← Issue №6/
week of Aug 9, 2026/
the whole section, in full
Hepatology, in full.
All 14 Hepatology papers in this issue,
as full cards, ranked by clinical utility. The issue page carries the strongest few;
this is the section, whole.
Actionability = is there something to do. Prevalence = how much of a general GI practice it touches. Stakes = how consequential the decision is. Evidence strength = how far the study design and the result support the action. Novelty = how likely you are not already doing it.
Hepatologyprospective cohort · n=2,817 · Aug 14, 2026 · Hepatology · IF 18.0
Clinical takeawaySWE demonstrated similar performance to VCTE for MASLD risk stratification. If SWE is available at your institution, this study supports its use as an alternative to VCTE. If your institution is implementing an elastography program and choosing between modalities, either is supported by this evidence; decide based on cost, operator expertise, and availability. Ongoing VCTE use does not require change.
What it foundSWE and VCTE showed similar 60-month risk prediction for liver-related events in MASLD (time-dependent AUROC: AGA 0.770 vs 0.775, EASL 0.804 vs 0.805; no significant difference between modalities).
ContextThis prospective cohort study validates SWE against hard clinical endpoints (liver-related events) in MASLD, showing similar risk stratification performance to VCTE and establishing SWE as a viable alternative modality.
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 This one is not: either no standard in the corpus matches it, or the comparison did not hold up on review and was withdrawn rather than published unverified.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.
Clinical takeawaySystematically screen all patients with steatotic liver disease for alcohol use using objective biomarkers such as phosphatidylethanol rather than patient report alone, structurally evaluate cardiometabolic risk factors (obesity, type 2 diabetes, hypertension, dyslipidemia), perform non-invasive fibrosis assessment, and crucially, reassess these factors repeatedly over time rather than applying static diagnostic labels once. Management should integrate alcohol reduction strategies, metabolic optimization, and liver-directed therapies in a multidisciplinary approach. Note that most emerging pharmacotherapies for metabolic steatohepatitis exclude patients with concurrent alcohol use, creating a gap between trial populations and real-world practice.
What it foundSteatotic liver disease comprises overlapping metabolic dysfunction-associated, metabolic and alcohol-related, and alcohol-related subtypes that transition dynamically over time as alcohol and metabolic risk factors fluctuate; misclassification is common due to under-reporting of alcohol and reliance on static diagnostic thresholds.
ContextChallenges the traditional siloed view of steatotic liver disease as separate entities (MASLD, MetALD, ALD) by emphasizing their overlapping nature and dynamic transitions. Highlights that current practice likely misclassifies patients due to under-reported alcohol and static diagnostic thinking. Identifies a real practice gap: trial design commonly excludes alcohol users, but real-world patients frequently have both metabolic dysfunction and alcohol exposure.
Refinessuggested applicable standard· American College of Gastroenterology (ACG), "ACG Clinical Guideline: Alcohol-Associated Liver Disease" (Jophlin, Singal, Bataller, et al.), Am J Gastroenterol 2024;119(1):30-54ShowHide
Decision at stakescreen for alcohol use disorder and provide multidisciplinary integrated care in patients with steatotic liver disease
Treatment of AUD with sustained abstinence is the most effective strategy to prevent progression and improve long-term outcomes at any stage of ALD; ACG recommends brief screening with a tool such as AUDIT-C (strong, high), brief motivational interventions (strong, low), and integrated multidisciplinary care combining behavioral therapy and/or pharmacotherapy (strong, low).…
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 standardShowHide
Treatment of AUD with sustained abstinence is the most effective strategy to prevent progression and improve long-term outcomes at any stage of ALD; ACG recommends brief screening with a tool such as AUDIT-C (strong, high), brief motivational interventions (strong, low), and integrated multidisciplinary care combining behavioral therapy and/or pharmacotherapy (strong, low). AUD pharmacotherapy recommendations are scoped specifically to COMPENSATED ALD and are not co-equal: baclofen is recommended as an option (strong recommendation, moderate evidence); acamprosate or naltrexone are only suggested as options (conditional, very low); gabapentin or topiramate are suggested as options (conditional, very low); disulfiram is suggested AGAINST along any spectrum of ALD (conditional, very low). For severe alcohol withdrawal, benzodiazepines are the treatment of choice but with explicitly cautious use and careful monitoring given their potential to precipitate or exacerbate hepatic encephalopathy (strong, moderate); AWS is managed per CIWA-Ar protocol, differentiating it from HE while acknowledging the two can coexist. For alcohol-associated hepatitis (AH), severity is stratified by MELD: MELD >20 defines severe AH, which carries high short-term mortality and should preferably be managed in hospital; MELD ≤20 defines moderate AH. In severe AH (MELD >20) ACG recommends corticosteroid therapy ONLY if there are no contraindications (strong, moderate); active infection (including untreated HBV infection), uncontrolled diabetes mellitus, gastrointestinal bleeding, and severe renal failure are contraindications to corticosteroid use, though corticosteroids can be started after adequate control or reversal of infection, renal failure, and gastrointestinal bleeding. Prednisolone is preferred over prednisone; both are dosed 40 mg/day for a total of 4 weeks, with IV methylprednisolone 32 mg/day as the alternative for patients unable to take oral medication; there is no evidence supporting rapid vs slow tapering after the 4-week course. Corticosteroid response is assessed by Lille score at day 7 OR day 4 (day-4 shown as accurate as day-7); among non-responders (Lille >0.45) corticosteroids should be discontinued. ACG recommends IV N-acetylcysteine as an adjuvant to corticosteroids in severe AH (strong, moderate), while explicitly noting that other society guidelines have not adopted this recommendation. ACG recommends AGAINST pentoxifylline (strong, moderate) and AGAINST universal prophylactic antibiotics in hospitalized severe AH (strong, moderate); data on G-CSF and microbiome-based therapies are insufficient. Nutrition: target 35 kcal/kg/day with 1.2-1.5 g/kg/day protein; patients consuming <21 kcal/kg/day should receive nutritional support, preferably oral/enteral, oral nutritional supplements first, escalating to enteral nutrition if caloric targets remain unmet (strong, moderate). Thiamine, vitamin B12 and zinc deficiencies are common in AH and should be supplemented. For severe AH unresponsive to medical management with high risk of death, early liver transplantation for highly selected patients should be considered according to regional and institutional protocols (conditional recommendation, low level of evidence); LT selection must not be based solely on an arbitrary duration of sobriety, and should rest on detailed psychosocial evaluation by a social worker and addiction specialist, optionally supported by tools such as SIPAT, HRAR, MAPS, HPSS or SALT. For severe AH with 4 or more organ failures, non-responsive to corticosteroids and ineligible for early LT, palliative care engagement is appropriate.
