← Issue №13/ week of Sep 27, 2026/ the whole section, in full

Hepatology, in full.

All 15 Hepatology papers in this issue, as full cards, ranked by clinical utility. The issue page carries the strongest few; this is the section, whole.

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most clinically useful first · the 2 the issue led with are ruled in green
Hepatology prospective cohort · n=9,761 · Sep 23, 2026 · Eur J Gastro Hep · IF 2.2

Allostatic load, unhealthy behaviors, and mortality risk among participants with and without metabolic dysfunction-associated steatotic liver disease.

New evidenceepidemiologyMASLDbiomarkerhealth services
Clinical takeawayCounsel MASLD patients on reducing chronic stress and improving health behaviors (diet, nicotine exposure, physical activity, sleep) to lower mortality risk, particularly emphasizing the combined impact of these factors.
What it foundHigh allostatic load plus poor health behaviors raised all-cause mortality risk 3.33-fold (95% CI 1.97-5.65) and cardiovascular mortality risk 3.66-fold (95% CI 1.31-10.23) in MASLD patients compared to those with low allostatic load and good health behaviors.
ContextConfirms and quantifies the independent and joint impact of chronic stress and health behaviors on mortality in MASLD, extending prior associations to specific risk levels, with particular significance for MASLD patients.
Measured against the standard of care· EASL-EASD-EASO 2026 Guidance on Resmetirom and Semaglutide as MASH-Targeted Therapy (J Hepatol, doi:10.1016/j.jhep.2026.08.028) / AASLD 2023 Practice Guidance (+ Oct 2024 resmetirom and Nov 2025 semaglutide updates) / AGA 2026 Clinical Care Pathway for MASLD (Gastroenterology, doi:10.1053/j.gastro.2026.01.047) / AGA 2026 Clinical Practice Update on MetALD (Clin Gastroenterol Hepatol, 2026) / EASL 2026 SLD trajectory guidance (JHEP Rep, doi:10.1016/j.jhepr.2026.101798)

Decision at stakelifestyle modification remains the foundation for all MASLD patients

No single passage of this standard matched the paper closely enough to quote, so none is shown. The standard is cited above.

Our full summary of this standard

This standard applies to MASLD: hepatic steatosis on imaging or biopsy, at least one cardiometabolic criterion, no other liver disease, and alcohol below the MetALD range. The AGA 2026 MetALD update sets MetALD at about 140-350 g/week of alcohol in women and 210-420 g/week in men, averaged over at least 3 months. MASLD therefore means under about 140 g/week (women) or 210 g/week (men), and drinking above the MetALD range is ALD. Assess alcohol use in every patient with steatotic liver disease at diagnosis and at least once a year, by interview, a validated questionnaire (e.g., AUDIT-C) and/or biomarkers such as phosphatidylethanol (PEth). Advise every patient with steatotic liver disease to stop drinking. Screen people with type 2 diabetes, people with overweight or obesity plus at least one more metabolic risk factor, and anyone with incidental steatosis or raised aminotransferases. Use FIB-4 first. A score below 1.3 (below 2.0 at age 65 or older) is low risk: the patient stays in primary care and repeats FIB-4 every 1-2 years. A score at or above the cutoff goes to a second-line test: VCTE, or ELF if elastography is not available. VCTE below 8 kPa is low risk. VCTE of 8 kPa or more, or ELF of 9.2 or more, means clinically significant fibrosis is likely and the patient should be referred to hepatology. Read liver stiffness with caution if the patient is actively drinking. Reserve biopsy for discordant or unclear results. Lifestyle change is the base of treatment for everyone: at least 5% weight loss improves steatosis, and 10% or more is usually needed for fibrosis to improve. Pharmacotherapy is recommended for adults with non-cirrhotic MASH and F2-F3 fibrosis (by non-invasive tests or biopsy), alongside structured lifestyle intervention and optimised management of comorbidities. The NIT ranges that stand in for F2-F3 differ by society. AASLD uses VCTE 8-15 kPa, MRE 3.1-4.4 kPa or ELF 9.2-10.5. EASL-EASD-EASO 2026 frames the treatable high-risk group as, for example, VCTE 10-20 kPa, MRE 3.1-5.0 kPa or ELF 9.8-11.3. Two drugs are approved: resmetirom (80 mg oral daily, or 100 mg at body weight of 100 kg or more; AASLD Oct 2024 guidance) and semaglutide 2.4 mg subcutaneously once weekly (FDA accelerated approval Aug 2025, AASLD Nov 2025 guidance; in ESSENCE, MASH resolved without fibrosis worsening in 62.9% vs 34.3% on placebo). EASL-EASD-EASO 2026 says to choose between them by patient preference, risks and cardio-renal-metabolic profile. Semaglutide may be preferred with obesity, type 2 diabetes, established cardiovascular disease or high cardiovascular risk. Resmetirom may be prioritised without obesity, or when the patient is already on or cannot tolerate a GLP-1 receptor agonist. On semaglutide, monitoring includes nutrition and sarcopenia assessment, and fibrosis NITs are used over time to judge response. In MASH cirrhosis, resmetirom and semaglutide appear safe but should not be used as MASH-targeted treatment until liver-related benefit is shown. Pioglitazone or vitamin E remain options under the AASLD 2023 guidance. Neither resmetirom nor semaglutide has been formally studied in MetALD. Manage cardiometabolic risk in every patient whatever the fibrosis stage, including statins for ASCVD and control of glucose and blood pressure. On semaglutide, watch for GI side effects and rare risks (AKI, gallbladder disease, pancreatitis, retinopathy, loss of lean mass). For MetALD, treat moderate or severe alcohol use disorder with medication plus behavioural therapy, correct micronutrient deficiencies (folate, thiamine, vitamin D), and do not offer bariatric or endobariatric procedures. HCC surveillance with ultrasound, with or without AFP, every 6 months is indicated only when cirrhosis is present.

