal hypertension, and structural distortion create a hostile hepatic environment that limits natural regeneration and increases the risk of decompensation. While liver transplantation remains the definitive treatment, donor shortages and limited accessibility continue to leave many patients without viable options. This has stimulated growing interest in therapies capable of restoring hepatic regeneration rather than solely slowing disease progression. The presented studies explored the use of HepLPC therapy in patients with cirrhosis through prospective, open-label clinical trials. Cells were administered using image-guided hepatic arterial infusion, a minimally invasive approach designed to deliver regenerative cells directly to the diseased liver while maintaining procedural safety. A key finding was the favorable early safety profile. Investigators reported few treatment-related adverse events and no significant treatment-related serious adverse events during follow-up. Successful completion of therapy without major procedural complications supported the feasibility of hepatic arterial delivery in carefully selected cirrhotic patients. Beyond safety, early signals of clinical benefit were observed. Serial assessments demonstrated improvements in global liver function, including trends toward lower Child-Pugh and MELD scores, suggesting potential enhancement of overall hepatic status. Recovery was also reflected in markers of hepatic synthetic function. Progressive increases in albumin, prealbumin, and cholinesterase levels suggested improved protein synthesis, while reductions in blood ammonia supported better detoxification capacity. Coagulation parameters, which are often impaired in advanced cirrhosis, also showed improvement following therapy, indicating broader recovery of hepatic synthetic pathways involved in hemostatic regulation. In addition, reductions in hepatic venous pressure gradient suggested potential improvement in portal hypertension and the underlying hepatic microenvironment. Long-term follow-up provided further encouraging observations. Imaging demonstrated reduction of ascites and improvement in portal hypertension–related manifestations, while some patients achieved sustained clinical stability without liver transplantation. Although these findings remain preliminary and require longer follow-up, HepLPC therapy introduces an important regenerative concept in hepatology. Rather than focusing exclusively on fibrosis suppression, this strategy aims to restore hepatic function and potentially modify the disease trajectory of decompensated cirrhosis.

The gut microbiome continues to emerge as an important contributor to outcomes in cirrhosis. At EASL Congress 2026, investigators presented findings from a multinational cohort study examining whether microbial composition and metabolic pathways could predict short-term hospitalization risk in patients with cirrhosis. The study evaluated microbiome profiles across international cohorts and demonstrated clear geographic differences in microbial diversity. However, despite these regional variations, a consistent pattern emerged among patients who required hospitalization within 90 days. These individuals generally exhibited lower microbial diversity compared with patients who remained clinically stable, suggesting that reduced microbial richness may reflect increased vulnerability and disease instability. Interestingly, geographic differences became less pronounced among higher-risk patients. While stable patients showed substantial microbiome variability between countries, hospitalized individuals appeared to converge toward a shared microbial pattern associated with advanced clinical risk. This finding suggests that disease-related microbial changes may outweigh regional influences as cirrhosis progresses. Beyond microbial composition, investigators identified important alterations in microbial metabolic pathways. Patients who were later hospitalized showed reduced activity in pathways involved in carbohydrate degradation, amino acid metabolism, and short-chain fatty acid fermentation. In contrast, pathways associated with stress adaptation, membrane biosynthesis, lipid metabolism, and nucleotide metabolism were relatively enriched. These findings point toward a microbiome that becomes increasingly stress-adapted and metabolically altered in higher-risk cirrhosis. Such pathway remodeling may have important biological consequences. Reduced fermentation and diminished production of beneficial microbial metabolites may impair intestinal barrier integrity and microbial homeostasis, while increased reliance on nitrogen- and sulfur-containing substrates could promote accumulation of potentially harmful metabolites. Several specific microbial pathways remained independently associated with hospitalization risk even after adjustment for MELD score, cirrhosis etiology, decompensation status, and commonly used therapies. Traditional clinical markers continued to retain prognostic value. Higher MELD scores, alcohol-related liver disease, ascites, and lactulose use were associated with greater hospitalization risk, whereas higher serum albumin levels appeared protective. Certain microbial species also showed important associations, with Enterococcus faecium linked to increased risk and beneficial commensals such as Bifidobacterium and Faecalibacterium associated with more favorable outcomes. Importantly, predictive models integrating microbiome and clinical data outperformed models based on clinical variables alone. These findings suggest that microbial profiling may become a valuable adjunct to conventional prognostic tools, potentially supporting earlier identification of high-risk patients and more personalized management strategies in cirrhosis.