Clinical takeawayUse standard statin dosing in MASLD for cardiovascular prevention. Hepatic steatosis does not impair LDL-C response and should not prompt dose modification or additional monitoring adjustments.
What it foundHepatic steatosis (≥5% liver fat fraction) does not significantly impair LDL-C response to statins; observed differences were 0.097 mmol/L per month (months 0-3, p=0.231) and -0.037 mmol/L per month (months 3-12, p=0.141), neither clinically nor statistically significant.
ContextMASLD is strongly associated with dyslipidemia and cardiovascular mortality. The concern was that hepatic steatosis might impair statin efficacy through altered drug metabolism. This prospective cohort confirms that statin-induced LDL-C reduction is unaffected by hepatic steatosis status.
Reinforcessuggested applicable standard· AASLD, "AASLD Practice Guidance on the clinical assessment and management of nonalcoholic fatty liver disease" (Rinella ME et al., Hepatology 2023;77(5):1797-1835). DOI 10.1097/HEP.0000000000000323, PMID 36727674.ShowHide
Decision at stakeUse standard statin dosing in patients with hepatic steatosis and do not reduce dose based on steatosis alone
Statins are safe and recommended in MASLD/MASH and compensated cirrhosis when indicated for cardiovascular risk reduction. Start per standard CV risk-based criteria with baseline LFTs; routine ALT monitoring on statin is not required and pre-existing transaminitis is not a contraindication. Hold or reduce only for clinically significant ALT elevation, severe muscle symptoms, or decompensated cirrhosis on an individualized basis.
Clinical takeawayCounsel patients taking acetaminophen on the hepatotoxic risk and overdose potential, particularly those using over-the-counter analgesics. Screen for acetaminophen use when evaluating unexplained transaminitis or ALT/AST elevation >100 U/L, given acetaminophen-alone products now account for one-third to one-half of medication-related liver injury cases.
What it foundAcetaminophen-alone exposures increased 349-380% from 2000 to 2024 and now account for one-third to one-half of medication-related liver injury cases (defined by ALT/AST >100 U/L), while APAP-combination products declined 60-85%.
ContextAcetaminophen's role in drug-induced liver injury is well-known. This analysis documents a major epidemiologic shift: acetaminophen-alone products now dominate (33-45% of cases, up 349-380%) while combination products declined 60-85% following FDA restrictions in the early 2010s, indicating regulatory efforts to limit APAP in combination formulations have redirected risk to isolated products.
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.
Towers EB … Farah R · Clinical Gastroenterology and Hepatology : the Official Clinical Practice Journal of the American Gastroenterological Association · IF 16.2 · PubMed ↗Permalink
Hepatologyprospective cohort · n=410 · Aug 9, 2026 · J Gastro Hep · IF 3.5
Clinical takeawayConsider iLivTouch-derived LIID and LSM as alternative non-invasive tools for identifying MASH and staging fibrosis when FIB-4, VCTE, MRE, or ELF are unavailable or discordant
What it foundLIID score showed AUROC 0.71 (95% CI 0.66-0.76) for MASH detection, with rule-out threshold <6.0 achieving 89.6% sensitivity and 78.2% NPV, and rule-in threshold >7.8 achieving 88.4% specificity and 70.5% PPV; LSM showed AUROC 0.86 for advanced fibrosis (95% CI 0.79-0.92), 0.75 for significant fibrosis (95% CI 0.69-0.79), and 0.78 for cirrhosis (95% CI 0.61-0.95).
ContextThis literature reports on noninvasive quantitative ultrasound-derived scoring methods for detecting metabolic dysfunction-associated steatohepatitis (MASH) and hepatic fibrosis in patients with metabolic dysfunction-associated steatotic liver disease (MASLD).
Reinforcessuggested applicable standard· AASLD 2023 Practice Guidance, updated by AASLD Practice Guidance October 2024 (resmetirom) and November 2025 (semaglutide)ShowHide
Decision at stakeUse non-invasive tests to identify MASH and assess fibrotic burden instead of liver biopsy
Diagnose MASLD by hepatic steatosis on imaging (or biopsy) plus at least one cardiometabolic criterion and exclusion of competing etiologies (significant alcohol use, other liver disease), then risk-stratify fibrosis using a sequential non-invasive approach: FIB-4 first, followed by a second-line imaging-based test (VCTE, MRE, or ELF) for indeterminate/high-risk FIB-4, with liver biopsy reserved for discordant or unclear cases.…
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 standardShowHide
Diagnose MASLD by hepatic steatosis on imaging (or biopsy) plus at least one cardiometabolic criterion and exclusion of competing etiologies (significant alcohol use, other liver disease), then risk-stratify fibrosis using a sequential non-invasive approach: FIB-4 first, followed by a second-line imaging-based test (VCTE, MRE, or ELF) for indeterminate/high-risk FIB-4, with liver biopsy reserved for discordant or unclear cases. Lifestyle modification (≥7-10% weight loss, Mediterranean diet, exercise) remains the foundation for all patients. For adults with MASH and F2-F3 fibrosis identified by non-invasive tests (VCTE 8-15 kPa, MRE 3.1-4.4 kPa, or ELF 9.2-10.5) rather than biopsy, AASLD now gives dedicated, updated practice guidance on both FDA-approved pharmacotherapies: resmetirom (Oct 2024 update) and semaglutide 2.4mg/week subcutaneous (Nov 2025 update, following August 2025 accelerated FDA approval based on ESSENCE trial data: 62.9% vs 34.3% MASH resolution without fibrosis worsening; 36.8% vs 22.4% ≥1-stage fibrosis improvement). Pioglitazone or vitamin E remain options per the 2023 base guidance. Manage cardiometabolic risk with statins for ASCVD reduction plus glycemic and blood-pressure control; for semaglutide specifically, routine hepatic panels are recommended only as clinically indicated (no discontinuations for LFT elevation in ESSENCE), with monitoring for GI adverse effects and rare risks (AKI, gallbladder disease, pancreatitis, thyroid C-cell tumors, retinopathy progression, lean mass loss). HCC surveillance with ultrasound and AFP every 6 months remains indicated only if cirrhosis is present.