EASL-EASD-EASO 2026 Guidance on Resmetirom and Semaglutide as MASH-Targeted Therapy (J Hepatol, doi:10.1016/j.jhep.2026.08.028) / AASLD 2023 Practice Guidance (+ Oct 2024 resmetirom and Nov 2025 semaglutide updates) / AGA 2026 Clinical Care Pathway for MASLD (Gastroenterology, doi:10.1053/j.gastro.2026.01.047) / AGA 2026 Clinical Practice Update on MetALD (Clin Gastroenterol Hepatol, 2026) / EASL 2026 SLD trajectory guidance (JHEP Rep, doi:10.1016/j.jhepr.2026.101798) · reviewed 2026-10-11 ↗
Hong D … Fu B · European Journal of Gastroenterology & Hepatology · IF 2.2 · PubMed ↗Permalink
Hepatology prospective cohort · n=1,007 · Sep 25, 2026 · Clin Gastro Hep · IF 16.2

Altered cognition and patient-reported outcomes predict 1-year hospitalization risk in a multi-center outpatient cirrhosis cohort.

New evidencecirrhosishepatic encephalopathyepidemiology
Clinical takeawayConsider incorporating Stroop testing (time-based cognitive assessment) and SF-36 general health subscale assessment into routine outpatient monitoring for cirrhosis patients with controlled etiology (median MELD 11) to improve hospitalization risk prediction.
What it foundHigher Stroop time (slower performance) and lower SF-36 general health score independently predicted all-cause (Stroop/SF-36, p<0.001 each), liver-related (Stroop, p=0.01; SF-36, p<0.001), and HE-related (Stroop/SF-36, p=0.02 each) hospitalizations in cirrhosis patients, adding predictive value beyond traditional risk factors (all C-index improvements p<0.001).
ContextThis study refines risk stratification in cirrhosis by demonstrating that PROs (SF-36) and cognitive testing (Stroop) add predictive value beyond traditional clinical parameters in a multicenter outpatient cohort.
Emergingsuggested applicable standard· American Association for the Study of Liver Diseases (AASLD), Kaplan DE, Ripoll C, Thiele M, et al. "AASLD Practice Guidance on risk stratification and management of portal hypertension and varices in cirrhosis." Hepatology. 2024;79(5):1180-1211.

Decision at stakeassessing hospitalization risk in outpatient cirrhosis management

No single passage of this standard matched the paper closely enough to quote, so none is shown. The standard is cited above.

