2025+奥地利多学会共识：代谢相关脂肪性肝病

Abbreviations

Al1-D2 Certainty of evidence and strength of recommendation according to the GRADE framework

ALD $^{2}$ Alcohol-related liver disease

ALTD alanine aminotransferase

AST Aspartate aminotransferase

AUD Alcohol use disorder

AUDIT Alcohol use disorders identification test AUDIT-C Alcohol use disorders identification test-consumption

J. Maria Brix· B. Ludvik

Karl Landsteiner Institute for Obesity and Metabolic Disorders, Vienna, Austria

M.Clodi

Clinical Division of Internal Medicine, Saint John of God Hospital, Linz, Austria

C.Datz

Department of Internal Medicine, General Hospital Oberndorf, Teaching Hospital of the Paracelsus Medical University Salzburg, Oberdorf, Austria

M.Effenberger.C.Ress.H.Tilg Division of Gastroenterology, Heparatology,Endocrinology and Metabolism, Department of Internal Medicine I,Medical University of Innsbruck, Innsbruck,Austria

D.Moritz Felsenreich

Division of Visceral Surgery, Department of General Surgery,Medical University of Vienna, Vienna, Austria

A. Maieron

Karl Landsteiner University of Health Sciences, Krems,Austria

consensus report

BIA Bioimpedance analysis

BMI Body mass index

BW Body weight

cACLD Compensated advanced chronic liver disease

CMRF Cardiometabolic risk factors

CSPH Clinically significant portal hypertension

DXA Dual-energy X-ray absorptiometry

ELF Enhanced liver fibrosis test

EtG Ethyl glucuronide

FIB-4 Fibrosis-4 score

FIT Fecal immochemical test

GFR Glomerular filtration rate

GRADE of recommendations, assess-ment, development, and evaluations

HCC Hepatocellular carcinoma

HPV Human papilloma virus

IFSO International Federation for the Surgery of Obesity and Metabolic Disorders

LSM Liver stiffness measurement

MASH Metabolic dysfunction-associated steato-hepatitis

MASLD Metabolic dysfunction-associated steatotic liver disease

MetALD Metabolic dysfunction and alcohol-re-lated steatotic liver disease

MRI Magnetic resonance imaging

MRI-PDFF Magnetic resonance imaging-proton density fat fraction

NAFLD Non-alcoholic fatty liver disease

NIT Noninvasive test

OAG Osterreichische Adipositas Gesellschaft/Austrian Society of Obesity

ODG Osterreichische Diabetes Gesellschaft/Austrian Society of Diabetology

A. Maieron

Department of Internal Medicine 2, Gastroenterology&Hepatology, University Hospital St, Dunant-Platz 1,3100 St.Polten, Austria

M. Peck-Radosavljevic

Innere Medizin und Gastroenterologie (IMuG), Klinikum

Klagenfurt, Klagenfurt am Wörseeer, Austria

T.-M. Scherzer

Department of Medicine I-Gastroenterology and Hepatology, University Hospital Wiener Neustadt, Wiener Neustadt,Austria

H. Sourij

Division of Endocrinology and Diabetology, Department of Internal Medicine, Medical University of Graz, Graz, Austria

M. Wagner

Division of Gastroenterology and Hepatology, Department of Internal Medicine, Medical University of Graz, Graz, Austria

Research Unit for Translational Nuclear Receptor Research,Division of Gastroenterology and Hepatology, Medical University of Graz, Graz, Austria

ÖGGH Osterreichische Gesellschaft fur Gas-troenterologie und Hepatologie/Austrian Society of Gastroenterology and Hepa-tology

PEth Phosphatidyl ethanol

SGLT2 Sodium/gluose cotransporter 2

SLD Steatotic liver disease

SWE Shear-wave elastography

VCTE Vibration-controlled transient elastogra-phy

Introduction

This joint consensus document of the Austrian So-cieties of Gastroenterology and Hepatology(OGGH),Diabetology(ODG), and Obesity(OAG) is intended to provide practical guidance for the management of persons with metabolic dysfunction-associated steatotic liver disease(MASLD), including persons with combined metabolic dysfunction and alcohol-related steatotic liver disease(MetALD). The man-agement of persons with alcohol-related liver disease(ALD) is not within the scope of this document and should be based on respective international guide-lines[1]. MASLD has previously been known as non-alcoholic fatty liver disease(NAFLD) and should be the term being used, while the term MetALD has been newly introduced[2]. Relevant aspects in the management of patients with compensated advanced chronic liver disease(CACLD) related to MASLD/MetALD are briefly outlined but further details should be derived from the respective Austrian (Billroth IV consensus and future versions) and international consensus statements (Baveno VII and future ver-sions) [3, 4]. As such, the management of persons with decompensated cirrhosis is not covered, un-BioTechMed,Graz, Austria