Clinical takeawayDo not add NAC to lifestyle counseling for MASLD. Although NAC was safe and well-tolerated, it provided no additional benefit over lifestyle intervention alone for fibrosis, insulin resistance, oxidative stress, or steatosis indices. Lifestyle modification remains the evidence-based foundation.
What it foundHigh-dose NAC (2400 mg/day) for 12 weeks did not significantly reduce serum malondialdehyde, fasting insulin, HOMA-IR, or hepatic fibrosis compared to lifestyle intervention alone in 60 non-diabetic MASLD patients; the control group (lifestyle alone) showed greater liver steatosis score reduction (p=0.004).
ContextNAC has theoretical antioxidant and hepatoprotective effects and has been studied in NASH/MASLD, but this RCT provides clear evidence it does not improve the hallmark features of the disease (steatosis, fibrosis, insulin resistance). Confirms that lifestyle intervention alone is the evidence-based foundation of MASLD management.
Emergingsuggested applicable standard· AASLD 2023 Practice Guidance, updated by AASLD Practice Guidance October 2024 (resmetirom) and November 2025 (semaglutide)ShowHide
Decision at stakeWhether N-acetylcysteine supplementation provides clinical benefit for non-diabetic MASLD patients
Diagnose MASLD by hepatic steatosis on imaging (or biopsy) plus at least one cardiometabolic criterion and exclusion of competing etiologies (significant alcohol use, other liver disease), then risk-stratify fibrosis using a sequential non-invasive approach: FIB-4 first, followed by a second-line imaging-based test (VCTE, MRE, or ELF) for indeterminate/high-risk FIB-4, with liver biopsy reserved for discordant or unclear cases.…
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 standardShowHide
Diagnose MASLD by hepatic steatosis on imaging (or biopsy) plus at least one cardiometabolic criterion and exclusion of competing etiologies (significant alcohol use, other liver disease), then risk-stratify fibrosis using a sequential non-invasive approach: FIB-4 first, followed by a second-line imaging-based test (VCTE, MRE, or ELF) for indeterminate/high-risk FIB-4, with liver biopsy reserved for discordant or unclear cases. Lifestyle modification (≥7-10% weight loss, Mediterranean diet, exercise) remains the foundation for all patients. For adults with MASH and F2-F3 fibrosis identified by non-invasive tests (VCTE 8-15 kPa, MRE 3.1-4.4 kPa, or ELF 9.2-10.5) rather than biopsy, AASLD now gives dedicated, updated practice guidance on both FDA-approved pharmacotherapies: resmetirom (Oct 2024 update) and semaglutide 2.4mg/week subcutaneous (Nov 2025 update, following August 2025 accelerated FDA approval based on ESSENCE trial data: 62.9% vs 34.3% MASH resolution without fibrosis worsening; 36.8% vs 22.4% ≥1-stage fibrosis improvement). Pioglitazone or vitamin E remain options per the 2023 base guidance. Manage cardiometabolic risk with statins for ASCVD reduction plus glycemic and blood-pressure control; for semaglutide specifically, routine hepatic panels are recommended only as clinically indicated (no discontinuations for LFT elevation in ESSENCE), with monitoring for GI adverse effects and rare risks (AKI, gallbladder disease, pancreatitis, thyroid C-cell tumors, retinopathy progression, lean mass loss). HCC surveillance with ultrasound and AFP every 6 months remains indicated only if cirrhosis is present.
New therapyMASLDhepatocellular carcinomacirrhosisartificial intelligence
Clinical takeawayDiscuss resmetirom or semaglutide with eligible MASH patients. Consult the product labeling for efficacy, safety, and selection criteria.
What it foundResmetirom (2024) and semaglutide (2025) received FDA accelerated approval as the first pharmacotherapies for MASH, ending a period with no approved medical treatments for the disease.
ContextThis confirms that MASLD management has evolved from observation-only (with biopsy as the sole severity assessment tool) to an era with noninvasive biomarkers, structured care pathways, and FDA-approved pharmacotherapies. MASLD affects >30% of the global population and remains a leading cause of cirrhosis and HCC.
Reinforcessuggested applicable standard· AASLD 2023 Practice Guidance, updated by AASLD Practice Guidance October 2024 (resmetirom) and November 2025 (semaglutide)ShowHide
Decision at stakeUse non-invasive biomarkers (FIB-4 and imaging) for fibrosis risk stratification rather than biopsy-first approach, and recognize resmetirom and semaglutide as evidence-based pharmacotherapies for MASH with F2-F3 fibrosis
…For adults with MASH and F2-F3 fibrosis identified by non-invasive tests (VCTE 8-15 kPa, MRE 3.1-4.4 kPa, or ELF 9.2-10.5) rather than biopsy, AASLD now gives dedicated, updated practice guidance on both FDA-approved pharmacotherapies: resmetirom (Oct 2024 update) and semaglutide 2.4mg/week subcutaneous (Nov 2025 update, following August 2025 accelerated FDA approval based on ESSENCE trial data: 62.9% vs 34.3% MASH resolution without fibrosis worsening; 36.8% vs 22.4% ≥1-stage fibrosis improvement).…
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 standardShowHide
Diagnose MASLD by hepatic steatosis on imaging (or biopsy) plus at least one cardiometabolic criterion and exclusion of competing etiologies (significant alcohol use, other liver disease), then risk-stratify fibrosis using a sequential non-invasive approach: FIB-4 first, followed by a second-line imaging-based test (VCTE, MRE, or ELF) for indeterminate/high-risk FIB-4, with liver biopsy reserved for discordant or unclear cases. Lifestyle modification (≥7-10% weight loss, Mediterranean diet, exercise) remains the foundation for all patients. For adults with MASH and F2-F3 fibrosis identified by non-invasive tests (VCTE 8-15 kPa, MRE 3.1-4.4 kPa, or ELF 9.2-10.5) rather than biopsy, AASLD now gives dedicated, updated practice guidance on both FDA-approved pharmacotherapies: resmetirom (Oct 2024 update) and semaglutide 2.4mg/week subcutaneous (Nov 2025 update, following August 2025 accelerated FDA approval based on ESSENCE trial data: 62.9% vs 34.3% MASH resolution without fibrosis worsening; 36.8% vs 22.4% ≥1-stage fibrosis improvement). Pioglitazone or vitamin E remain options per the 2023 base guidance. Manage cardiometabolic risk with statins for ASCVD reduction plus glycemic and blood-pressure control; for semaglutide specifically, routine hepatic panels are recommended only as clinically indicated (no discontinuations for LFT elevation in ESSENCE), with monitoring for GI adverse effects and rare risks (AKI, gallbladder disease, pancreatitis, thyroid C-cell tumors, retinopathy progression, lean mass loss). HCC surveillance with ultrasound and AFP every 6 months remains indicated only if cirrhosis is present.
