Metabolic dysfunction-associated steatotic liver disease

• Metabolic dysfunction-associated steatotic liver disease (MASLD) is the 2023 name for the condition formerly called non-alcoholic fatty liver disease (NAFLD): fat in the liver together with at least one of five cardiometabolic risk factors, in the absence of harmful alcohol intake.
• It affects more than 30% of adults worldwide and is the commonest chronic liver disease. Most people have no symptoms.
• Most patients do not die of liver failure: cardiovascular disease is the leading cause of death, although steatohepatitis and fibrosis can progress to cirrhosis, liver failure and hepatocellular carcinoma.
• The extent of liver fibrosis, not the amount of fat, determines outcome. Fibrosis is assessed non-invasively in steps: FIB-4 first, then vibration-controlled elastography or the enhanced liver fibrosis (ELF) blood test, with biopsy reserved for uncertainty.
• The cornerstones of treatment are losing 5-10% or more of body weight, Mediterranean-style eating, regular exercise, no alcohol, and vigorous treatment of cardiovascular risk. Resmetirom and, since 2025, semaglutide are approved for selected patients, and guidelines still differ in how to use them.

By the end of this page you should be able to:

1. Define MASLD and place it within the 2023 steatotic liver disease (SLD) nomenclature, including MASH, MetALD and alcohol-associated disease.
2. List the five adult cardiometabolic criteria and explain how alcohol intake determines whether SLD is MASLD, MetALD or ALD.
3. Explain the pathophysiology from insulin resistance and lipotoxicity through inflammation to fibrosis.
4. Use FIB-4, elastography and ELF in the correct order to estimate fibrosis stage, and know when to biopsy.
5. Give evidence-based weight loss targets, dietary and exercise advice, and describe the approved drug options and their limits.
6. Explain screening for hepatocellular carcinoma and varices in MASLD-related cirrhosis.
7. Adjust care in children and in low-resource settings.

MASLD is the presence of excess fat (triglyceride) in the liver in someone who has at least one cardiometabolic risk factor and drinks no more than a mild amount of alcohol, with no other clear cause for the steatosis.^[1][3] Under the microscope the earliest stage is simple steatosis; metabolic dysfunction-associated steatohepatitis (MASH, formerly NASH) is steatosis plus hepatocyte ballooning and lobular inflammation, which drives fibrosis. Fibrosis is staged F0 (none) through F4 (cirrhosis), and it is fibrosis stage, not the amount of fat, that determines prognosis.^[2]

In June 2023 a multi-society Delphi consensus renamed and redefined the field. Steatotic liver disease (SLD) is now the umbrella term for every cause of excess liver fat. Within it sit:^[1][4]

• MASLD - steatosis plus at least one cardiometabolic risk factor and little or no alcohol.
• MetALD - steatosis plus cardiometabolic risk factors and moderate alcohol intake (140-350 g/week for females, 210-420 g/week for males).
• Alcohol-associated (alcohol-related) liver disease (ALD) - steatosis driven by heavy alcohol use, defined as more than 50 g/day in females or more than 60 g/day in males in the mixed picture; purely alcohol-driven disease uses the same thresholds with little metabolic disease.
• Specific aetiologies - drug-induced, monogenic or other causes such as lysosomal acid lipase deficiency, hypobetalipoproteinaemia or Wilson disease.
• Cryptogenic SLD - steatosis with no identifiable cause, which may be reclassified as understanding improves.^[1]

Multiple aetiologies can coexist in one patient, so the alcohol history must be taken seriously even when the metabolic profile looks classic.^[1][4]

The old term NAFLD largely maps onto MASLD: studies show 99.8% concordance between the populations in clinical cohorts and virtually identical non-invasive test performance, so the existing evidence base applies to MASLD.^[3]

• Steatosis (fatty liver): excess triglyceride in hepatocytes, usually from insulin resistance and excess energy.
• Steatohepatitis (MASH/NASH): steatosis plus hepatocyte ballooning and lobular inflammation.
• Fibrosis / cirrhosis: the scar that determines prognosis.
• At-risk steatohepatitis: MASH with at least stage 2 (F2) fibrosis - the group most likely to benefit from drug therapy.