M. Wagner

BioTechMed,Graz,Austria

H. Hofer

Department of Internal Medicine I, Gastroenterology and Hepatology, Rheumatology, Endocrinology and Diabetology,Klinikum Wels-Grieskirchen, Wells, Austria

Clinical Research Institute for Inflammation Medicine,Johannes Kepler University, Linz, Austria

F.W.Kiefer

Division of Endocrinology& Metabolism, Department of Medicine III, Medical University of Vienna, Vienna, Austria

M. Roden

Department of Endocrinology and Diabetology, Medical Faculty and University Hospital, Heinrich Heine University,Düsseldorf, Germany

Leibniz Institute for Diabetes Research at Heinrich Heine University, Institute for Clinical Diabetology, German Diabetes Center, Düsseldorf, Germany

German Center for Diabetes Research(DZD e.V.),Munchen-Neuherberg, Germany

consensus report

less specifically stated. The certainty in the evidence and strength of recommendations was determined in analogy to the grading of recommendations, as-sessment, development, and evaluations(GRADE)framework(https://dev-bestpractice.bmjgroup.com/info/us/toolkit/learn-ebm/what-is-grade/)[5], if ap-plicable:

● Very low(D): the true effect is probably markedly different from the estimated effect./ Any estimate of effect is very uncertain.

● Low(C): the true effect might be markedly differ-ent from the estimated effect./ Further research is very likely to have an important impact on our confidence in the estimate of effect and is likely to change the estimate.

● Moderate(B): the authors believe that the true ef-fect is probably close to the estimated effect. / Fur-ther research is likely to have an important impact on our on our confidence in the estimate of effect and may change the estimate.

● High(A): the authors have a lot of confidence that the true effect is similar to the estimated effect./Further research is very unlikely to change our con-fidence in the estimate of effect.

Strength of recommendation:

● Weak(2):indicates that engaging in a shared deci-sion-making process is essential.

● Strong(1): suggests that it is not usually necessary to present both options.

Definitions

● MASLD/MetALD are defined by the presence of steatosis on imaging(i.e., conventional B-mode ultrasound or quantitative techniques, computed tomography, or magnetic resonance imaging[MRI])or histology and at least one cardiometabolic risk factor(Fig.1;[2,6-8]).

●Metabolic dysfunction-associated steatohepatitis(MASH) is defined by hepatic steatosis and histo-logical liver parenchymal injury, characterized by hepatocellular ballooning and lobular inflamma-tion[7,9].

●Histologically, hepatic fibrosis is staged as follows:no fibrosis(F0), mild fibrosis(F1), moderate/signifi-cant fibrosis(F2), advanced fibrosis(F3), and cir-rhosis(F4). As non-invasive tests(NIT) are limited in their discriminative ability for individual stages,fibrosis should be classified by NIT as follows: sig-nificant fibrosis(≥F2, i.e., presence of F2, F3, or F4),advanced fibrosis/cirrhosis(≥F3, i.e., presence of F3 or F4), or cirrhosis(F4)[10,11].

●Individuals with steatotic liver disease(SLD; i.e.,umbrella term for persons with steatosis) con-suming<20/30g alcohol per day(females/males)should be classified as MASLD, and those with cur-rent or historic alcohol consumption of 20-50/30-60g per day(females/males) as MetALD. Individuals with hepatic steatosis and either current or historic alcohol consumption>50/60g per day(females/males), or current diagnosis or history of alcohol use disorder should be classified as ALD[2, 6, 12,13].

 Fig.1 Diagnosis and work-up of steatic liver disease(SLD) and its sub-enities. ALD alcohol-related liver dis-ease, AUD alcohol use disorder, BIA biopedance analy-sis, BMI body mass index, CMRF cardiometabolic risk fac-tors,DXA dual-energy X-ray absorptiometry,ETG ethyl glu-

curonide,MASLD metabolic dysfunction-associated steatotic liver disease, MetALD metabolic dysfunction and alcohol-related steatotic liver disease, PEth phosphatidylethanol,SLD steatotic liver disease

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● Depending on the clinical context, SLD due to causes other than MASLD/MetALD or ALD(e.g.,drug-induced liver injury, genetic metabolic disor-ders such as lysosomal acid lipase deficiency or hy-pobetalipoproteinemia, HIV-associated and other forms of lipodystrophy, endocrine diseases, and celiac disease) should be considered[6].(CI).

● Steatosis may have resolved at the time of diagno-sis of the most severe cases of SLD(i.e., cirrhosis).Thus, individuals may still be classified as MASLD/MetALD/ALD in the absence of steatosis in cases of high clinical suspicion [14]. (C2).