Clinical takeawayFor PBC patients on UDCA, assess ALP at 1 year; if ALP ≥1.67x ULN (or bilirubin 1-2x ULN) in Australia, escalate to second-line therapy including PPAR agonists, fenofibrate, or obeticholic acid (subject to precautions). Also escalate if inadequate biochemical response or bothersome symptoms. At diagnosis, identify high-risk patients (male, age <45, ALP >1.5x ULN, anti-gp210 positive, or significant fibrosis) for closer monitoring and earlier therapy consideration.
What it foundAbout 40% of PBC patients have inadequate UDCA response; established progression risk factors are male gender, age <45 years, ALP >1.5x ULN, anti-gp210 antibodies, and significant fibrosis; in Australia, second-line therapy is reimbursed when ALP ≥1.67x ULN or bilirubin 1-2x ULN after 1 year of UDCA.
ContextThis review consolidates established PBC management (UDCA for transplant-free survival) with evolving emphasis on ALP normalization as an aspirational treatment target. Risk stratification and Australian-specific reimbursement thresholds provide practical guidance for clinicians managing PBC in that setting.
Refinessuggested applicable standard· American Association for the Study of Liver Diseases, 'Primary Biliary Cholangitis: 2021 Practice Guidance', 2021ShowHide
Decision at stakeSet the biochemical response target for UDCA efficacy assessment at 12 months
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.
Clinical takeawayBe aware of BEACON-HCC as emerging North American expert consensus on HCC treatment allocation that prioritizes newer modalities (TARE, EBRT, systemic-locoregional combinations) and refined prognostic factors (tumor burden, vascular invasion) beyond BCLC 2025. Prospective validation against clinical outcomes is planned; do not adopt as primary guidance until this evidence materializes.
What it foundBEACON-HCC is a consensus treatment allocation framework developed by 20 North American experts incorporating TARE, EBRT, systemic-locoregional combinations, and nuanced prognostic factors (tumor burden, vascular invasion), achieving 96.6% agreement with external expert recommendations versus 72.4% for BCLC 2025 in a 29-case pilot.
ContextBEACON-HCC reflects current expert opinion on incorporating newer treatment options into HCC allocation. The 96.6% concordance with external experts shows strong agreement on the framework structure among specialists, but this is consensus opinion from a 29-case pilot exercise, not empirical validation. Clinical outcomes validation is pending.
Refinessuggested applicable standard· American Association for the Study of Liver Diseases (AASLD), 'AASLD Practice Guidance on prevention, diagnosis, and treatment of hepatocellular carcinoma,' Hepatology, 2023 (78(6):1922-1965).ShowHide
Decision at stakeAllocate HCC therapy based on BCLC staging framework incorporating tumor stage, liver function, and performance status
…AASLD 2023 stages confirmed HCC using the BCLC framework and links stage to therapy (curative resection, ablation, or transplantation within Milan criteria for very-early/early disease; TACE and other locoregional therapy for intermediate disease; systemic therapy for advanced disease).…
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 standardShowHide
Perform HCC surveillance in adults with cirrhosis of any etiology who are able to benefit from HCC treatment, accordingly, do not enroll patients with Child-Turcotte-Pugh class C cirrhosis unless they are candidates for (or listed for) liver transplantation, and do not surveil those with life-limiting comorbidity (life expectancy <1-2 years) that transplantation cannot remedy, and in select non-cirrhotic chronic HBV carriers at elevated risk (e.g., active hepatitis/high viral load, family history of HCC, African/African-American ancestry, Asian men >40 and Asian women >50; AASLD references risk scores such as PAGE-B but stops short of mandating a specific numeric cutoff). Surveillance is abdominal ultrasound PLUS serum AFP at ~6-month (semiannual) intervals, a change from prior AASLD guidance, which had left AFP optional (Strong recommendation). Pursue diagnostic evaluation for an AFP ≥20 ng/mL or for a rising AFP, defined as a doubling of AFP or an increase on two consecutive tests even if the absolute value is <20 ng/mL. Any suspicious ultrasound observation ≥1 cm, or an inadequate/limited ultrasound, should be evaluated with multiphasic contrast-enhanced CT or MRI interpreted with CT/MRI LI-RADS. AASLD 2023 stages confirmed HCC using the BCLC framework and links stage to therapy (curative resection, ablation, or transplantation within Milan criteria for very-early/early disease; TACE and other locoregional therapy for intermediate disease; systemic therapy for advanced disease). Its first-line systemic options for advanced HCC with preserved liver function (Child-Pugh A) are atezolizumab+bevacizumab OR durvalumab+tremelimumab (STRIDE) as preferred, with sorafenib, lenvatinib, or durvalumab monotherapy as alternatives when the preferred combinations are contraindicated. After potentially curative therapy, continue surveillance for recurrence given high recurrence risk (AASLD monitors with cross-sectional contrast-enhanced imaging, not ultrasound, in the early post-treatment period).
Clinical takeawayIn infection-triggered HRS-AKI with high disease severity (MELD >29, stage 3 AKI present in 67% of cohort), high-dose albumin (>50 g/day, mean 66 g/day) was not associated with increased respiratory failure compared to standard dosing (2/54, 3.7% vs. 2/89 standard-dose patients, 2.2%), prolonged hospital stay, or reduced 6-month survival (p=0.141). The respiratory failures observed were related to infection complications (pneumonia, aspiration), not albumin toxicity. Respiratory failure concern alone should not restrict albumin dosing in this severely ill population. Limitation: observational study with severity-based allocation; patients assigned to high-dose albumin had higher baseline MELD, stage 3 AKI, and infection-driven AKI, yet similar outcomes-reassuring but does not establish that higher-dose benefit extends to less-severe HRS-AKI.
What it foundHigh-dose albumin (>50 g/day, mean 66 g/day) in infection-triggered HRS-AKI resulted in respiratory failure in 2/54 cases (3.7%), similar to standard dosing (2/89 cases, 2.2%), without increased hospital stay or reduced 6-month survival (p=0.141).