Alcohol use disorder remains a major contributor to cirrhosis progression, hepatic decompensation, and reduced transplant eligibility. While alcohol abstinence continues to be the foundation of treatment, maintaining long-term abstinence is often difficult, and currently available pharmacologic therapies may have limitations in patients with advanced liver disease. At EASL Congress 2026, investigators presented real-world evidence suggesting that GLP-1 receptor agonists may offer benefits extending beyond metabolic control in patients with alcohol-related liver disease. GLP-1 receptor agonists, commonly prescribed for type 2 diabetes and obesity, have attracted attention because of their potential influence on alcohol-related behaviors and liver injury. Their proposed mechanisms include modulation of brain reward pathways involved in alcohol craving, particularly within dopaminergic circuits, alongside metabolic and anti-inflammatory effects. These agents may reduce insulin resistance, decrease hepatic steatosis, promote weight loss, and suppress inflammatory and fibrogenic pathways, providing a biologically plausible role in alcohol-related liver disease. The study utilized data from the TriNetX network, including 111 healthcare organizations across the United States. Investigators evaluated patients with alcohol-related liver disease and type 2 diabetes over a five-year period. After extensive matching for demographic, metabolic, laboratory, and treatment-related variables, two comparable cohorts of approximately 9,000 patients each were analyzed—one receiving GLP-1 receptor agonists and one without GLP-1 therapy. Results demonstrated significant associations between GLP-1 therapy and improved alcohol-related outcomes. Patients receiving treatment experienced fewer alcohol intoxication events and reduced alcohol withdrawal episodes over follow-up. Liver-related outcomes were also favorable, with lower rates of alcohol-associated hepatitis, cirrhosis progression, hepatic decompensation, and overall hospitalization compared with matched controls. Event curves remained consistently separated over time, suggesting sustained benefit. Investigators also explored additional endpoints, including alcohol remission, transplant-related outcomes, and biomarkers of alcohol use. Although several trends favored GLP-1 therapy, these findings did not consistently achieve statistical significance, partly because objective alcohol biomarkers such as phosphatidylethanol were infrequently available. Despite encouraging findings, important limitations remain. The study was retrospective and observational, relied on coding data, and could not confirm long-term treatment adherence or establish direct causality. Overall, this large U.S. cohort suggests that GLP-1 receptor agonists may have a promising adjunctive role in alcohol-related liver disease and cirrhosis. However, prospective randomized studies remain necessary before defining their place alongside established therapies for alcohol use disorder.

Understanding the true burden of steatotic liver disease remains an important public health challenge. At EASL Congress 2026, findings from the multinational LiverScreen study provided valuable insight into the prevalence and severity of metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction-associated alcohol-related liver disease (MetALD), and alcohol-related liver disease (ALD) across Europe. The LiverScreen project involved more than 30,000 individuals over 40 years of age from nine European countries and used liver stiffness measurement and ALT testing as initial screening tools. Participants with abnormal findings underwent further hepatology evaluation, including repeat elastography, imaging, laboratory assessment, and liver biopsy when appropriate. Classification followed the updated steatotic liver disease nomenclature. The study demonstrated that MASLD is by far the most common form of steatotic liver disease in the general population. However, an important clinical paradox emerged. Although MASLD accounted for most detected cases, disease severity increased progressively from MASLD to MetALD and ALD. Patients with alcohol-related phenotypes showed substantially higher rates of elevated liver stiffness and advanced fibrosis, indicating greater risk of clinically significant liver disease. Several factors independently increased the likelihood of liver stiffness elevation. Type 2 diabetes, obesity, multiple cardiometabolic risk factors, and excess alcohol consumption all contributed to worsening liver disease severity. Importantly, investigators observed a synergistic relationship between alcohol exposure and diabetes or glucose intolerance, suggesting that metabolic dysfunction and alcohol together may accelerate hepatic injury more aggressively than either factor alone. The study also highlighted a major challenge in population-based liver disease research: underreporting of alcohol intake. In a Danish sub-cohort, phosphatidylethanol (PEth), an objective alcohol biomarker, revealed substantial discrepancies between self-reported alcohol use and biological assessment. Many participants initially classified as MASLD or MetALD would have met criteria for more alcohol-related disease categories when PEth results were considered. These findings suggest that the true burden of MetALD and ALD may be considerably underestimated. Among patients undergoing specialist evaluation and biopsy, advanced fibrosis was more frequent in MetALD and ALD than in MASLD, further reinforcing the greater severity associated with alcohol-related disease phenotypes. Overall, the LiverScreen study emphasizes that prevalence alone does not reflect disease impact. While MASLD remains the dominant phenotype across Europe, alcohol-related liver disease carries disproportionate severity and may be more common than currently recognized when objective alcohol assessment is incorporated.