● Notably, the presence of fibrosis in persons with obesity and MASLD indicates clinical obesity, i.e.,illness [15].

Prevalence

● The prevalence of MASLD in the general popula-tion of Austria is estimated to lie between 35-55%,depending on the diagnostic modality for hepatic steatosis[16-19], 3-7% are estimated to have signi-icant fibrosis(liver stiffness measurement, LSM by vibration-controlled transient elastography, VCTE≥8kPa) and~1% advanced fibrosis,(LSM≥12kPa)[16,19-22].

● About 3-5% of the global population are estimated to have MASH, but data from Austria are lacking[19].

● The prevalence of MASLD in individuals with type 2 diabetes mellitus(70-75\%) and overweight/obesity(70-80\%) is estimated to be higher, with consecutive higher rates of advanced fibrosis(~5-7\%)[16,17,23,24].

Risk factors for disease progression

● Fibrosis stage determines the risk of liver-related events and thus subsequent management. More-over, it is linked to cardiovascular events and other complications including malignancies[25-27].(Al).

● Although the presence of MASH(i.e.,steatohepatitis as evidenced by steatosis, ballooning degeneration of hepatocytes, and inflammation on histology)drives fibrosis progression, it cannot be reliably non-invasively assessed by monitoring transami-nases, and specifically developed tests require fur-ther validation [6, 7, 28]. As the additional value for risk stratification on top of fibrosis stage is unclear[25, 29, 30], management decisions are currently guided by fibrosis stage [6, 7, 28]. (Bl).

● Both metabolic dysfunction(especially type 2 dia-betes mellitus and obesity) and alcohol have inde-pendent but also synergistic amplifying effects on disease phenotype and progression [31-33].(B1).

●The following groups are at considerable risk for ad-vanced fibrosis: type 2 diabetes mellitus,(abdom-inal) obesity, males> 50 years and postmenopausal women[6,7,16].(B1).

Alcohol consumption and assessment

● The current amount and drinking pattern as well as history of alcohol intake should be evaluated and documented in all individuals with suspected or di-agnosed liver disease[6, 12, 13]. The daily amount of alcohol should be derived from the individual's typ-ical weekly consumption.(BI).

● Alcohol use disorder (AUD) should be evaluated by validated instruments (e.g., by AUDIT or AUDIT-C,with a threshold for hazardous consumption of $\geq 8$ points for AUDIT, $\geq 3$ points for AUDIT-C in females, and≥4 points for AUDIT-C in males)[6,12,13]. (Cl).

● Alcohol intake may be evaluated by specific biomark-ers(e.g., phosphatidylethanol(PEth) or ethyl glu-curonide(EtG))[6,12,13].(C2).

● Complete alcohol abstinence may be encouraged in all persons with SLD, considering the harmful effects of alcohol consumption on overall health [6,34]. (A2).

● Complete alcohol abstinence should be recom-mended in persons with liver fibrosis[6, 7].(BI).

Case finding

● Screening for SLD in the general population is not recommended [6,7].(C1)

● Case finding for liver fibrosis in SLD should be per-formed in the following at-risk groups[6,7]:

- Type 2 diabetes mellitus.

- Obesity(abdominal/visceral) plus≥1 additional cardiometabolic risk factors. Obesity is defined by BMI≥30kg/m2 and/or waist circumference≥102cm for men and≥88cm for women and/or other measures of visceral obesity[15].

- Persistently elevated liver enzymes (i.e., aspartate aminortransferase, AST, alanine aminotransferase,ALT).

- Hazardous/harmful alcohol consumption(alco-hol consumption>20/30g per day for females/males or AUDIT-C≥3/4 points or AUDIT≥8 points).(Cl).

Fibrosis assessment and risk stratification

● Early fibrosis detection and management of comor-bidities may help to prevent its progression to cir-rhosis and related complications [6].(C2).

● NIT such as blood-based scores(e.g., fibrosis-4,FIB-4 score calculated as follows: age(years)AST(U/L))/(platelet count(109/L) $\times$ ∞LT(U/L))[35] or elastography should be used to estimate the proba-bility of fibrosis and liver-related events in MASLD/MetALD, considering the clinical scenario(i.e., ex-pected prevalence of fibrosis) and potential con-founding factors[6,7].(B1).

● As NIT are more informative than AST, ALT, or gamma-glutamyl transferase alone, the latter should

consensus report

 Fig.2 Interpretation of VCTE, SWE, and ELF and result-ing monitoring recommendations. Numbers in grey indicate cut-offs supported by less evidence. cACLD compensated advanced chronic liver disease, ELF Enhanced Liver Fibro-

not be used for guiding management of people with MASLD/MetALD [6]. (B1).