Our full summary of this standard

Scope: this primary document covers portal hypertension and varices in cirrhosis ONLY. Everything else in the current entry (HCC surveillance, transplant referral, nutrition, vaccination, ascites/SBP/HE/HRS/ACLF management) belongs to the separate documents listed as supporting sources and must not be attributed to this guidance. Risk-stratify compensated advanced chronic liver disease (cACLD) with non-invasive tests before defaulting to endoscopy. By vibration-controlled transient elastography, liver stiffness (LSM) under 10 kPa excludes cACLD, 10 to 14.9 kPa is suggestive and warrants further testing, and 15 kPa or above rules cACLD in. Clinically significant portal hypertension (CSPH, i.e. HVPG above 10 mm Hg) is ruled in non-invasively by LSM at or above 25 kPa alone, or LSM 20 to 24.9 kPa with platelets below 150 x 10^9/L, or LSM 15 to 19.9 kPa with platelets below 110 x 10^9/L. Where spleen stiffness measurement is available, values below 21 kPa argue against CSPH and above 50 kPa argue for it. These non-invasive cutoffs are conditional probability thresholds, not universal diagnostic rules, and hold only when their derivation conditions are met. They were established in compensated advanced chronic liver disease of viral (treated or untreated HBV/HCV), alcohol-related, or non-obese (BMI under 30) MASLD etiology, and are not validated for and should not be applied to cholestatic (e.g. PBC, PSC), vascular, or other etiologies, in which different cutoffs apply. They also require a technically reliable liver stiffness measurement by vibration-controlled transient elastography, fasting, at least 10 valid acquisitions, and an IQR/median ratio below 30 percent, and are confounded by factors that raise liver stiffness independently of fibrosis, including ALT flares or acute hepatitis, extrahepatic cholestasis, hepatic congestion (right heart failure), and recent food intake; Baveno VII recommends confirming an LSM-based rule-in on a repeat measurement obtained on a separate day. The spleen stiffness cutoffs apply only to a dedicated 100 Hz spleen module, carry a higher technical failure rate, are machine-dependent, and are not interchangeable with values obtained using the standard 50 Hz liver probe. Where these population or acquisition conditions are not met, the numeric thresholds do not reliably classify CSPH, and HVPG measurement or endoscopy is required rather than a non-invasive determination. Preserve the gray zone: LSM 15 to 25 kPa without a qualifying platelet count is explicitly indeterminate (roughly 40 to 60 percent of cACLD patients) and calls for HVPG and/or endoscopy rather than assumption in either direction. Once CSPH is established, offer a non-selective beta-blocker, carvedilol preferred at 12.5 mg/day, to lower portal pressure and prevent FIRST decompensation, on the strength of PREDESCI. This is a treat-the-pressure strategy rather than a treat-the-varices one: because a patient already on NSBB for CSPH would not have management changed by the finding, screening endoscopy becomes unnecessary for most such patients. Screening EGD is still indicated where elastography is unavailable, technically difficult, or gives discordant results, and for patients who do not meet non-invasive criteria. Standard beta-blocker contraindications (severe asthma, advanced heart block, bradyarrhythmias) continue to apply. For varices needing treatment managed endoscopically, band ligation is repeated every 2 to 4 weeks until obliteration, with surveillance endoscopy at 6 months and annually thereafter. Gastric/cardiofundal varices are treated with cyanoacrylate injection or EUS-guided coil embolization rather than banding, with hepatology involvement. In acute variceal hemorrhage, consider preemptive (early) TIPS within 24 to 72 hours in high-risk patients: Child-Turcotte-Pugh class B with score above 7 and active bleeding at endoscopy despite vasoactive therapy, or CTP class C with score 10 to 13. Keep the document's own qualifier: there is no established universal MELD or CTP cutoff at which TIPS is mandatory, and the decision is case-by-case with hepatology consultation. Statin use in compensated cirrhosis is NOT a recommendation traceable to this document; the current entry's statin sentence needs its own source or removal. Verification note: the Hepatology full text is paywalled (402/403 on direct fetch). Document identity, title, year, volume, pages and authorship were confirmed via Crossref and PubMed metadata; the numeric thresholds above were corroborated from two independent peer-reviewed commentaries on this specific guidance and match the Baveno VII rule-of-five, but were not read verbatim from the primary PDF. A human should confirm the exact guidance-statement wording against the full text before this entry is treated as quotation-grade.

American Association for the Study of Liver Diseases (AASLD), Kaplan DE, Ripoll C, Thiele M, et al. "AASLD Practice Guidance on risk stratification and management of portal hypertension and varices in cirrhosis." Hepatology. 2024;79(5):1180-1211. · reviewed 2026-07-23 ↗
Bajaj JS … Reddy KR · Clinical Gastroenterology and Hepatology : the Official Clinical Practice Journal of the American Gastroenterological Association · IF 16.2 · PubMed ↗Permalink
Hepatology review · Sep 22, 2026 · Clin Gastro Hep · IF 16.2

AGA Clinical Practice Update on the Evaluation and Management of Metabolic Dysfunction- and Alcohol-Associated Liver Disease: Expert Review.

Guideline / reviewalcohol-associated liver diseaseMASLDguideline
Clinical takeawayClassify patients with steatotic liver disease into MASLD, MetALD, or alcohol-associated liver disease using alcohol consumption thresholds and cardiometabolic risk factors. Advise all patients with MetALD to discontinue alcohol use, acknowledging potential periods of reduction or intermittent use. Implement a tiered, noninvasive strategy for fibrosis assessment.
What it foundMetALD is defined by alcohol consumption thresholds of ≈140-350 g/wk in women and 210-420 g/wk in men, alongside cardiometabolic risk factors. All patients with steatotic liver disease should be assessed initially and at least annually for alcohol use via patient interview, validated questionnaires, and/or serum/urine biomarkers.
ContextRefines the classification and management of steatotic liver disease, introducing specific alcohol consumption thresholds for MetALD, emphasizing alcohol cessation, and detailing a tiered noninvasive approach for fibrosis assessment.
Measured against the standard of care· EASL-EASD-EASO 2026 Guidance on Resmetirom and Semaglutide as MASH-Targeted Therapy (J Hepatol, doi:10.1016/j.jhep.2026.08.028) / AASLD 2023 Practice Guidance (+ Oct 2024 resmetirom and Nov 2025 semaglutide updates) / AGA 2026 Clinical Care Pathway for MASLD (Gastroenterology, doi:10.1053/j.gastro.2026.01.047) / AGA 2026 Clinical Practice Update on MetALD (Clin Gastroenterol Hepatol, 2026) / EASL 2026 SLD trajectory guidance (JHEP Rep, doi:10.1016/j.jhepr.2026.101798)