Overlap and variant syndromes in autoimmune liver disease remain among the most challenging areas in hepatology because patients often present with findings that do not fit neatly into a single diagnosis. At EASL Congress 2026, experts emphasized that conditions such as MASLD-AIH, PSC-AIH, and PBC-AIH require careful interpretation of biochemical, serological, histological, and radiological findings rather than reliance on a single marker or scoring system. One major challenge involves distinguishing autoimmune hepatitis (AIH) from metabolic dysfunction-associated steatotic liver disease (MASLD). Patients with obesity, diabetes, hepatic steatosis, positive autoantibodies, and elevated liver enzymes frequently create diagnostic uncertainty. Importantly, the presence of ANA, SMA, or mildly elevated IgG does not automatically confirm AIH, as these abnormalities may also occur in MASLD. Features raising suspicion for AIH include markedly elevated ALT levels, significant autoantibody titers, IgG elevation, and liver injury disproportionate to expected metabolic disease activity. In such situations, liver biopsy becomes essential. Histological evaluation, particularly the presence and severity of interface hepatitis and lymphoplasmacytic infiltration, helps distinguish true autoimmune disease from steatohepatitis with incidental immune findings. The session also explored the evolving relationship between AIH and primary sclerosing cholangitis (PSC). In younger patients, AIH may initially dominate the clinical picture and respond to immunosuppression, while cholestatic features later emerge, suggesting progression toward PSC. Rising alkaline phosphatase levels, positive ANCA, inflammatory bowel disease, or ductular changes should prompt cholangiographic evaluation. MRCP was highlighted as the key diagnostic investigation because liver biopsy may fail to identify large-duct PSC. PBC-AIH was discussed as a variant syndrome rather than a true overlap syndrome in most patients. Persistent or disproportionate transaminase elevation, elevated IgG, and inadequate explanation by cholestatic disease alone should prompt reconsideration of the diagnosis. Reassessment following UDCA therapy and careful histological evaluation remain central to management decisions. A unifying message emerged throughout the discussion: diagnostic discordance should trigger further investigation. When laboratory findings, imaging, clinical behavior, or histology do not align with the expected disease pattern, clinicians should reconsider the diagnosis. Liver biopsy remains central in many cases, while MRCP is essential when PSC is suspected. Recognizing evolving disease phenotypes and diagnostic inconsistencies is critical for accurate diagnosis and individualized management.