● The following NIT thresholds rule out advanced fibrosis: FIB-4<1.3(<2 for age>65 years), LSM<8kPa by VCTE or shear-wave elastography(SWE), or enhanced liver fibrosis(ELF) test<7.7[6, 7](Fig.2 and 3).(Bl).

● LSM values≥8kPa by VCTE or SWE are suggestive of significant fibrosis while≥10kPa are suggestive of cACLD and indicate an increased risk of liver-re-lated events. Values≥12-15kPa rule in advanced liver fibrosis, along with ELF>9.8[6,7,36] (Fig. 2 and 3). (BI).

● In cases of elevated LSM and recent excessive al-cohol consumption (e.g.,>50/60 per day or AUD)in combination with AST>70 U/L or elevated biliru-bin, elastography should be performed after 2-4 weeks of alcohol abstinence [8, 37]. The use of LSM can still reliably rule out advanced fibrosis in this situation [8,37]. (C2).

● A sequential approach is recommended for identify-ing persons with liver fibrosis related to SLD(Fig. 3),applying a simple, nonproprietary blood-based NIT as first-line test (currently suggested: FIB-4) and, in case fibrosis cannot be ruled out, either elastogra-phy or ELF test [6,7]. (C1).

● If elastography is easily accessible(e.g., in sec-ondary or tertiary care), it may be applied as a first-line test.(D2).

● None of the available NIT to assess MASH can cur-rently be recommended to guide clinical decision making $[7,8,28,38,39]$ . (Bl).

sis test, HCC hepatocellular carcinoma, LSM liver stiffness measurement, SWE shear-wave elastography, VCTE vibra-tion-controlled transient elastography

Risk stratification regarding CSPH

● LSM<15kPa and platelet count≥150G/L rule out clinically significant portal hypertension(CSPH) in adults with MASLD/MetALD[3,4,40,41].(BI).

● LSM≥25kPa rules in CSPH in non-obese individu-als with MASLD/MetALD[3,4,40,41].(Cl).

● In obese persons, the ANTICIPATE±NASH(LSM by VCTE, platelet count,±BMI) or the NICER model(LSM and spleen stiffness measurement by VCTE,platelet count, BMI) may be applied to estimate the probability of CSPH[3,4,41,42].(DI).

Steatosis assessment

● Given its broad availability, conventional B-mode ultrasound is currently recommended as the pri-mary diagnostic modality for establishing the diag-nosis of SLD, although it has limited sensitivity for mild steatosis[6,8].(A1).

● MRI-based steatosis assessment by magnetic reso-nance spectroscopy or proton density fat fraction(MRI-PDFF) is currently considered the gold stan-dard of steatosis assessment, but is limited by its cost and availability, and is therefore not recom-mended for broad clinical use [6,10].

● Although SLD is defined by hepatic steatosis, its presence does not impact management of liver dis-ease. Thus, steatosis assessment is currently only recommended when the goal is to establish a diag-nosis of SLD and when this changes clinical man-agement. (C2).

consensus report

 Fig.3 Algorithm for risk assessment in individuals with MASLD/MetALD, applicable for case finding of fibrosis asso-ciated with SLD.1 Age-adjusted cut-off<2 to rule out ad-vanced fibrosis if age>65 years.2 If a false positive result is suspected, repeat after 2-4 weeks. ALD alcohol-related liver disease, ALT alanine aminotransferase, AST aspartate aminotransferase, cACLD compensated advanced chronic liver disease, CMRF cardiometabolic risk factors, ELF En-

hanced Liver Fibrosis test, HCC hepatocellular carcinoma,LSM liver stiffness measurement, MASH metabolic dysfunc-tion-associated steatohepatitis, MASLD metabolic dysfunc-tion-associated steatotic liver disease, MetALD steatotic liver disease with metabolic-dysfunction and alcohol-related com-ponents, SLD steatotic liver disease, SWE shear-wave elas-tography,VCTE vibration-controlled transient elastography

consensus report

Liver biopsy

● Liver biopsy should be reserved for the exclusion of other liver diseases[6]. (AI).

● Although required for the diagnosis of MASH, liver biopsy is not routinely indicated in this respect un-less it changes clinical management[6].(AI).

● Liver biopsy is not indicated for fibrosis assessment[6].(AI).

General management

● Comorbidities associated with MASLD/MetALD should be assessed/documented in all individu-als and re-evaluated during follow-up to capture cardiometabolic risk [6] (BI):

- Overweight/obesity.

- Prediabetes and type 2 diabetes mellitus.

- Arterial hypertension.

- Dyslipidemia.

- Obstructive sleep apnea syndrome.

- Cardiovascular disease.

- Chronic kidney disease.

- In females: polycystic ovary syndrome.