Decision at stakethe classification and management of patients with MetALD

This standard applies to MASLD: hepatic steatosis on imaging or biopsy, at least one cardiometabolic criterion, no other liver disease, and alcohol below the MetALD range. The AGA 2026 MetALD update sets MetALD at about 140-350 g/week of alcohol in women and 210-420 g/week in men, averaged over at least 3 months. MASLD therefore means under about 140 g/week (women) or 210 g/week (men), and drinking above the MetALD range is ALD. …

From our summary of this standard, unedited — the part the paper bears on. … marks omitted text. Our wording, not the guideline's; read the source for its own text.

Our full summary of this standard

This standard applies to MASLD: hepatic steatosis on imaging or biopsy, at least one cardiometabolic criterion, no other liver disease, and alcohol below the MetALD range. The AGA 2026 MetALD update sets MetALD at about 140-350 g/week of alcohol in women and 210-420 g/week in men, averaged over at least 3 months. MASLD therefore means under about 140 g/week (women) or 210 g/week (men), and drinking above the MetALD range is ALD. Assess alcohol use in every patient with steatotic liver disease at diagnosis and at least once a year, by interview, a validated questionnaire (e.g., AUDIT-C) and/or biomarkers such as phosphatidylethanol (PEth). Advise every patient with steatotic liver disease to stop drinking. Screen people with type 2 diabetes, people with overweight or obesity plus at least one more metabolic risk factor, and anyone with incidental steatosis or raised aminotransferases. Use FIB-4 first. A score below 1.3 (below 2.0 at age 65 or older) is low risk: the patient stays in primary care and repeats FIB-4 every 1-2 years. A score at or above the cutoff goes to a second-line test: VCTE, or ELF if elastography is not available. VCTE below 8 kPa is low risk. VCTE of 8 kPa or more, or ELF of 9.2 or more, means clinically significant fibrosis is likely and the patient should be referred to hepatology. Read liver stiffness with caution if the patient is actively drinking. Reserve biopsy for discordant or unclear results. Lifestyle change is the base of treatment for everyone: at least 5% weight loss improves steatosis, and 10% or more is usually needed for fibrosis to improve. Pharmacotherapy is recommended for adults with non-cirrhotic MASH and F2-F3 fibrosis (by non-invasive tests or biopsy), alongside structured lifestyle intervention and optimised management of comorbidities. The NIT ranges that stand in for F2-F3 differ by society. AASLD uses VCTE 8-15 kPa, MRE 3.1-4.4 kPa or ELF 9.2-10.5. EASL-EASD-EASO 2026 frames the treatable high-risk group as, for example, VCTE 10-20 kPa, MRE 3.1-5.0 kPa or ELF 9.8-11.3. Two drugs are approved: resmetirom (80 mg oral daily, or 100 mg at body weight of 100 kg or more; AASLD Oct 2024 guidance) and semaglutide 2.4 mg subcutaneously once weekly (FDA accelerated approval Aug 2025, AASLD Nov 2025 guidance; in ESSENCE, MASH resolved without fibrosis worsening in 62.9% vs 34.3% on placebo). EASL-EASD-EASO 2026 says to choose between them by patient preference, risks and cardio-renal-metabolic profile. Semaglutide may be preferred with obesity, type 2 diabetes, established cardiovascular disease or high cardiovascular risk. Resmetirom may be prioritised without obesity, or when the patient is already on or cannot tolerate a GLP-1 receptor agonist. On semaglutide, monitoring includes nutrition and sarcopenia assessment, and fibrosis NITs are used over time to judge response. In MASH cirrhosis, resmetirom and semaglutide appear safe but should not be used as MASH-targeted treatment until liver-related benefit is shown. Pioglitazone or vitamin E remain options under the AASLD 2023 guidance. Neither resmetirom nor semaglutide has been formally studied in MetALD. Manage cardiometabolic risk in every patient whatever the fibrosis stage, including statins for ASCVD and control of glucose and blood pressure. On semaglutide, watch for GI side effects and rare risks (AKI, gallbladder disease, pancreatitis, retinopathy, loss of lean mass). For MetALD, treat moderate or severe alcohol use disorder with medication plus behavioural therapy, correct micronutrient deficiencies (folate, thiamine, vitamin D), and do not offer bariatric or endobariatric procedures. HCC surveillance with ultrasound, with or without AFP, every 6 months is indicated only when cirrhosis is present.