MASLD occurs in children and adolescents as well as adults, particularly with excess adiposity and insulin resistance. The nomenclature provides age-adjusted cardiometabolic criteria for younger patients (for example BMI percentiles rather than adult cut-offs) and is intended to apply across the lifespan. Detailed diagnosis and management in children are addressed separately from adult practice. In practice lifestyle improvement is the foundation of care at every age, and decisions about bariatric surgery or drugs in minors should involve paediatric hepatology.^[1][4]

MASLD is the commonest chronic liver disease worldwide, affecting more than 30% of the global population and about 25-30% of adults in general-population studies.^[4][2] In much of the world it is still under-recognised because it is usually silent.

• Obesity. Total body fat and, more importantly, visceral (android) fat distribution are strongly linked to MASLD and disease progression; gynoid distribution appears protective. Lean people can still develop MASLD when visceral adiposity and insulin resistance are present.^[2]
• Type 2 diabetes mellitus is the strongest single risk factor. The prevalence of MASLD in people with type 2 diabetes ranges from 30% to 75%, and advanced fibrosis is found in 6-19% of screened patients with diabetes.^[2]
• Dyslipidaemia is present roughly twice as often as in people without MASLD, and the lipoprotein pattern is more atherogenic.^[2]
• Hypertension is also common and additive to other metabolic factors in predicting fibrosis progression.^[2]
• Polycystic ovary syndrome carries a 2- to 4-fold increased prevalence of MASLD and a higher rate of steatohepatitis and advanced fibrosis independent of age and BMI.^[2]
• Obstructive sleep apnoea is associated with more advanced histology through intermittent hypoxia and worse insulin resistance.^[2]
• Hypothyroidism, hypogonadism and growth hormone deficiency are associated with NAFLD in some studies through effects on body fat distribution and insulin resistance, although causal directions are uncertain.^[2]
• Lean MASLD. An estimated 4.1% of adults in the United States and up to 19% in Asia have MASLD despite a body mass index below 25 kg/m2 (23 kg/m2 in Asian people), often mediated by visceral adiposity and genetic susceptibility.^[2]
• Genetics. The PNPLA3 I148M variant impairs triglyceride lipolysis in hepatocytes and is linked to more advanced disease and hepatocellular carcinoma; variants in TM6SF2 and MBOAT7 also raise risk, while HSD17B13 and CIDEB loss-of-function variants appear protective. Genetic testing does not currently change routine management.^[2]

The population prevalence of steatohepatitis and fibrosis is rising in parallel with obesity and metabolic disease: one prospective colon-cancer screening cohort found NASH in 14% of asymptomatic adults, and estimates project marked increases in advanced fibrosis and liver-related death by 2030.^[2]

The fundamental problem is a mismatch between lipid supply and disposal. Energy oversupply, insulin resistance in adipose tissue, muscle and liver, and excessive de novo lipogenesis (driven strongly by dietary fructose and other sugars) increase free fatty acid delivery to the liver. Subcutaneous adipose tissue expansion has a finite capacity; once it is exceeded, fat overflows into visceral depots and the liver.^[2] MASLD is also associated with a 2- to 5-fold increased risk of incident type 2 diabetes, so the relationship is bidirectional.^[2]

Not all fat is equal. Lipotoxic injury arises when hepatocytes are exposed to toxic lipid species such as diacylglycerols, ceramides and free cholesterol rather than to safely stored triglyceride. Mitochondrial dysfunction, endoplasmic reticulum stress and the release of damage-associated molecules activate resident Kupffer cells and recruit inflammatory cells. This produces hepatocyte ballooning, lobular inflammation and cell death on top of the steatosis - the constellation called steatohepatitis. Insulin resistance worsens as disease progresses.^[2]

Genetic factors modify this response: the PNPLA3 I148M variant alters hepatocyte lipid droplet handling, while host and environmental modifiers such as saturated fat intake, alcohol, the gut microbiome, uric acid and periodic hypoxia from obstructive sleep apnoea all influence activity.^[2]

Sustained inflammation activates hepatic stellate cells, which deposit collagen. Fibrosis stage, not steatosis, is the dominant predictor of liver-related outcomes and death. In paired-biopsy cohorts fibrosis progresses roughly one stage every 7 years in NASH versus 14 years in simple steatosis, and even patients without fibrosis on the first biopsy have higher liver-related and non-hepatic cancer risk than the general population. Cirrhosis develops in a minority, but once it is present the risk of hepatic decompensation is 3-20% per year.^[2]