● Individuals with MASLD/MetALD should be in-formed about the increased risk of extrahepatic malignancies and counselled about extrahepatic cancer screening recommendations [6]. (BI).

Specifically, the following investigations are recom-mended:

- Colonocoscopy every 7-10 years starting at the age of 45 years or fecal immunochemical test (FIT)-based colorectal cancer screening every 2 years.

- Biannual self-examination for skin lesions/cancer.

- Immunization for human papilloma virus (HPV).

- In females:

- Yearly PAP smear and HPV testing every 3 years.

- Mammography every second year starting at the age of 40 years.

- In males:

- Prostate cancer screening starting from the age of 45 years.

● In persons with type 2 diabetes, linkage to special-ists in diabetes care and disease management pro-grams is encouraged.(BI).

● Hepatology consultation is indicated in persons with NIT suggestive of significant fibrosis [6, 7, 38].(CI).

Nonpharmacological therapy

● Lifestyle modification is the foundation of MASLD/MetALD management [6]. (Al).

● A multidisciplinary approach is recommended to treat cardiometabolic comorbidities in MASLD/MetALD [6,7]. (B1).

● Weight loss by lifestyle intervention (i.e., dietary, ex-ercise, and behavioral therapy) is recommended in MASLD/MetALD [6,7]. (AI).

● In adults with MASLD and overweight/obesity,weight management should aim at a sustained re-duction of≥5% to improve hepatic steatosis,7-10%to improve hepatic inflammation, and≥10% to im-prove liver fibrosis. Improvement of fibrosis is the key treatment goal, i.e., weight loss≥10% should be intended [6, 43]. (BI). The same may apply to MetALD. (C2).

● Diet and exercise interventions may be also rec-ommended in normal weight adults with MASLD to reduce liver fat, although there is currently no evidence regarding their impact on inflammation,fibrosis, or adverse liver-related outcomes [6, 44].(C2).

● For adults with MASLD, improving diet quality (i.e.,Mediterranean) as well as limiting the consumption of fructose (e.g., sugar-sweetened beverages) and ultraprocessed food is recommended [6, 45-48].(B1). The same may apply to persons with MetALD,who may also be advised to abstain from alcohol.(D2).

● Physical activity and exercise (both aerobic and re-sistance; >150min/week of moderate or >75min/week of vigorous intensity) should be recommended and tailored to the individual's preference and abil-ity. This usually corresponds to 3-5 sessions of 30-60min [6, 49-53]. (AI). The same may apply to persons with MetALD.(C2).

● In adults with MASLD/MetALD,nutraceuticals can-not be recommended as there is insufficient ev-idence regarding their health benefits, including their effectiveness in ameliorating hepatic inflam-mation/fibrosis or preventing adverse liver-related outcomes [6]. (C1).

● Observational studies have linked coffee consump-tion to improved liver health in MASLD[6,7,54-57].(CI).

General management in cACLD/cirrhosis

● Dietary and lifestyle recommendations should be adapted to the severity of liver disease, nutritional status, and the presence of sarcopenia/sarcopenic obesity in persons with cACLD/cirrhosis[6, 58, 59].(BI).

● A high-protein diet (>1.2-1.5g/kg bodyweight/day)as well as a late evening snack are recommended for persons with a CACLD/cirrhosis and sarcopenia/sarcopenic obesity[6, 58, 59].(Bl).

● In persons with cACLD/compensated cirrhosis and obesity, moderate weight reduction can be sug-gested, with an emphasis on high protein intake and physical activity to maintain muscle mass and reduce the risk of sarcopenia[6].(C2).

● Further management should be based on the Bill-roth IV consensus or subsequent versions [3].

consensus report

Pharmacological treatment

● Individuals with MASLD/MetALD and evidence of significant liver fibrosis(i.e.,≥8kPa) should be con-sidered for MASH-targeted therapies(in particu-lar, resmetromel[60] and semagulotide[61], once approved).(DI). Individuals with cACLD(LSM≥10kPa) have the highest/most/murgent need for medic-inal treatment due to their increased risk for adverse liver-related events[3,4,62,63].(CI).

● Resmetromen cannot be recommended for adults with a high probability of cirrhosis (i.e., $\geq 20 kPa$ )until phase 3 data establishing its safety and effi-cacy in this population are available (i.e., MASTRO-NASH OUTCOMES; NCT05500222](6, 64).(D2).

● Incretin-based therapies, currently indicated for type 2 diabetes as well as weight management in people with obesity or BMI≥27 kg/m2 and comor-bidities, should be used in people with MASLD/MetALD and evidence of significant liver fibrosis(i.e.,≥8kPa), as they improve cardiometabolic out-comes and MASH[6,38].(B1). Specifically, the large phase 3 study on high-dose(2.4mg) semaglutide demonstrated improvement of MASH and fibrosis[61]. Also, a smaller phase 2 study on tirzepatide indicated its efficacy in improving MASH and also found a reduction in fibrosis[65]. Similar findings have been obtained with survodutide[66], which has not been approved for type 2 diabetes, obesity,or MASH at the time of this consensus.