ContextClinicians often restrict albumin in HRS-AKI due to worry about respiratory failure, which may inadvertently limit adequate renal perfusion support during AKI recovery. This study challenges that concern by showing similar low respiratory failure rates across a wide dosing range, though the groups differed in severity at baseline.
Reinforcessuggested applicable standard· International Club of Ascites (ICA) & Acute Disease Quality Initiative (ADQI), "Acute kidney injury in patients with cirrhosis: Acute Disease Quality Initiative (ADQI) and International Club of Ascites (ICA) joint multidisciplinary consensus meeting," Journal of Hepatology, 2024ShowHide
Decision at stakeuse albumin 20-25% at 20-40 g/day (adjusted daily to volume status) alongside vasoconstrictors in HRS-AKI
…Give 20-25% albumin 20-40 g/day with any vasoconstrictor, adjusted daily to volume status and withheld for fluid overload/pulmonary edema.…
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 standardShowHide
Per the 2024 ADQI-ICA joint consensus (which updates the 2015 ICA-AKI criteria referenced in AASLD 2021), in a patient with cirrhosis and ascites: DIAGNOSE HRS-AKI when all of (a) cirrhosis with ascites; (b) AKI by KDIGO/ICA criteria, serum creatinine rise ≥0.3 mg/dL (26.5 µmol/L) within 48h or ≥50% from a baseline known or presumed within the prior 7 days, and/or urine output ≤0.5 mL/kg/h for ≥6h (strong recommendation, grade A); (c) absence of improvement in serum creatinine and/or urine output within 24h following adequate volume resuscitation WHEN CLINICALLY INDICATED, the consensus recommends AGAINST systematic 48h albumin administration as a diagnostic requisite (strong recommendation, grade D), and only where volume status is equivocal is a single fluid challenge (250-500 mL crystalloid, or 1-1.5 g/kg of 20-25% albumin) assessed within 24h; and (d) absence of strong evidence for an alternative primary cause of AKI (e.g., septic shock requiring vasopressors, acute glomerular injury, obstruction, or nephrotoxin-induced AKI) (not graded). HRS-AKI is a phenotype specific to advanced cirrhosis and ascites: coexisting CKD, tubular injury or proteinuria do NOT exclude it, and it may coexist with, or be superimposed on, other AKI etiologies rather than requiring pure exclusion. TREAT: immediately on diagnosis start a vasoconstrictor plus 20-25% albumin (strong recommendation, grade A). Terlipressin is first-line, continuous IV infusion 2-12 mg/day, titrated up by ≥2 mg/day every 24h to a maximum 12 mg/day if serum creatinine has not fallen ≥25%; or IV bolus 1-2 mg every 6h, escalated from 1 mg to 2 mg every 6h on that same ≥25% serum-creatinine response threshold, with the 12 mg/day maximum applying only to continuous infusion and not to bolus dosing. If terlipressin is unavailable or contraindicated, norepinephrine (continuous infusion 0.5-3 mg/h, up-titrated 0.5 mg/h every 4h to raise MAP ≥10 mmHg; requires ICU care and a central line) may be more appropriate. Midodrine 7.5-15 mg PO every 8h plus octreotide 100-200 µg SC every 8h with albumin is third-line, considered only if terlipressin is contraindicated AND transfer to ICU for norepinephrine is not possible. Give 20-25% albumin 20-40 g/day with any vasoconstrictor, adjusted daily to volume status and withheld for fluid overload/pulmonary edema. Discontinue vasoconstrictors when serum creatinine returns to within 0.3 mg/dL of baseline, for a severe adverse reaction, if kidney function does not improve after 48h at maximum tolerated dose, if RRT is indicated, or at a maximum of 14 days of therapy (strong recommendation, grade B). Initiation of RRT should be individualized to clinical context and anticipated or observed life-threatening AKI-related complications (best-practice statement) rather than framed strictly as a transplant-bridge measure. Recommend expedited evaluation for liver transplantation following an episode of AKI (best-practice statement); LT in selected patients is the definitive treatment for HRS-AKI regardless of vasoconstrictor response (strong recommendation, grade A), with vasoconstrictors serving as a bridge to transplantation or renal recovery rather than a cure.
Clinical takeawayEducate patients and families that HBV is lifelong (80% don't understand). Involve families in care planning. Target additional support to high-risk non-adherers: less educated, without family support, or rural residents. Simplify care pathways and improve affordability, especially in endemic regions.
What it foundTreatment uptake in chronic HBV is predicted by higher education (OR 2.0; 95% CI 1.3-3.1), family support (OR 1.9; 95% CI 1.3-2.8), and urban residence (OR 1.7; 95% CI 1.1-2.5); only 20.5% of patients recognize HBV as a lifelong condition requiring continuous care.
ContextQuantifies well-established barriers to HBV adherence-education, family support, socioeconomic access-in the endemic regions where treatment gaps are most significant.
Reinforcessuggested applicable standard· American Association for the Study of Liver Diseases / Infectious Diseases Society of America (AASLD/IDSA), "AASLD/IDSA Practice Guideline on Treatment of Chronic Hepatitis B," Hepatology, 2026ShowHide
Decision at stakeHow to implement CHB treatment recommendations considering patient values, knowledge gaps, and socioeconomic barriers to care.
