Steatotic Liver Disease
MASLD per the Rinella criteria, MetALD versus alcohol-associated bands, FIB-4 and FibroScan thresholds for staging, resmetirom (Rezdiffra) approval scope, the GLP-1 and dual-incretin trials in MASH, severe alcoholic hepatitis (STOPAH), early liver transplantation criteria, and HCC surveillance once cirrhosis lands.
- Audio chapterSingle-voice audio, listen on the commute.
- ABIM-format MCQs5-option vignettes with full wrong-answer teaching.
- Study guideTables, decision trees, primary sources.
- AI tutorChapter-grounded, answers the question you're stuck on.
What this chapter covers
- Section 21.1: MASLD nomenclature and cardiometabolic criteria
The 2023 multi-society Delphi consensus retired the NAFLD and NASH labels in favor of a positive, mechanism-anchored nomenclature that names what the disease is rather than what it is not.
- Section 21.2: MASLD pathophysiology, lean MASLD, cryptogenic cirrhosis
MASLD is fundamentally a disease of insulin resistance with genetic susceptibility layered on top, and the histologic phenotype reflects the failure of the hepatocyte to keep up with a steady oversupply of fatty acids.
- Section 21.3: Noninvasive fibrosis assessment in MASLD
The clinical question in any MASLD patient is not whether there is steatosis but whether there is advanced fibrosis, because fibrosis stage is what predicts liver-related mortality.
- Section 21.4: Lifestyle and bariatric surgery
Lifestyle modification is the only intervention with histologic-improvement evidence across the MASLD spectrum, and the dose-response of weight loss to liver outcomes is one of the few precise numbers in hepatology.
- Section 21.5: MASLD pharmacotherapy
The MASLD pharmacotherapy field changed dramatically in March 2024 when resmetirom became the first FDA-approved drug for MASH.
- Section 21.6: Alcohol-associated liver disease spectrum
Alcohol-associated liver disease is a continuum from steatosis through alcoholic steatohepatitis to fibrosis to cirrhosis, with each stage carrying a different reversibility profile and a different management implication.
- Section 21.7: Severe alcoholic hepatitis and STOPAH
Severe alcoholic hepatitis is the acute clinical syndrome that sits on top of underlying ALD and that demands a structured diagnosis and a structured management.
- Section 21.8: Early liver transplantation for severe AH
Severe alcoholic hepatitis that does not respond to corticosteroids carries a 6-month mortality of 70 to 80 percent without further intervention, and the historical answer to that mortality was that liver transplantation was not an option until the patient demonstrated 6 months of abstinence.
Podcast episodes
- 01
MASLD: Diagnosis Through Pharmacotherapy
Episode one of the Steatotic Liver Disease chapter reframes fatty liver as MASLD, a positive diagnosis built on hepatic steatosis plus at least one of five cardiometabolic criteria rather than an exclusion. The organizing idea: fibrosis stage, not the transaminase or the degree of steatosis, is the prognostic anchor, so the workup runs a tiered noninvasive sequence and management is graded by how much fibrosis is present. It walks the biology of insulin resistance and lipotoxicity, the PNPLA3 and TM6SF2 variants, lean disease and cryptogenic cirrhosis as the same entity, then the FIB-4 into elastography algorithm. Management climbs from weight-loss targets through bariatric surgery, including compensated cirrhosis, to the newly on-label drugs resmetirom and semaglutide.
Read the transcript → - 02
Associated Liver Disease and Early Transplant
Episode two moves along the alcohol continuum to alcohol-associated liver disease, one biology read across steatosis, steatohepatitis, and cirrhosis, then zeroes in on the acute superimposed syndrome of severe alcoholic hepatitis. The organizing idea: severe disease is defined by a Maddrey above thirty-two or a MELD over twenty, treated with prednisolone only after infection is excluded, with the day-seven Lille score as the binary decision to continue or stop. It works through the AST-greater-than-ALT lab signature, the ethanol-metabolism mechanism that drives it, and the drug interactions that follow. The close is early transplant for selected steroid nonresponders, which retired the old six-month sobriety rule in favor of a structured psychosocial assessment.
Read the transcript →
Key topics
- Positive cardiometabolic diagnosis and the five criteria
- Steatohepatitis versus bland steatosis and fibrosis as the prognostic anchor
- Alcohol continuum and the intermediate category
- Insulin resistance, lipotoxicity, and the PNPLA3 and TM6SF2 variants
- Lean disease and cryptogenic cirrhosis
- Noninvasive fibrosis testing: FIB-4, transient elastography, MR elastography
- Lifestyle, diet, and weight-loss targets
- Bariatric surgery including compensated cirrhosis
- Pharmacotherapy: resmetirom, semaglutide, pioglitazone, vitamin E
- Three-stage spectrum: steatosis, steatohepatitis, cirrhosis
- Ethanol metabolism, the NADH shift, and drug interactions
- Risk modifiers: sex, genetics, and the acetaldehyde variant
- The AST-greater-than-ALT lab pattern
- Severe alcoholic hepatitis and the consensus diagnostic criteria
- Maddrey and MELD severity thresholds
- Prednisolone therapy and mandatory infection screening
- The day-seven Lille response decision
- Early transplant selection criteria
Sources
Guidelines, consensus statements, and validated instruments this chapter draws on. Named here because the chapter applies them directly.
Professional society guidelines
- American Association for the Study of Liver Diseases (AASLD)
- American College of Gastroenterology (ACG)
- American Gastroenterological Association (AGA)
Consensus statements
- Baveno VII consensus (portal hypertension)
Scoring systems
- FIB-4 index
- Lille model (alcohol-associated hepatitis)
- MELD score
- Maddrey discriminant function
- Child-Pugh score