EASL-EASD-EASO 2026 Guidance on Resmetirom and Semaglutide as MASH-Targeted Therapy (J Hepatol, doi:10.1016/j.jhep.2026.08.028) / AASLD 2023 Practice Guidance (+ Oct 2024 resmetirom and Nov 2025 semaglutide updates) / AGA 2026 Clinical Care Pathway for MASLD (Gastroenterology, doi:10.1053/j.gastro.2026.01.047) / AGA 2026 Clinical Practice Update on MetALD (Clin Gastroenterol Hepatol, 2026) / EASL 2026 SLD trajectory guidance (JHEP Rep, doi:10.1016/j.jhepr.2026.101798) · reviewed 2026-10-11 ↗
Arab JP … Fontana RJ · Clinical Gastroenterology and Hepatology : the Official Clinical Practice Journal of the American Gastroenterological Association · IF 16.2 · PubMed ↗Permalink
Hepatology prospective cohort · n=4,192 · Sep 22, 2026 · Clin Transl Gastro · IF 3.4

Validation of a machine learning model to non-invasively exclude spontaneous bacterial peritonitis.

New evidenceartificial intelligencebiomarker
Clinical takeawayConsider using this ML model as an adjunctive tool to non-invasively exclude SBP in cirrhotic VA patients with ascites, particularly in resource-limited settings, but do not replace guideline-mandated paracentesis when indicated.
What it foundA machine learning model excluded SBP with negative predictive values of 93.6%, 92.0%, and 90.9% at <5%, <10%, and <15% probability thresholds in a national VA cohort, and 100%, 97.5%, and 95.4% in a manual confirmation subgroup.
ContextThis validates a previously developed ML model in a contemporary VA cohort post-2020, confirming its utility in post-COVID-19 healthcare settings.
Measured against the standard of care· AASLD 2021 Practice Guidance (Biggins et al., Hepatology) / AGA Clinical Practice Update 2025 (Orman et al., Gastroenterology 2025;169(7):1547-1557)

No single passage of this standard matched the paper closely enough to quote, so none is shown. The standard is cited above.

Our full summary of this standard

Perform a diagnostic paracentesis as soon as possible in any patient with new-onset ascites that can be sampled. Also perform one in any patient with cirrhosis and ascites who is admitted to hospital. AASLD 2021 says this applies to emergent admission for any reason. AGA 2025 BPA 2 names admission for ascites- or encephalopathy-related symptoms. The tap rules out SBP even without signs of infection, because up to one-third of SBP is asymptomatic. Repeat it whenever signs, symptoms or labs suggest infection, and in tense ascites with AKI. Paracentesis is safe with coagulopathy: INR >1.5 or platelets <50×10^9/L is not a contraindication, and routine FFP or platelet transfusion is not recommended. Possible exceptions are DIC, and uremia with thrombocytopenia, where desmopressin may be considered. Initial fluid testing: neutrophil (PMN) count, total protein, and ascitic albumin with a same-day serum albumin to calculate the SAAG. AGA 2025 adds Gram stain and culture to the initial panel for new-onset ascites and hospitalized patients. AASLD 2021 treats culture as part of the SBP workup rather than the routine panel. Either way, inoculate ≥10 mL into aerobic and anaerobic blood-culture bottles at the bedside before antibiotics. Amylase, cytology, glucose, LDH, AFB/ADA and triglycerides are ordered only for a clinical reason. SAAG ≥1.1 g/dL means portal hypertension (~97% accuracy). SAAG <1.1 g/dL points to a non-portal-hypertensive cause: carcinomatosis, TB peritonitis, nephrotic syndrome, pancreatic or chylous ascites. Within high-SAAG ascites, total protein <2.5 g/dL suggests cirrhosis (also massive liver metastases or late Budd-Chiari). Total protein ≥2.5 g/dL suggests a cardiac or postsinusoidal cause (heart failure, portal vein thrombosis, SOS, early Budd-Chiari), so work up with echocardiography, hepatic-vein Doppler or right-heart catheterization. SBP is diagnosed by ascitic PMN >250/mm^3, with or without a positive culture, once a surgically treatable source has been excluded. SBE is diagnosed by pleural fluid PMN >250/mm^3 in a hepatic hydrothorax after pneumonia and other secondary causes are excluded. It is treated with antibiotics and no chest tube.