• Progression. Fibrosis and steatohepatitis are the principal predictors of disease progression. Bridging fibrosis (stage 3) and cirrhosis carry an exponentially greater risk of liver-related morbidity and mortality than earlier stages.^[2]
• Cardiovascular disease causes more deaths than any other condition among people with MASLD, followed by non-hepatic malignancy and then liver disease. A strong association exists with atherosclerotic heart disease, heart failure and atrial fibrillation. Optimising blood pressure, lipids, glucose control and smoking cessation is therefore central to care.^[2]
• Hepatocellular carcinoma (HCC) can occur with or without cirrhosis, although the risk rises dramatically with fibrosis stage. In cirrhosis, HCC surveillance is essential.
• Other complications. Chronic kidney disease is about twice as prevalent in people with MASLD. Endocrine associations (PCOS, hypothyroidism, hypogonadism, growth hormone deficiency) are common enough to ask about.^[2]
• Liver transplantation. NASH-related cirrhosis is already the leading indication for liver transplantation in women and in people over 65, and is on a par with alcohol overall. NASH cirrhosis is likely to keep rising.^[2]

MASLD is usually silent. When symptoms occur they are non-specific: fatigue, right upper quadrant discomfort or fullness, or general malaise. Signs of chronic liver disease (hepatomegaly, splenomegaly, stigmata of cirrhosis) appear only in advanced disease. Jaundice and ascites indicate decompensated cirrhosis, which is very late. Therefore the disease is most often found incidentally on imaging done for another reason, or during work-up for abnormal liver enzymes.^[2]

Examination should focus on features that point to MASLD and its complications: body fat distribution (android or gynoid, lipodystrophy), signs of insulin resistance (acanthosis nigricans, dorsal cervical fat pad), and stigmata of advanced liver disease (firm liver, splenomegaly, spider naevi, palmar erythema, gynaecomastia).^[2] "Normal ALT" should be interpreted correctly: many laboratories set the upper limit too generously, whereas in MASLD the true normal is 29-33 U/L in men and 19-25 U/L in women. A raised ALT with a normal FIB-4 should not be ignored; abnormal liver enzymes still warrant assessment for fibrosis and exclusion of other causes.^[2][3]

Hepatic steatosis is not specific to MASLD. The broad differential is the differential of SLD itself: MASLD/MetALD/ALD, drug-induced liver injury, and monogenic or secondary causes such as lysosomal acid lipase deficiency, hypobetalipoproteinaemia, Wilson disease, coeliac disease and lipodystrophy. Other chronic liver diseases (chronic hepatitis B and C, autoimmune hepatitis, haemochromatosis) may coexist or mimic MASLD, and some (notably hepatitis C) also cause steatosis. Haemochromatosis is usually distinguished by a markedly raised transferrin saturation rather than the mild rise seen in MASLD.

Common drug culprits that can cause macrovesicular steatosis or steatohepatitis include amiodarone, tamoxifen, methotrexate, corticosteroids, 5-fluorouracil and irinotecan.^[2] When the picture is atypical (young patients, lean patients, severe disease, no metabolic risk factors), consider coeliac disease, Wilson disease and lipodystrophic states, and test when clinically suspected.^[2]

In most patients MASLD is discovered incidentally. The initial work-up has three aims: confirm and characterise steatosis, quantify alcohol use, and exclude other liver diseases.^[2][3]

• Steatosis on imaging. Ultrasound is the usual starting point. It detects moderate to severe steatosis, is poor at mild steatosis and cannot grade fibrosis. It is low-cost and widely available, and is often the "incidental steatosis" that triggers the whole assessment.
• Laboratory panel. Hepatic panel including ALT and AST, full blood count with platelets, fasting glucose and HbA1c, fasting lipid profile, renal function and urine protein. Hepatitis C screening should be considered if not previously done, and AST is needed for FIB-4.^[2]
• History. Weight trajectory, medical comorbidities, current and recent medications, family history of diabetes or cirrhosis, screening for obstructive sleep apnoea, and a careful alcohol history (type, amount, pattern, duration, frequency).^[2]
• Physical examination. Body fat distribution, features of insulin resistance, and careful signs of advanced liver disease or portal hypertension.^[2]
• Second-line tests when liver enzymes are elevated, the profile is atypical, or both: autoimmune serologies, transferrin saturation, ceruloplasmin, alpha-1 antitrypsin level and phenotype, coeliac serology (tissue transglutaminase IgA, with duodenal biopsy if positive).^[2]