…Qualifiers the guideline stresses: the decision weighs exposure risk and the vaccine/immunity status of contacts, favoring treatment if contacts are unvaccinated, vaccine-nonresponsive, immunocompromised, or of unknown vaccine status; persons requesting treatment for prevention may be prescribed it since risks may not be disclosed; explicitly, people with CHB must NOT be restricted in daily activities, contact sports, school, or professional training and must NOT be required to take antivirals because of transmission risk in those settings; routine contact, shared meals, and hugging are not transmission routes (avoid sharing toothbrushes/razors); most healthcare workers with CHB are NOT high-risk, but those performing SHEA Category III exposure-prone procedures may require antivirals (SHEA target HBV DNA <1000 IU/mL); neither CDC nor SHEA requires disclosure to patients or staff; anti-stigma framing is part of the recommendation.…
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 standardShowHide
The 2026 AASLD/IDSA guideline addresses six PICO questions only; it states explicitly that all other 2018 AASLD recommendations for CHB management remain applicable, and that screening/diagnosis were out of scope. Baseline evaluation and the standard treatment indications (cirrhosis with detectable HBV DNA; HBeAg-positive immune-active with ALT >2x ULN and HBV DNA >20,000 IU/mL; HBeAg-negative immune-active with ALT >2x ULN and HBV DNA >2,000 IU/mL; prophylaxis for reactivation risk during immunosuppression) derive from the 2018 document, not this update, which lists 'treatment of HBeAg-positive and -negative immune active CHB with ALT >2x ULN', treatment of children, treatment of cirrhosis, low-level viremia, virologic breakthrough, and special populations (transplant, acute HBV, HCV/HDV/HIV coinfection) as topics 'well covered in previous AASLD 2018 Guidance and for which recommendations have not changed'. Preferred agents remain entecavir, TDF, or TAF. THE SIX 2026 RECOMMENDATIONS: (1) PMTCT, for pregnant persons with HBV DNA >200,000 IU/mL at any time point during pregnancy, regardless of HBeAg status, AASLD RECOMMENDS initiating TDF or TAF at gestational week 28 (STRONG recommendation, MODERATE certainty, the only strong recommendation in the guideline); TDF has a more extensive safety record in pregnancy than TAF. Implementation qualifiers: initiate immediately if care is first sought after week 28; initiate at week 16 if infant HBIG will be unavailable (with subsequent infant vaccination); consider earlier initiation when amniocentesis is anticipated (transmission risk is increased with HBV DNA >2,000,000 IU/mL) or when preterm labor risk is high; continue TDF/TAF if already on it, switch entecavir or other agents to TDF/TAF; if treatment was solely for perinatal prophylaxis it may be discontinued at delivery, with HBV DNA and ALT monitored every 1-3 months for up to 6 months for withdrawal flare and treatment reinitiated if ALT >=5x ULN; use TDF or TAF in breastfeeding persons requiring treatment. (2) HORIZONTAL TRANSMISSION, for HBsAg-positive viremic persons not meeting disease-specific treatment indications who are in high-risk scenarios for transmission to others, AASLD SUGGESTS a shared decision-making approach regarding antiviral treatment (CONDITIONAL, VERY LOW certainty). Qualifiers the guideline stresses: the decision weighs exposure risk and the vaccine/immunity status of contacts, favoring treatment if contacts are unvaccinated, vaccine-nonresponsive, immunocompromised, or of unknown vaccine status; persons requesting treatment for prevention may be prescribed it since risks may not be disclosed; explicitly, people with CHB must NOT be restricted in daily activities, contact sports, school, or professional training and must NOT be required to take antivirals because of transmission risk in those settings; routine contact, shared meals, and hugging are not transmission routes (avoid sharing toothbrushes/razors); most healthcare workers with CHB are NOT high-risk, but those performing SHEA Category III exposure-prone procedures may require antivirals (SHEA target HBV DNA <1000 IU/mL); neither CDC nor SHEA requires disclosure to patients or staff; anti-stigma framing is part of the recommendation. (3) IMMUNE-TOLERANT PHASE, defined as HBeAg-positive, HBV DNA >10^7 IU/mL, and normal ALT; AASLD SUGGESTS antiviral therapy for those over age 40 years, OR with significant liver inflammation (grade >=2) or fibrosis (>=F2) on biopsy or noninvasive tests (CONDITIONAL, VERY LOW certainty). For persons under age 40 who are interested in starting treatment earlier, AASLD suggests shared decision-making weighing risk factors and the benefits and risks of treatment. Accurate phase identification requires persistently normal ALT on >=2 measurements >=6 months apart, using ULN 35 U/L (males) and 25 U/L (females). (4) INDETERMINATE ('grey zone') PHASE, the HBeAg-negative indeterminate phase is defined as HBsAg-positive, HBeAg-negative persons whose ALT and/or HBV DNA fall outside the thresholds for HBeAg-negative immune-active CHB (ALT >2x ULN and HBV DNA >2,000 IU/mL) and outside those for inactive CHB (HBV DNA <2,000 IU/mL with normal ALT), comprising predominantly two subgroups, (I) normal (<ULN) or mildly elevated (<2x ULN) ALT with HBV DNA >=2,000 IU/mL, or (II) elevated ALT (>ULN) with HBV DNA <2,000 IU/mL, with ALT interpreted against ULN 35 U/L (males) and 25 U/L (females) and phase assigned on >=2 ALT and HBV DNA measurements over a 6-12 month period; in adults who are HBsAg-positive, HBeAg-negative, without cirrhosis and in the indeterminate phase so defined, AASLD SUGGESTS antiviral therapy using a shared decision-making approach assessing risks and benefits, and re-evaluating that decision at each follow-up visit if treatment has not been initiated (CONDITIONAL, VERY LOW certainty). Decision-relevant factors include fibrosis stage, age, and sex, e.g. age >40, male sex, and low-normal platelets (<180 k/mm3) favor treatment. (5) DISCONTINUATION, in adults with CHB who are HBeAg-negative, without cirrhosis, with sustained undetectable HBV DNA on nucleos(t)ide analogue therapy, AASLD SUGGESTS NOT withdrawing NA therapy until HBsAg loss (CONDITIONAL, VERY LOW certainty). If a patient nonetheless has a strong desire to stop, shared decision-making applies and ALL of the following must be met: no history of advanced fibrosis/cirrhosis, hepatic decompensation (variceal bleed, ascites, encephalopathy, hepatorenal syndrome), HCC, or extrahepatic HBV complications; if HBeAg-positive at treatment start, HBeAg seroconversion to anti-HBe-positive for >=1 year with undetectable HBV DNA >=2 years; if HBeAg-negative at start, undetectable HBV DNA >=2 years; no HIV or HDV coinfection; quantitative HBsAg <100 IU/mL; and willingness to adhere to frequent monitoring. After stopping, monitor ALT and HBV DNA every 1-3 months for 6 months, then every 3 months for 6-12 months, then every 3-6 months. Restart antivirals IMMEDIATELY if HBV DNA >=10,000 IU/mL (4 log IU/mL) at any time regardless of ALT, OR ALT >=5x ULN regardless of HBV DNA, OR total bilirubin >2.5 mg/dL. (6) HCC SURVEILLANCE (all CONDITIONAL, VERY LOW certainty; modality/interval per AASLD 2023 HCC Practice Guidance), Rec 6: after HBsAg loss, continue surveillance in those with cirrhosis, family history of HCC, men who lost HBsAg after age 40, and women who lost HBsAg after age 50. Rec 7: in HBV-HDV coinfection, surveil adults independent of cirrhosis status; in children, individualize because HCC risk in that population is unknown. Rec 8: in HBV-HIV coinfection, surveil men >=18 years and women >=40 years. Rec 9: in HBV-HCV coinfection, AASLD recommends treating HCV and suggests HCC surveillance per HBV mono-infection criteria. Where a person has more than one coinfection, the surveillance recommendation should follow the coinfection carrying the highest associated risk. The guideline notes that most of its recommendations rest on low or very low certainty evidence and that shared decision-making, not uniform policy, is the intended mode of application.