AASLD 2021 Practice Guidance (Biggins et al., Hepatology) / AGA Clinical Practice Update 2025 (Orman et al., Gastroenterology 2025;169(7):1547-1557) · reviewed 2026-10-11 ↗
Tsai SY … Bajaj JS · Clinical and Translational Gastroenterology · IF 3.4 · PubMed ↗Permalink
Hepatology review · Sep 21, 2026 · J Gastro Hep · IF 3.5

Translational Hepatology From Bedside to Global Policy: How Robust Clinical and Translational Research Reshapes Global Practice Guidelines and Patient Outcomes.

New therapytranslationalguidelinecost-effectivenessviral hepatitis
Clinical takeawayConsider STRIDE regimen as frontline dual immunotherapy for HBV-predominant unresectable hepatocellular carcinoma, particularly in cirrhotic patients with portal hypertension, as it establishes a VEGF-free standard.
What it foundSTRIDE regimen (single-dose tremelimumab plus regular durvalumab) improved median overall survival to 25.26 vs. 14.09 months (compared to standard therapy) in HBV-predominant unresectable hepatocellular carcinoma.
ContextThis confirms and extends prior evidence supporting dual immunotherapy in HBV-predominant uHCC, establishing STRIDE as a VEGF-free standard in APASL guidelines.
No standard claimed for this paper

Every paper is compared to the standard governing its question. This one is not: either no standard in the corpus matches it, or the comparison did not hold up on review and was withdrawn rather than published unverified. Both are logged.

Lau G · Journal of Gastroenterology and Hepatology · IF 3.5 · PubMed ↗Permalink
Hepatology retrospective · n=24 · Sep 22, 2026 · Dig Liver Dis · IF 4.2

Early predictors of pruritus response in children with PFIC treated with odevixibat.

New evidencepediatricbiomarker
Clinical takeawayMonitor sBA levels at 1 and 3 months in children with PFIC on odevixibat; reductions ≥48% at 1 month or ≥52% at 3 months from baseline suggest likelihood of pruritus response by 6 months.
What it foundReductions in serum bile acid (sBA) levels ≥48% at 1 month (AUC 0.771; sensitivity 0.75, specificity 0.83) and ≥52% at 3 months (AUC 0.885; sensitivity 0.81, specificity 1.00) from baseline predicted pruritus response (≥1-point improvement) at 6 months in children with PFIC treated with odevixibat.
ContextIdentifies early biomarkers for response to odevixibat in children with PFIC, a rare but debilitating condition with limited treatment options.
No standard claimed for this paper

Every paper is compared to the standard governing its question. This one is not: either no standard in the corpus matches it, or the comparison did not hold up on review and was withdrawn rather than published unverified. Both are logged.

Di Giorgio A … D'Antiga L · Digestive and Liver Disease : Official Journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver · IF 4.2 · PubMed ↗Permalink
Hepatology prospective cohort · n=18,000 · Sep 22, 2026 · Lancet GH · IF 39.1

Prevalence of liver fibrosis and steatotic liver disease in community-dwelling adults in China (the CHESS-LiverHealth project): cross-sectional baseline data from a prospective cohort study.

EpidemiologyepidemiologyMASLDalcohol-associated liver diseasebiomarker
Clinical takeawayNo clinical action yet: epidemiological data establishing baseline prevalence in China. Consider heightened awareness for liver fibrosis and steatotic liver disease in high-risk groups (obesity, diabetes, alcohol use).
What it foundPrevalence of liver fibrosis (LSM ≥8 kPa) was 4.4%, and steatotic liver disease (CAP ≥248 dB/m) was 43.7% in community-dwelling Chinese adults, with MASLD accounting for 39.5% of cases.
ContextThis literature reports a high prevalence of liver fibrosis and steatotic liver disease in community-dwelling adults in China, associated with overweight, obesity, diabetes, and harmful alcohol consumption.
No standard claimed for this paper

Every paper is compared to the standard governing its question. This one is not: either no standard in the corpus matches it, or the comparison did not hold up on review and was withdrawn rather than published unverified. Both are logged.

Liu S … Qi X · Lancet Gastroenterology & Hepatology · IF 39.1 · PubMed ↗Permalink
Hepatology review · Sep 25, 2026 · Gastroenterology · IF 25.1

Global burden of liver disease: 2026 update.

Epidemiologyepidemiologyhealth servicescost-effectivenessviral hepatitis
Clinical takeawayNo clinical action yet: this is an epidemiology review highlighting global disparities in liver disease burden and access to care.
What it foundChronic liver disease affects over 1.5 billion people globally, with cirrhosis and primary liver cancer causing 2.4 million deaths annually, disproportionately in low- and middle-income countries.
ContextConfirms the substantial and growing global burden of liver disease, driven by alcohol-associated liver disease, MASLD, and viral hepatitis, with widening regional disparities in outcomes.
No standard claimed for this paper

Every paper is compared to the standard governing its question. This one is not: either no standard in the corpus matches it, or the comparison did not hold up on review and was withdrawn rather than published unverified. Both are logged.