Alcohol must be quantified in everyone with steatosis. In the 2023 AASLD guidance alcohol intake is broadly classified as mild (up to 20 g/day in females and 30 g/day in males), moderate (21-39 g and 31-59 g respectively) and heavy (40 g or more and 60 g or more). Moderate drinking is associated with a higher chance of advanced fibrosis, especially with obesity or type 2 diabetes, so "mild" intake is not automatically harmless. Heavy drinking should be avoided entirely. In MASLD-related cirrhosis, all alcohol should be stopped.^[2][3]

The nomenclature then decides labelling: MASLD implies little or no alcohol; steatosis plus cardiometabolic factors and 140-350 g/week in females or 210-420 g/week in males is MetALD; steatosis driven by more than 50 g/day (females) or 60 g/day (males) is counted as alcohol-associated liver disease.^[1][4]

Because fibrosis stage drives prognosis and management, and liver biopsy is invasive, both AASLD (2023) and EASL (2024) recommend a stepwise approach using non-invasive tests, starting in primary care. The objective of the first step is to exclude advanced fibrosis using a test with a high negative predictive value; patients with diabetes need more frequent re-testing.^[2][3]

Liver biopsy is no longer required for routine management. It remains the reference standard for diagnosing steatohepatitis and is useful when non-invasive tests disagree, or when an alternative diagnosis is suspected. Repeat non-invasive testing over time can monitor progression at a population level, but no single test has been validated as a treatment-response surrogate in an individual.^[3]

FIB-4 performs less well in people with diabetes and in the very young and very old, which is why combined use (FIB-4 then elastography) is preferred. VCTE results are confounded by obesity, food intake and acute inflammation, and an adequate scan can be difficult in severe obesity. ELF is a blood test sent to a reference laboratory. Magnetic resonance elastography is the most accurate imaging method but is costly. The presence of cirrhosis should be confirmed or excluded with caution, as false positives and false negatives occur.^[2][3]

The diagnosis of MASLD requires steatosis plus at least one of five adult cardiometabolic risk factors. These are the thresholds used in the 2023 AASLD consensus materials:^[4]

AASLD also uses ALT thresholds of greater than 33 U/L in males and greater than 25 U/L in females as the "elevated" liver enzymes that should trigger this pathway.^[4]

MASLD is histologically graded as no steatohepatitis (MASL, or benign steatosis) or steatohepatitis (MASH), and fibrosis staged F0 to F4. For everyday practice non-invasive markers substitute fairly well for biopsy; the useful cut-offs are these:^[2][3]

A VCTE result of 20 kPa or more, or a platelet count below 150 × 10^9/L in compensated disease, is the point at which endoscopy for varices should be performed (see below).^[3]

Management is individualised and, ideally, delivered by a multidisciplinary team, because liver outcomes depend at least as much on cardiometabolic disease as on the liver itself.^[3] The backbone is non-pharmacological; drugs and procedures are added for selected patients and according to local approval.^[3]

Weight loss is the only intervention with proven histological benefit. EASL 2024 recommends: at least 5% reduction in body weight to reduce liver fat, 7-10% to improve necro-inflammation, and 10% or more to improve fibrosis.^[3] Even modest losses help, and severe obesity often needs combined dietary, psychological and eventually surgical or pharmacological support.

• Diet. Improving diet quality along Mediterranean lines - more vegetables, fruit (not juice), legumes, nuts, olive oil, whole grains, unprocessed fish and poultry, and less ultra-processed food, sugar-sweetened beverages and foods high in saturated fat - improves hepatic injury. A hypocaloric plan is preferred for overweight patients. There is no evidence that nutraceuticals improve outcomes, and they are not recommended.^[3]
• Exercise. Advise at least 150 minutes per week of moderate-intensity or 75 minutes of vigorous-intensity physical activity, tailored to preference and ability, because cardiometabolic benefits are strong and hepatic benefit is supported, although less robust.^[3]
• Coffee. Drinking coffee (caffeinated or decaffeinated) is associated in observational studies with less liver damage and fewer liver-related outcomes in MASLD. It is safe for most adults and a reasonable daily habit, with pregnancy and gastro-oesophageal cautions.^[3]
• Alcohol. Discourage all alcohol; in advanced fibrosis or cirrhosis it should be stopped completely and permanently. Both alcohol and obesity potentiate liver injury.^[3][2]
• Normal-weight (lean) patients. Weight-loss advice may not be appropriate, but dietary change and activity can still reduce liver fat.^[3]