● In persons with MASLD/MetALD and evidence of significant liver fibrosis(i.e.,≥8kPa), incretin-based therapies should be prescribed by specialists in in-ternal medicine, endocrinology and/or diabetology,or gastroenterology and/or hepatology.(DI).

● From the hepatological perspective, pioglatizone is safe to use in persons without cirrhosis, however, it is not approved for and cannot be recommended as MASH-targeted therapy [6,67].(B2).

● Metformin is safe to use in MASLD/MetALD and should be used for its respective indication, namely type 2 diabetes, but cannot be recommended as MASH-targeted therapy[6].(CI).

● Sodium-glucose co-transporter 2(SGLT2) inhibitors are safe to use in MASLD/MetALD and should be used for their respective indications, namely type 2 diabetes, heart failure, and chronic kidney disease,but cannot be recommended as a MASH-targeted therapy at this point [6], although an investigator-initiated trial suggests efficacy in improving MASH and also found a reduction in fibrosis[68].(C1).

● Insulin therapy should be used for its respective in-dication, type 1 and type 2 diabetes, but cannot be recommended as MASH-targeted therapy [69].(C1).

● Despite limited evidence, individuals with MASLD/MetALD and a history of liver transplantation may be managed similarly.(D2).

Pharmacological treatment in cACLD/cirrhosis

● While metformin can be used in adults with cACLD and preserved renal function(GFR>30ml/min), it should not be used in adults with decompensated cirrhosis[6].(CI).

Given the risk of hypoglycemia, sulfonylureas should be avoided in decompensated cirrhosis[6].(DI).

● Incretin-based therapies can be used in adults with Child-Pugh class A cirrhosis [6,70-72].(B1).

Hepatic impairment studies on semaglutide[70],tirzepatide[73], and survodutide[71] indicate that no pharmacokinetic-related dose adjustment is needed in mild to severe hepatic impairment(i.e.,Child-Pugh classes A-C), although the potential risk of sarcopenia requires particular attention.(D1).

● Limited clinical experience indicates that incretin-based therapies may be used for weight manage-ment on the waiting list for liver transplantation[74], although the risk of sarcopenia requires partic-ular caution.(D2).

● SGLT2 inhibitors are safe to use in people with Child-Pugh class A and B cirrhosis[6].(D2).

● Statins should be used in cACLD/cirrhosis accord-ing to guidelines for reducing cardiovascular events[3, 4, 6].(B1). In persons with Child-Pugh B/C,statins may be used at a lower dose due to an oth-erwise increased risk of rhabdomyolysis(e.g., 3%with simvastatin 40mg(75]) and persons should be followed closely for muscle and liver toxicity.(CI)Simvastatin at max. 20mg daily[75, 76] or atorvas-tatin 10mg daily[77] have been shown to be safe in randomized controlled clinical trials including Child-Pugh B/C patients, while for rosvastatin,only pharmacokinetic data are available, suggesting that a dose of 5 mg daily may be preferred[78].

● If CSPH is present, carvedilol should be used unless contraindicated [3, 4].(C1).

Metabolic/bariatric surgery

● In persons with MASLD without cirrhosis who have an indication for metabolic/bariatric surgery, tech-niques supported by the International Federation for the Surgery of Obesity and Metabolic Disorders(IFSO) may be considered, as metabolic/bariatric surgery has long-term benefits on liver health and may induce remission of type 2 diabetes and im-provement of cardiometabolic risk factors [79]. (C2).

● In people with MASLD-related compensated ad-vanced chronic liver disease/cirrhosis but without clinically significant portal hypertension,metabolic/bariatric surgery can be considered, but careful evaluation by a multidisciplinary team with expe-rience in bariatric/metabolic surgery in this partic-ular population is mandatory. Preoperative evalu-ation should follow the respective European Asso-ciation for the Study of the Liver Clinical Practice Guidelines[80,81].(D2).

consensus report

● Metabolic/bariatric endoscopic procedures require further evidence before being applied as a MASH-targeted therapy [6].(D2).

Natural history and general management

● As fibrosis determines outcomes in SLD, it should be considered the central parameter for liver disease monitoring and clinical decision-making [6, 7, 25,29,30]. (Al).

● Regression of fibrosis in persons with advanced fi-brosis/cirrhosis is associated with a reduced risk of liver-related outcomes[62,82-84].(Bl).