Devarbhavi H … Kamath PS · Gastroenterology · IF 25.1 · PubMed ↗Permalink
Hepatology prospective cohort · n=679 · Sep 21, 2026 · Gut · IF 24.6

Hospitalisation in cirrhosis is linked to distinct gut microbiome structural and functional profiles: a multinational metagenomic study.

New evidencemicrobiomebiomarkerepidemiologyartificial intelligence
Clinical takeawayNo clinical action yet: a microbiome signature associated with hospitalization risk in cirrhosis, not yet validated for clinical use.
What it foundA combined clinical-microbiome model predicted 90-day hospitalization in cirrhosis with AUC 0.84, outperforming clinical-only (AUC 0.79) and microbiome-only (AUC 0.74) models.
ContextExtends prior evidence linking gut microbiome to cirrhosis outcomes by identifying specific taxa and functional pathways associated with hospitalization risk across diverse populations.
No standard claimed for this paper

Every paper is compared to the standard governing its question. This one is not: either no standard in the corpus matches it, or the comparison did not hold up on review and was withdrawn rather than published unverified. Both are logged.

Nikitina D … Bajaj JS · Gut · IF 24.6 · PubMed ↗Permalink
Hepatology guideline · Sep 24, 2026 · Gut · IF 24.6

Expert consensus on clinical trials for use of systemic therapy in patients with hepatocellular carcinoma undergoing surgical and locoregional therapies.

Guideline / reviewhepatocellular carcinomaguideline
Clinical takeawayNo clinical action yet: expert consensus on trial design for HCC systemic therapy in earlier disease stages, not yet tested in practice.
What it foundConsensus statements defined for trial design in HCC systemic therapy, including high-risk recurrence criteria (patients at highest risk of recurrence, with 2-year event-free survival as primary outcome) and comparator arms (systemic therapy for patients with larger tumour burden and locally advanced disease).
ContextRefines trial design for HCC systemic therapy in earlier stages, addressing heterogeneity and defining endpoints for neoadjuvant/perioperative (2-year event-free survival) and combination therapy trials (progression-free survival and overall survival).
No standard claimed for this paper

Every paper is compared to the standard governing its question. This one is not: either no standard in the corpus matches it, or the comparison did not hold up on review and was withdrawn rather than published unverified. Both are logged.

Yarchoan M … Singal AG · Gut · IF 24.6 · PubMed ↗Permalink
Hepatology retrospective · n=4,351 · Sep 25, 2026 · Clin Gastro Hep · IF 16.2

Extrahepatic Autoimmune Disease in People With Primary Biliary Cholangitis: Nationwide Occurrence and Relation to Outcome.

New evidenceepidemiologyautoimmune hepatitisPBC
Clinical takeawayBe aware that EHAIDs are common in PBC patients, but they do not appear to influence liver outcomes.
What it found27.3% of PBC patients had extrahepatic autoimmune diseases (EHAIDs), most commonly hypothyroidism (35.6%) and Sjögren's syndrome (18.3%), with 80.7% of EHAIDs present at baseline. No association was found between EHAIDs and liver transplant-free survival (aHR 0.81, 95% CI 0.63-1.05) or disease progression (aHR 0.92, 95% CI 0.65-1.32).
ContextConfirms EHAIDs are frequent in PBC but do not impact liver prognosis, aligning with prior evidence but providing robust nationwide data.
Reinforcessuggested applicable standard· American Association for the Study of Liver Diseases, 'Primary Biliary Cholangitis: 2021 Practice Guidance', 2021

Decision at stakethe presence of extrahepatic autoimmune diseases does not alter the management of primary biliary cholangitis

Treat with first-line ursodeoxycholic acid (UDCA) 13-15 mg/kg/d divided, and assess biochemical response at 12 months using Paris-II plus continuous risk scores (Globe, UK-PBC). Escalate to a second-line agent (obeticholic acid [contraindicated in cirrhosis with portal hypertension or prior decompensation], seladelpar, elafibranor, or a fibrate) when response is inadequate, guided by a Child-Pugh/portal-hypertension hard gate, and manage pruritus with a stepwise ladder (cholestyramine → rifampin → sertraline → naltrexone). Refer for transplant evaluation for decompensation, refractory pruritus, or rising bilirubin.