Because cardiovascular disease is the leading cause of death in MASLD, aggressive management of blood pressure, lipids, glucose control and smoking cessation is recommended for everyone.^[2] In practice this means:

• Statins are safe in MASLD across the whole disease spectrum, including compensated cirrhosis, and reduce cardiovascular morbidity and mortality; a meta-analysis level evidence base supports moderate- to high-intensity statins as first-line lipid-lowering therapy. Statins are under-used in MASLD in real-world practice. Caution is required in decompensated cirrhosis, where the risk of statin-related adverse events is higher.^[2]
• Fibrates or prescription omega-3 fatty acids / icosapent ethyl are used when triglycerides are severely elevated (over 500 mg/dL) ^[2], with caution combining fibrates and statins.- Pioglitazone can be considered to optimise glycaemic control because of concomitant lipid benefits.^[2]
• Cardiovascular risk scores should be used, and antiplatelet, antihypertensive and glucose-lowering therapy matched to standard guidelines.

EASL 2024 and AASLD 2023 disagree on emphasis, and the honest position is that none of the pharmacologic options has proven benefit on long-term liver-related clinical outcomes.

• Bariatric/metabolic surgery should be considered in non-cirrhotic MASLD with an approved indication (for example BMI criteria), because it can induce durable improvements in liver injury, fibrosis remission, type 2 diabetes, and cardiometabolic risk factors. In compensated cirrhosis it can be considered only after careful multidisciplinary assessment of indication, surgical type and portal hypertension; bariatric surgery is contraindicated in decompensated cirrhosis. Metabolic or endoscopic weight-loss procedures are not yet validated as MASH therapy.^[3]
• Endoscopic bariatric procedures and nutraceuticals are not recommended as liver-directed therapy.^[3]

In MASLD-related cirrhosis the standard HCC surveillance programme (ultrasound every 6 months, usually with alpha-fetoprotein) applies, and risk-stratification tools may refine scheduling; none are yet validated in phase III/IV studies. HCC surveillance is not recommended in non-cirrhotic MASLD below F3 fibrosis; in F3 it may be considered based on individual risk.^[3]

For portal hypertension, measurement of liver stiffness (VCTE 15 kPa or less together with platelets 150 × 10^9/L or more) can be used to rule out clinically significant portal hypertension. Where present (or where compensated advanced chronic liver disease shows VCTE 20 kPa or more or platelets below 150 × 10^9/L), upper endoscopy should be performed to screen for varices unless criteria to start non-selective beta-blockers already apply.^[3] Patients with cirrhosis also need HCC, varices and decompensation monitoring as standard.^[2]

Adults with MASLD who are transplant candidates need multidisciplinary evaluation for cardiometabolic disease because they carry a higher risk of cardiovascular events before, during and after transplantation. Weight optimisation matters: dietary change and supervised exercise are first line to reduce BMI below 40 kg/m2 (ideally below 35 kg/m2), with emaciating sarcopenia avoided; pharmacological weight loss may be considered after careful risk-benefit assessment; sleeve gastrectomy may be considered in compensated cirrhosis without clinically significant portal hypertension, but bariatric surgery is contraindicated in decompensated cirrhosis. After transplantation, MASLD frequently recurs, particularly in those with multiple metabolic risk factors, so long-term control of weight and cardiometabolic disease is essential.^[3]

In children and adolescents the evidence base is thinner. Lifestyle modification (dietary quality, activity) remains the foundation; weight loss targets are individualised. Drug therapy in minors is generally limited to clinical trials; vitamin E 800 IU/day has been studied in biopsy-proven NASH in children, but screening and management decisions should follow paediatric guidance and specialist input.^[2]

Obesity and gestational weight gain compound fatty liver risk. Drug choices in pregnancy should be managed as a multidisciplinary decision, weight-loss medicines are generally avoided, and advice about alcohol is absolute. Gestational diabetes screening should be treated as standard.