Clinical takeawayPursue 6-monthly ultrasound and serum AFP surveillance for at-risk patients; use noninvasive fibrosis assessment in primary care settings to identify patients requiring surveillance and ensure referral to specialist hepatology care; establish clear multidisciplinary referral pathways.
What it foundConsensus recommends 6-monthly ultrasound and serum AFP for HCC surveillance, with particular emphasis on using noninvasive fibrosis assessment in primary healthcare to identify at-risk patients requiring surveillance.
ContextThis literature reports a Malaysian multidisciplinary consensus on evidence-based approaches to hepatocellular carcinoma prevention and early detection.
Reinforcessuggested applicable standard· American Association for the Study of Liver Diseases (AASLD), 'AASLD Practice Guidance on prevention, diagnosis, and treatment of hepatocellular carcinoma,' Hepatology, 2023 (78(6):1922-1965).ShowHide
Decision at stakeSurveillance interval and modality: ultrasound plus serum AFP every 6 months for at-risk cirrhotic patients
…Surveillance is abdominal ultrasound PLUS serum AFP at ~6-month (semiannual) intervals, a change from prior AASLD guidance, which had left AFP optional (Strong recommendation).…
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 standardShowHide
Perform HCC surveillance in adults with cirrhosis of any etiology who are able to benefit from HCC treatment, accordingly, do not enroll patients with Child-Turcotte-Pugh class C cirrhosis unless they are candidates for (or listed for) liver transplantation, and do not surveil those with life-limiting comorbidity (life expectancy <1-2 years) that transplantation cannot remedy, and in select non-cirrhotic chronic HBV carriers at elevated risk (e.g., active hepatitis/high viral load, family history of HCC, African/African-American ancestry, Asian men >40 and Asian women >50; AASLD references risk scores such as PAGE-B but stops short of mandating a specific numeric cutoff). Surveillance is abdominal ultrasound PLUS serum AFP at ~6-month (semiannual) intervals, a change from prior AASLD guidance, which had left AFP optional (Strong recommendation). Pursue diagnostic evaluation for an AFP ≥20 ng/mL or for a rising AFP, defined as a doubling of AFP or an increase on two consecutive tests even if the absolute value is <20 ng/mL. Any suspicious ultrasound observation ≥1 cm, or an inadequate/limited ultrasound, should be evaluated with multiphasic contrast-enhanced CT or MRI interpreted with CT/MRI LI-RADS. AASLD 2023 stages confirmed HCC using the BCLC framework and links stage to therapy (curative resection, ablation, or transplantation within Milan criteria for very-early/early disease; TACE and other locoregional therapy for intermediate disease; systemic therapy for advanced disease). Its first-line systemic options for advanced HCC with preserved liver function (Child-Pugh A) are atezolizumab+bevacizumab OR durvalumab+tremelimumab (STRIDE) as preferred, with sorafenib, lenvatinib, or durvalumab monotherapy as alternatives when the preferred combinations are contraindicated. After potentially curative therapy, continue surveillance for recurrence given high recurrence risk (AASLD monitors with cross-sectional contrast-enhanced imaging, not ultrasound, in the early post-treatment period).
Clinical takeawayNo clinical action yet: Phase 1 study in a pre-selected patient population. Efficacy in typical CHB and optimal dosing remain to be determined in Phase 2-3 trials.
What it foundIn virally suppressed, HBeAg-negative CHB patients on stable nucleos(t)ide analogue therapy, AHB-137 300 mg achieved mean HBsAg reductions of 0.7-1.0 log10 IU/mL, with HBsAg loss (<0.05 IU/mL) in 3 patients.
ContextCurrent CHB management relies on nucleos(t)ide analogues (first-line) or pegylated interferon. AHB-137 targeting HBV mRNA represents a novel mechanism distinct from existing therapies. This first-in-human data demonstrates early HBsAg activity in a highly selected population of already-suppressed patients; treatment-related adverse events (primarily mild to moderate injection-site reactions and headaches) occurred in 71% of CHB patients, with no serious adverse events or discontinuations. Whether this activity translates to improved outcomes in treatment-naive or typical CHB patients, and how tolerability scales with dosing and duration in Phase 2-3, remains unknown.
Emergingsuggested applicable standard· American Association for the Study of Liver Diseases / Infectious Diseases Society of America (AASLD/IDSA), "AASLD/IDSA Practice Guideline on Treatment of Chronic Hepatitis B," Hepatology, 2026ShowHide
Decision at stakepotential role of novel antisense oligonucleotide therapies in chronic hepatitis B 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 standardShowHide
The 2026 AASLD/IDSA guideline addresses six PICO questions only; it states explicitly that all other 2018 AASLD recommendations for CHB management remain applicable, and that screening/diagnosis were out of scope. Baseline evaluation and the standard treatment indications (cirrhosis with detectable HBV DNA; HBeAg-positive immune-active with ALT >2x ULN and HBV DNA >20,000 IU/mL; HBeAg-negative immune-active with ALT >2x ULN and HBV DNA >2,000 IU/mL; prophylaxis for reactivation risk during immunosuppression) derive from the 2018 document, not this update, which lists 'treatment of HBeAg-positive and -negative immune active CHB with ALT >2x ULN', treatment of children, treatment of cirrhosis, low-level viremia, virologic breakthrough, and special populations (transplant, acute HBV, HCV/HDV/HIV coinfection) as topics 'well covered in previous AASLD 2018 Guidance and for which recommendations have not changed'. Preferred agents remain entecavir, TDF, or TAF. THE SIX 2026 RECOMMENDATIONS: (1) PMTCT, for pregnant persons with HBV DNA >200,000 IU/mL at any time point during pregnancy, regardless of HBeAg status, AASLD RECOMMENDS initiating TDF or TAF at gestational week 28 (STRONG recommendation, MODERATE certainty, the only strong recommendation in the guideline); TDF has a more extensive safety record in pregnancy than TAF. Implementation qualifiers: initiate immediately if care is first sought after week 28; initiate at week 16 if infant HBIG will be unavailable (with subsequent infant vaccination); consider earlier initiation when amniocentesis is anticipated (transmission risk is increased with HBV DNA >2,000,000 