● Improvement in disease activity and resolution of steatohepatitis have been linked to fibrosis regres-sion [85,86]. (Bl).

Monitoring of comorbidities

● Comorbidities associated with MASLD/MetALD and cardiovascular risk should be assessed/docu-mented in all individuals at diagnosis and re-evalu-ated during follow-up at regular intervals according to respective guidelines [6,7]. (AI).

● During follow-up, special attention should be paid to diabetes mellitus and obesity due to their partic-ularly strong associations with liver fibrosis progres-sion [6,7].(B1)

● Extrahepatic cancer screening is recommended ac-cording to the respective guidelines [6,7]. (BI)

● Alcohol consumption is an independent risk factor for the progression of SLD and should be assessed and documented in all individuals with suspected liver disease [6, 7]. (Al) While data on the impact,interval and modality of re-evaluation of alcohol consumption are lacking, we recommend re-as-sessment at regular intervals and according to the overall clinical context (e.g., when dynamics in NIT/laboratory parameters are observed), given the dy-namic nature of alcohol consumption and associ-ated harms [7].(D1).

Monitoring of fibrosis

● It is encouraged to repeat NIT to estimate disease progression or regression [62, 63, 83, 84].(C2).Currently, there is insufficient evidence to define thresholds for a clinically significant change or re-sponse to treatment. (D2).

● Monitoring of fibrosis should preferably be done with the same NIT used for initial evaluation to assess changes over time.(D1).

● A gradual and consistent increase in NIT assessing fibrosis over time likely indicates worsening of fibro-sis and increased risk of complications, while a de-crease likely indicates improvement of fibros and a decreased risk of complications [62,63,83,84].(C2).

● In individuals with LSM values suggestive of cACLD(≥10kPa),a regression to LSM<10kPa is associated

with improved outcomes [62,63,83,84]. (C2). There is currently limited evidence regarding the prognos-tic utility of dynamics in other NIT. (D2).

● NIT dynamics should be interpreted in the overall clinical context.(D1).

● Liver biopsy is not indicated for the purpose of fi-brosis monitoring[6].(B1).

Monitoring intervals

● In persons with FIB-4<1.3 or in whom advanced fi-brosis was ruled out (e.g., LSM<8kPa, ELF<7.7), it is encouraged to repeat FIB-4 every 2 years to re-assess fibrosis probability [6, 7]. Other NIT may be repeated based on the overall clinical context/risk factors. (D2).

● In persons with cACLD (LSM≥10kPa), NIT should be repeated every 12 months [3, 4]. (CI).

● In people with LSM-8-10kPa, there is currently in-sufficient evidence to recommend specific inter-vals for monitoring of liver disease but may be per-formed every 12 months based on the presence of risk factors.(D2).

● When monitoring a liver-directed treatment, it is recommended to repeat ALT/AST every 6 months and NIT for fibrosis every 12 months.(D2).

Monitoring steatosis

● Regular monitoring of hepatic steatosis using ul-trasound-based modalities is currently not recom-mended, as dynamics cannot be reliably assessed [7,10] and as changes in the degree of hepatic steatosis do not impact clinical management.(Cl).

● MRI-PDFF can be used to assess changes in hepatic steatosis, but it is not recommended for broad clin-ical use [6, 10] (C1).

HCC surveillance

●HCC surveillance should be done according to re-spective guidelines and is not different to other chronic liver disease entities [6, 87]. (BI).

●HCC surveillance by ultrasound and alpha-fetopro-tein is indicated in persons with SLD-related cirrho-sis [6,87]. (BI). LSM ≥ 15kPa may be used as non-invasive cut-off to guide surveillance [88-90] (Fig.3).(C2).

● HCC surveillance in other people than those with cirrhosis is currently not recommended due to cost effectiveness considerations [6,87]. (C2).

Acknowledgements Panel 1:Definition,prevalence,and nat-ural history: Alexander Bräuer, Herbert Tilg, Elmar Aigner;coordination: Georg Semmler. Panel 2: Case finding, diag-nosis, and risk stratification: Johanna Brix, Christian Datz,Andreas Maieron, Harald Sourrij; coordination: Georg Semm-ler. Panel 3: Management: Florian Kiefer, Martin Clodi, Maria Effenberger, Daniel Moritz Felsenreich, Thomas-Matthias Scherzer; coordination: Mattias Mandorfer. Panel 4: Phar-

consensus report

macological therapy: Peter Fasching, Harald Hofer, Bernhard Ludvik, Lars Stechmesser, Michael Trauner; coordination:Mattias Mandorfer. Panel 5: Monitoring: Markus Peck-Ra-dosarlvjevic, Claudia Ress, Martin Wagner; coordination:Georg Semmler.