Left-sided portal hypertension is a distinct and often underrecognized form of portal hypertension caused by splenic vein obstruction rather than primary liver disease. Presented at EASL Congress 2026, this session highlighted how the condition differs fundamentally from classical portal hypertension associated with cirrhosis and why recognizing its unique features is essential for accurate diagnosis and management. Unlike cirrhotic portal hypertension, patients with left-sided portal hypertension usually maintain preserved liver function and rarely develop ascites. The condition is primarily characterized by splenomegaly, thrombocytopenia, and the development of gastric varices, particularly involving the gastric fundus. These clinical features create a disease pattern that is hemodynamically and clinically distinct from conventional portal hypertensive syndromes. The underlying mechanism begins with obstruction or thrombosis of the splenic vein, which disrupts normal venous drainage from the spleen. This results in the formation of collateral pathways that redirect blood flow, predominantly toward the gastric fundus, leading to isolated gastric varices. An important distinguishing feature is that blood flow in the left gastric vein remains hepatopetal, contrasting with the altered hemodynamics commonly seen in cirrhotic portal hypertension. Endoscopy plays a valuable role in diagnosis. Isolated fundal gastric varices are the most common finding, although diffuse reticular variceal patterns may also occur. Recognition of these patterns, particularly in the absence of significant liver disease, should raise suspicion for left-sided portal hypertension. Associated findings such as splenic vein abnormalities and splenomegaly further strengthen the diagnosis. Pancreatic disease remains the leading cause of this condition. Both acute and chronic pancreatitis frequently lead to splenic vein thrombosis, while pancreatic tumors, pseudocysts, and post-surgical pancreatic changes represent additional etiologies. Less commonly, hypercoagulable states may contribute, and thrombophilia evaluation may be appropriate when clinical findings suggest an underlying systemic predisposition. Although progression to clinically significant variceal bleeding is relatively uncommon, delayed diagnosis remains an important challenge because splenic vein pathology may be overlooked on routine imaging. Careful evaluation of thrombocytopenia, splenomegaly, and gastric varices is therefore critical. Overall, left-sided portal hypertension should be viewed as a unique vascular disorder rather than a variant of cirrhotic portal hypertension. Early recognition of its characteristic clinical, endoscopic, and radiological features is essential to prevent complications and guide appropriate management.

The updated EASL 2025 treatment recommendations for HBeAg-negative chronic hepatitis B aim to simplify treatment decisions and improve identification of patients who may benefit from antiviral therapy. Presented at EASL Congress 2026, these revised indications move beyond older frameworks by incorporating non-invasive assessment of liver disease severity and reducing the number of patients categorized within the clinically uncertain “grey zone.” To evaluate the real-world impact of these changes, investigators studied a cohort of 1,501 treatment-naïve patients with HBeAg-negative chronic hepatitis B. Patients previously classified as inactive infection or placed within the grey-zone category under earlier guidelines were reassessed using both the 2017 and 2025 EASL recommendations. Follow-up incorporated liver stiffness measurements and histological evaluation to better characterize disease activity and treatment eligibility. A major finding was the significant reduction in grey-zone classification under the updated criteria. While the classification of inactive HBV infection remained largely stable, nearly half of the patients previously lacking a clear treatment indication were reclassified as having definite eligibility for therapy. This shift represents an important advance because grey-zone patients have historically posed challenges in clinical decision-making and often required prolonged observation before treatment decisions could be made. The revised recommendations also expanded identification of patients requiring antiviral treatment. Using the EASL 2025 criteria, over one-third of patients fulfilled treatment indications. Detectable HBV DNA combined with increased liver stiffness emerged as the most frequent reason for treatment eligibility, underscoring the growing role of non-invasive fibrosis assessment in routine hepatology practice. Additional patients qualified based on elevated HBV DNA together with abnormal ALT levels. Importantly, the updated recommendations showed stronger alignment with real-world physician behavior. Patients meeting the new criteria were considerably more likely to receive antiviral therapy during follow-up than those without treatment indications, and this pattern remained consistent over time. This suggests that the revised algorithm more accurately reflects how clinicians already approach treatment decisions in practice. Overall, the EASL 2025 treatment framework offers clearer clinical stratification for HBeAg-negative chronic hepatitis B. By simplifying thresholds and incorporating liver stiffness assessment, the new guidance reduces diagnostic uncertainty, limits grey-zone classification, and supports earlier and more precise antiviral treatment decisions in everyday clinical care.