MASLD prevalence is rising fastest in low- and middle-income settings, where ultrasound, elastography and ELF are often unavailable, yet the principles of care scale well:

• Recognise MASLD clinically from metabolic risk or incidentally noted steatosis, and use history and examination to risk-stratify. True ALT normal cut-offs should guide interpretation where laboratory ranges are generous.
• FIB-4 requires only age, AST, ALT and platelets, and can be calculated in many primary care settings. Use VCTE when available; otherwise rely on FIB-4 and clinical judgement, and refer at high scores.
• Liver biopsy needs not be performed when it will not change management. Most patients can be managed with diet, activity and cardiometabolic care.
• Low-cost measures (avoid sugary drinks, reduce refined starch, increase walking, treat hypertension and diabetes, use statins when indicated, and avoid alcohol) remain the most effective interventions.
• Work through local referral networks for compensated and decompensated cirrhosis; HCC surveillance with ultrasound where feasible.
• Adapt recommendations to local regulations, resources and cost structures, as the European guidelines themselves advise.^[3]

• MASLD, the new name for NAFLD, is SLD plus at least one of five cardiometabolic risk factors.
• MASH (formerly NASH) is steatohepatitis that drives fibrosis; MetALD and ALD are defined by alcohol quantity.
• It affects about one in three adults worldwide; most are asymptomatic.
• Cardiovascular disease, not liver failure, is the commonest cause of death.
• Fibrosis stage (>steatosis) determines outcome and the need for specialist care.
• True normal ALT is 29-33 U/L in men and 19-25 U/L in women.
• FIB-4 first, then VCTE or ELF; biopsy for uncertainty. Cut-offs: FIB-4 under 1.3 low, 1.3-2.67 indeterminate, over 2.67 high; VCTE under 8, 8-12 and 12 kPa or more; ELF under 7.7, 7.7-9.7 and 9.8 or more.
• Reassess FIB-4 every 1-2 years with diabetes/two or more risk factors, or 2-3 years otherwise.
• Weight loss targets: at least 5% to reduce liver fat, 7-10% to improve inflammation, 10% or more to improve fibrosis.
• Mediterranean-style diet, 150 minutes/week of moderate activity, coffee is probably protective, and alcohol should be discouraged, and stopped in advanced fibrosis.
• Statins are safe in MASLD across the spectrum and reduce cardiovascular events.
• Resmetirom 80/100 mg daily and semaglutide 2.4 mg weekly are now approved (accelerated) for non-cirrhotic MASH with F2-F3 fibrosis; EASL still does not recommend GLP-1 receptor agonists, pioglitazone or vitamin E as MASH-targeted therapy.
• Bariatric surgery can help with metabolic disease and MASH in non-cirrhotic, approved cases; it is contraindicated in decompensated cirrhosis.
• HCC surveillance every 6 months applies in cirrhosis; varices screening at VCTE 20 kPa or more or platelets below 150 × 10^9/L.
• Children need age-adjusted criteria; low-resource care relies on FIB-4, lifestyle and risk-factor control.

1. A 52-year-old woman with type 2 diabetes has steatosis on ultrasound. Her FIB-4 is 1.1. What is the most appropriate next step, and when should you re-test? Answer: Advanced fibrosis is unlikely. Manage in primary care with lifestyle and cardiometabolic optimisation, and repeat FIB-4 in 1-2 years because she has type 2 diabetes. No need for elastography or biopsy at this stage.

2. A 46-year-old man, BMI 31, drinks 25 g of alcohol daily. Does he have MASLD or MetALD? Answer: He has both cardiometabolic risk factors and moderate alcohol intake, so this is MetALD. If the alcohol were 20 g/day or less it would be MASLD.

3. A patient has FIB-4 1.9. Which non-invasive thresholds rule advanced fibrosis in or out on the next test? Answer: VCTE below 8 kPa (or ELF below 7.7) makes advanced fibrosis unlikely; VCTE 12 kPa or more (or ELF 9.8 or more) makes it likely; 8-12 kPa or ELF 7.7-9.7 is indeterminate and needs referral or biopsy.

4. Which patients should be considered for resmetirom, and what is the dose? Answer: Adults with non-cirrhotic MASH and F2-F3 fibrosis who are eligible locally, with diet and exercise, receive 80 mg daily if under 100 kg and 100 mg daily if 100 kg or more.

5. Why is a BMI of 24.5 an unreliable reassurance in an Indian patient with visceral obesity? Answer: MASLD cardiometabolic criteria use a lower BMI threshold in Asian people (23 kg/m2 or more), and waist circumference, glucose, lipids and blood pressure may be abnormal even at relatively low BMI. Visceral fat carries most of the risk.

Alcohol-associated liver disease; Cirrhosis; Diabetes mellitus type 2; Hepatocellular carcinoma; Metabolic syndrome; Obesity and overweight; Pancreatitis (acute); Primary liver transplantation; Variceal bleeding.