Author Contribution All authors contributed to the con-ception of the consensus. Recommendations were drafted by the respective panellists(see acknowledgements section) and critically reviewed by all panellists as well as discussed in consensus meetings. All authors approved the final version to be published.

Funding Open access funding provided by Medical University of Vienna.

Conflict of Interest M. Mandorfer received grant support from Echosens, served as a speaker and/or consultant and/or advisory board member for AbbVie, AstraZeneca, Echosens,Ell Lilly, Gilead, Isen, Takeda, and W. L. Gore &Asso-ciates, and received travel support from AbbVie and Gilead.G. Semmler received travel support from Amgen. E. Aigner served as speaker and/or advisory board member for Sanofi-Aventis, Gilead, Eli Lilly, Boehringer Ingelheim, Bayer, Falk Pharma, Amicus, Takeda, and Roche. A. Brauer served as speaker and/or consultant and/or advisory board member for Eli Lilly and Novo Nordisk and received travel support from Boehringer Ingelheim, Eli Lilly, and Novo Nordisk.J. Maria Brix served as speaker and/or consultant and/or advisory board member for AstraZeneca, Decom,Boehringer Ingelheim, Eli Lilly, Medtronic, and Novo Nordisk. M. Efrenberger served as a speaker and/or consultant and/or advisory board member for Ipsen and received travel support from Ipsen. A. Maeronist served as speaker and/or consultant and/or advisory board member for Joehringer Ingelheim, Eli Lilly, MSD, and Madrigal. B. Ludvik received grant support from Boehringer Ingelheim, Novo Nordisk, Madrigal, Eli Lilly, and Amgen and served as a speaker/advisor for As-trazeneca, Amgen, Boehringer Ingelheim, Eli Lilly, and Novo Nordisk. M. Peck-Radosavjelvic served as speaker and/or advisory board member for AstraZeneca, BMS, Boehringer Ingelheim, Eli Lilly, isal, Falk, Gilead, Isen, Intercept-Advanz, Merz, MSD, Roche, Sanofi, Shionogi, and Sobi.L. Stechemseers served as speaker and/or consultant and/or advisory board member for Boehringer Ingelheim, Eli Lilly, and Novo Nordisk. M. Trauner received grant support from Albireo, Alnylam, Cambymab, Falk Pharma, Genentech, Gilead,Intercept,MSD, Takeda and UltraGenya; horizona for con-sulting from AbbVie, Albireo, Agomab, Alfasigma, Boehringer Ingelheim, Biomx, Chemomab, Dolvigo Therapeutics, Falk Pharma, Genfit, Gilead, GSK, Hightide, Intercept, Ipsen, Janssen, Mircum, Novartis, Phen, Plrecta, Regity-Edus, ProQR Therapeutics, Siemens, and Shire; speaker fees from Albibre, Boehringer Ingelheim, BMS, Falk Foundation,Gilead, Ipsen, Intercept-Intercept, Mirum, MSD, and Madrigal as well as travel support from AbbVie, Falk Foundation, Gilead, Jannsen,Intercept, and Ipsen. He is also co-inventor of patents on the medical use of 24-nurorosodeoxychic acid(service inventions as employee) filed by the Medical Uni-versity of Graz. H. Hofer served as a speaker and/or advisory board member for AbbVie, Falk Pharma, Gilead, Ipsen, Eli Lilly,Boehringer Ingelheim, and Madrigal. FW. Kiefer served as speaker and/or consultant and/or advisory board member for Abbvie, Falk Pharma, Gilead, Ipsen, Eli Lilly,Boehringer Ingelheim, and Madrigal. FW. Kiefer served as speaker and/or consultant and/or advisory board member for AstraZeneca, Boehringer Ingelheim, Eli Lilly, Novartis.

Novo Nordisk, and Sanofi Aventis. P. Fasching served as speaker and/or consultant and/or advisory board member for Boehringer Ingelheim, Ell Lilly, and Novo Nordisk and received travel support from Boehringer Ingelheim and Novo Nordisk. M. Roden received grant support for investigator-initiated research from Boehringer Ingelheim, Novo Nordisk,and Sanofi-Aventis to the German Diabetes Center (DDZ)and served as a speaker and/or consultant and/or advi-sory board member for AstraZeneca, Echosens, Eli Lilly,Madrigal, MSD, Novo Nordisk, Pfizer, Synlab, and Target RWE. M. Clodi, C. Datz, D. Moritz Felsenreich, C. Ress, T.-M. Scherzer, H. Sourij, M. Wagner, and H. Tilg have nothing to disclose.

Ethical standards For this article no studies with human participants or animals were performed by any of the authors.All studies mentioned were in accordance with the ethical standards indicated in each case.

Open Access This article is licensed under a Creative Com-mons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permis-sion directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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