Achieving sustained virological response (SVR) remains a major therapeutic goal in chronic hepatitis D, and new real-world evidence presented at EASL Congress 2026 provides important insights into treatment outcomes with bulevirtide. Findings from the French ANRS HEP-Delta cohort suggest that the duration of HDV RNA suppression during therapy may play a crucial role in predicting long-term viral control after treatment discontinuation. The study explored whether maintaining undetectable HDV RNA for at least 96 weeks before stopping therapy could predict sustained response in routine clinical practice. Investigators analyzed data from 364 patients treated with bulevirtide, either as monotherapy or in combination with interferon. The cohort reflected real-world practice, including patients with varied backgrounds and a substantial burden of cirrhosis. A key observation was the strong association between prolonged HDV RNA negativity and post-treatment viral control. Patients who maintained undetectable HDV RNA for longer durations, particularly beyond 96 weeks, experienced significantly higher rates of sustained virological response after stopping bulevirtide. These findings support the concept that extended viral suppression may serve as an important marker of durable treatment success. The study also highlighted the influence of treatment strategy. Patients receiving early combination therapy with bulevirtide and interferon achieved higher rates of undetectable HDV RNA at the end of treatment compared with those receiving bulevirtide alone. Although treatment durations were similar, interferon appeared to enhance virological suppression and increase the likelihood of achieving end-of-treatment viral negativity. Another important issue discussed was the role of assay sensitivity in monitoring treatment response. Comparisons between different HDV RNA assays revealed that some samples classified as negative by one platform remained detectable on another, suggesting that assay selection can influence interpretation of virological response and potentially affect treatment decisions. Further analysis identified lower baseline HDV RNA levels and longer periods of viral suppression as independent predictors of undetectable HDV RNA at treatment completion. However, among patients receiving combination therapy, additional factors such as cirrhosis status and intermittent viral positivity also influenced outcomes. Overall, the French HEP-Delta experience reinforces the importance of prolonged HDV suppression during bulevirtide therapy. Maintaining HDV RNA negativity for more than 96 weeks emerged as a strong indicator of sustained response following treatment discontinuation, supporting its potential role as a practical marker for long-term treatment success in chronic hepatitis D.

The management of metabolic dysfunction-associated steatohepatitis (MASH) is evolving rapidly, with increasing emphasis on selecting the right patients, monitoring treatment response, and identifying when therapy should be continued or reconsidered. During EASL Congress 2026, experts discussed a practical approach to initiating, monitoring, and stopping anti-MASH therapy. A central message was that treatment should primarily target patients with clinically significant fibrosis, particularly those with moderate-to-advanced fibrosis (F2–F3), where the risk of disease progression becomes more substantial. Patients with early-stage disease generally derive limited benefit from pharmacological therapy, while evidence supporting routine treatment in advanced cirrhosis remains insufficient. Accurate fibrosis staging is therefore essential before initiating therapy. Liver biopsy is no longer routinely required for treatment selection. Instead, non-invasive tests have become central to clinical decision-making. Tools such as FibroScan, magnetic resonance elastography, and ELF scoring help identify suitable treatment candidates while reducing procedural burden. However, interpretation should never rely on a single measurement alone and must be integrated with clinical findings, laboratory parameters, and imaging results. Excluding advanced cirrhosis remains particularly important because most available evidence for anti-MASH therapy comes from non-cirrhotic populations. Findings such as thrombocytopenia, portal hypertension, markedly elevated liver stiffness, or discordant non-invasive assessments should raise suspicion for advanced disease and prompt further evaluation. Resmetirom was highlighted as an important therapeutic option. By activating thyroid hormone receptor-β pathways, it promotes hepatic fat clearance and improves metabolic activity within the liver. Current evidence supports its use in patients with MASH and significant fibrosis, while caution is advised in advanced cirrhosis, uncontrolled thyroid disease, alcohol-related liver disease, and patients with significant portal hypertensive complications. Monitoring treatment response relies largely on non-invasive biomarkers rather than repeat biopsy. Improvements in liver stiffness, ALT levels, or hepatic fat content after approximately one year may indicate meaningful biological response and support continuation of therapy. Temporary liver enzyme elevations during early resmetirom treatment were described as generally self-limited and not necessarily indicative of hepatotoxicity. Semaglutide was also discussed as an important metabolic strategy, particularly because it addresses obesity, insulin resistance, and diabetes while contributing to weight loss and hepatic improvement. Ultimately, continuation of therapy should be guided by objective evidence of benefit, whereas absence of measurable response may support reconsideration of treatment strategy.