American Association for the Study of Liver Diseases, 'Primary Biliary Cholangitis: 2021 Practice Guidance', 2021 · reviewed 2026-07-21 ↗
Weijsters GHX … Dutch PBC Study Group · Clinical Gastroenterology and Hepatology : the Official Clinical Practice Journal of the American Gastroenterological Association · IF 16.2 · PubMed ↗Permalink
Hepatology prospective cohort · n=156 · Sep 22, 2026 · Gut · IF 24.6

Integrative multi-omics landscape and diagnostic-therapeutic modelling of steatohepatitic hepatocellular carcinoma.

Basic sciencehepatocellular carcinomabiomarkerbasic sciencetranslational
Clinical takeawayNo clinical action yet: a mechanistic finding in mice (FABP4 deletion suppressed tumor growth) and preliminary multi-omics profiling in humans. FABP4 is a potential target but requires validation.
What it foundAn SH-HCC index reliably differentiated SH-HCC from conventional HCC, and a diagnostic model based on 12 lipid species achieved AUC=0.909 in an independent cohort. Drug response analysis suggested reduced responsiveness to sorafenib and immunotherapy in SH-HCC, while transarterial chemoembolisation remained effective.
ContextSH-HCC is a poorly understood subtype of HCC with distinct molecular features, including a lipid-rich phenotype and altered immune microenvironment, with potential therapeutic implications.
No standard claimed for this paper

Every paper is compared to the standard governing its question. This one is not: either no standard in the corpus matches it, or the comparison did not hold up on review and was withdrawn rather than published unverified. Both are logged.

Zhang L … Yu D · Gut · IF 24.6 · PubMed ↗Permalink
Hepatology meta analysis · n=548 · Sep 24, 2026 · Aliment Pharm Ther · IF 6.7

Meta-Analysis: The Placebo Response in Modern Treatments for Cholestatic Pruritus: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

New evidencemeta-analysissystematic review
Clinical takeawayNo clinical action yet: this meta-analysis quantifies placebo effects in cholestatic pruritus trials, which informs trial design but does not directly impact patient management.
What it foundPlacebo groups in cholestatic pruritus trials showed a pooled standardized mean change of -0.49 (95% CI, -0.72 to -0.27) overall and -0.57 (95% CI, -0.81 to -0.33) for moderate-to-severe pruritus, with a 30.0% overall response rate.
ContextConfirms the substantial placebo effect in cholestatic pruritus trials, highlighting variability across outcome instruments and the need for careful endpoint selection in future studies.
No standard claimed for this paper

Every paper is compared to the standard governing its question. This one is not: either no standard in the corpus matches it, or the comparison did not hold up on review and was withdrawn rather than published unverified. Both are logged.

Silveira IB … Cançado GGL · Alimentary Pharmacology & Therapeutics · IF 6.7 · PubMed ↗Permalink
Hepatology prospective cohort · n=20 · Sep 23, 2026 · J Hepatology · IF 40.1

EBV-reactive KIR+ CX3CR1+ CD8+ T cells mediate liver transplantation tolerance.

Basic sciencebasic sciencetranslationalbiomarkerpediatric
Clinical takeawayNo clinical action yet: a mechanistic finding in mice and in vitro studies, with preliminary human data in a small pediatric trial (n=20).
What it foundEBV-derived peptides presented by HLA-E on alloreactive CD4+ T cells prime KIR+ CX3CR1+ CD8+ T cells, which suppress alloreactive CD4+ T cells via perforin and granzyme B, promoting liver transplant tolerance.
ContextOpens a new question on the role of EBV and KIR+ CX3CR1+ CD8+ T cells in liver transplant tolerance, a previously unclear mechanism.
No standard claimed for this paper

Every paper is compared to the standard governing its question. This one is not: either no standard in the corpus matches it, or the comparison did not hold up on review and was withdrawn rather than published unverified. Both are logged.

Liu Y … Xia Q · Journal of Hepatology · IF 40.1 · PubMed ↗Permalink
Hepatology review · Sep 24, 2026 · Hepatology · IF 18.0

The hepatic sinusoid as a regulatory niche: From cellular specialization to precision hepatology.

Basic sciencebasic sciencetranslationalbiomarker
Clinical takeawayNo clinical action yet: a mechanistic review of liver sinusoidal biology in preclinical models and human tissue research.
What it foundThe hepatic sinusoid is a multicellular, spatially organized regulatory niche coordinating vascular exchange, immune surveillance, metabolic zonation, tissue repair, and systemic communication.
ContextReframes liver diseases (fibrosis, portal hypertension, MASLD, liver cancer) as disorders of sinusoidal communication and niche organization, linking sinusoidal dysfunction to aging and extrahepatic axes.
No standard claimed for this paper

Every paper is compared to the standard governing its question. This one is not: either no standard in the corpus matches it, or the comparison did not hold up on review and was withdrawn rather than published unverified. Both are logged.

Fernández-Iglesias A … Gracia-Sancho J · Hepatology · IF 18.0 · PubMed ↗Permalink
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