IU/mL) or when preterm labor risk is high; continue TDF/TAF if already on it, switch entecavir or other agents to TDF/TAF; if treatment was solely for perinatal prophylaxis it may be discontinued at delivery, with HBV DNA and ALT monitored every 1-3 months for up to 6 months for withdrawal flare and treatment reinitiated if ALT >=5x ULN; use TDF or TAF in breastfeeding persons requiring treatment. (2) HORIZONTAL TRANSMISSION, for HBsAg-positive viremic persons not meeting disease-specific treatment indications who are in high-risk scenarios for transmission to others, AASLD SUGGESTS a shared decision-making approach regarding antiviral treatment (CONDITIONAL, VERY LOW certainty). Qualifiers the guideline stresses: the decision weighs exposure risk and the vaccine/immunity status of contacts, favoring treatment if contacts are unvaccinated, vaccine-nonresponsive, immunocompromised, or of unknown vaccine status; persons requesting treatment for prevention may be prescribed it since risks may not be disclosed; explicitly, people with CHB must NOT be restricted in daily activities, contact sports, school, or professional training and must NOT be required to take antivirals because of transmission risk in those settings; routine contact, shared meals, and hugging are not transmission routes (avoid sharing toothbrushes/razors); most healthcare workers with CHB are NOT high-risk, but those performing SHEA Category III exposure-prone procedures may require antivirals (SHEA target HBV DNA <1000 IU/mL); neither CDC nor SHEA requires disclosure to patients or staff; anti-stigma framing is part of the recommendation. (3) IMMUNE-TOLERANT PHASE, defined as HBeAg-positive, HBV DNA >10^7 IU/mL, and normal ALT; AASLD SUGGESTS antiviral therapy for those over age 40 years, OR with significant liver inflammation (grade >=2) or fibrosis (>=F2) on biopsy or noninvasive tests (CONDITIONAL, VERY LOW certainty). For persons under age 40 who are interested in starting treatment earlier, AASLD suggests shared decision-making weighing risk factors and the benefits and risks of treatment. Accurate phase identification requires persistently normal ALT on >=2 measurements >=6 months apart, using ULN 35 U/L (males) and 25 U/L (females). (4) INDETERMINATE ('grey zone') PHASE, the HBeAg-negative indeterminate phase is defined as HBsAg-positive, HBeAg-negative persons whose ALT and/or HBV DNA fall outside the thresholds for HBeAg-negative immune-active CHB (ALT >2x ULN and HBV DNA >2,000 IU/mL) and outside those for inactive CHB (HBV DNA <2,000 IU/mL with normal ALT), comprising predominantly two subgroups, (I) normal (<ULN) or mildly elevated (<2x ULN) ALT with HBV DNA >=2,000 IU/mL, or (II) elevated ALT (>ULN) with HBV DNA <2,000 IU/mL, with ALT interpreted against ULN 35 U/L (males) and 25 U/L (females) and phase assigned on >=2 ALT and HBV DNA measurements over a 6-12 month period; in adults who are HBsAg-positive, HBeAg-negative, without cirrhosis and in the indeterminate phase so defined, AASLD SUGGESTS antiviral therapy using a shared decision-making approach assessing risks and benefits, and re-evaluating that decision at each follow-up visit if treatment has not been initiated (CONDITIONAL, VERY LOW certainty). Decision-relevant factors include fibrosis stage, age, and sex, e.g. age >40, male sex, and low-normal platelets (<180 k/mm3) favor treatment. (5) DISCONTINUATION, in adults with CHB who are HBeAg-negative, without cirrhosis, with sustained undetectable HBV DNA on nucleos(t)ide analogue therapy, AASLD SUGGESTS NOT withdrawing NA therapy until HBsAg loss (CONDITIONAL, VERY LOW certainty). If a patient nonetheless has a strong desire to stop, shared decision-making applies and ALL of the following must be met: no history of advanced fibrosis/cirrhosis, hepatic decompensation (variceal bleed, ascites, encephalopathy, hepatorenal syndrome), HCC, or extrahepatic HBV complications; if HBeAg-positive at treatment start, HBeAg seroconversion to anti-HBe-positive for >=1 year with undetectable HBV DNA >=2 years; if HBeAg-negative at start, undetectable HBV DNA >=2 years; no HIV or HDV coinfection; quantitative HBsAg <100 IU/mL; and willingness to adhere to frequent monitoring. After stopping, monitor ALT and HBV DNA every 1-3 months for 6 months, then every 3 months for 6-12 months, then every 3-6 months. Restart antivirals IMMEDIATELY if HBV DNA >=10,000 IU/mL (4 log IU/mL) at any time regardless of ALT, OR ALT >=5x ULN regardless of HBV DNA, OR total bilirubin >2.5 mg/dL. (6) HCC SURVEILLANCE (all CONDITIONAL, VERY LOW certainty; modality/interval per AASLD 2023 HCC Practice Guidance), Rec 6: after HBsAg loss, continue surveillance in those with cirrhosis, family history of HCC, men who lost HBsAg after age 40, and women who lost HBsAg after age 50. Rec 7: in HBV-HDV coinfection, surveil adults independent of cirrhosis status; in children, individualize because HCC risk in that population is unknown. Rec 8: in HBV-HIV coinfection, surveil men >=18 years and women >=40 years. Rec 9: in HBV-HCV coinfection, AASLD recommends treating HCV and suggests HCC surveillance per HBV mono-infection criteria. Where a person has more than one coinfection, the surveillance recommendation should follow the coinfection carrying the highest associated risk. The guideline notes that most of its recommendations rest on low or very low certainty evidence and that shared decision-making, not uniform policy, is the intended mode of application.
Clinical takeawayNo clinical action yet: this is a review of preclinical technology platforms. LOC systems are research tools that may eventually improve drug development by predicting hepatotoxicity in human-relevant conditions, but they have no direct bedside diagnostic or therapeutic application.
What it foundLiver-on-chip (LOC) systems are microscale in vitro devices incorporating human cells within engineered microdevices with dynamic flow through microchannels, designed to recreate liver spatial oxygen and nutrient gradients and physiologic complexity superior to 2D cell culture for modeling liver disease and screening drug toxicity.
ContextLiver-on-chip represents an evolution bridging traditional 2D cell culture and animal models, offering a human-cell platform for understanding hepatotoxicity and disease mechanisms; the technology remains in development for clinical and commercial implementation.
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.