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-based 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 an acute syndrome superimposed on underlying ALD.
- 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
Steatotic Liver Disease: MASLD to Drug Therapy
The organizing idea is that fibrosis stage, not ALT or the amount of fat, predicts the outcome, so every decision in MASLD follows from it. The episode first diagnoses MASLD positively from steatosis plus one cardiometabolic criterion and classifies it by alcohol in grams a week. It then explains why fat becomes injury and why genetics such as PNPLA3 drive progression, and it flags lean MASLD and burned-out cryptogenic cirrhosis. Staging comes next, with FIB-4, then FibroScan read with its pitfalls, then MR elastography. Treatment follows: weight loss as a dose, diet and exercise, bariatric surgery, and then semaglutide, resmetirom, pioglitazone, and vitamin E, with the statin always continued.
Read the transcript → - 02
Steatotic Liver Disease: Alcohol and Transplant
The organizing idea is that abstinence is the treatment at every stage of alcohol-associated liver disease, and that severe alcoholic hepatitis is an acute syndrome with its own decision sequence. The episode begins with what reverses at each stage, how alcohol injures the liver, and what the AST-to-ALT pattern means. It then covers why women, PNPLA3 carriers and ALDH2 star two carriers are harmed at lower doses. It moves to diagnosing alcoholic hepatitis by NIAAA criteria without a biopsy, scoring severity, excluding infection, giving prednisolone, and stopping or continuing it at day seven by Lille score. It closes with nutrition, early transplant selection, and alcohol use disorder treatment afterward.
Read the transcript →
Key topics
- New SLD, MASLD, MASH, and MetALD nomenclature
- Diagnostic criteria for MASLD
- Alcohol in grams a week and the MetALD category
- Pathogenesis from insulin resistance to lipotoxicity
- PNPLA3, TM6SF2, and HSD17B13 genetics
- Fibrosis stage as the prognostic driver
- Lean MASLD and cryptogenic cirrhosis
- FIB-4, FibroScan, and MR elastography staging
- Weight loss, diet, exercise, and bariatric surgery
- Semaglutide, resmetirom, pioglitazone, and vitamin E
- Stages and reversibility of alcohol-associated liver disease
- Alcohol metabolism and liver injury
- AST to ALT pattern and the AST over 400 rule
- Susceptibility: sex, genes, viral hepatitis, bariatric surgery
- ALDH2 star two and cancer risk
- NIAAA criteria for alcoholic hepatitis
- MELD and Maddrey severity scores
- Prednisolone, contraindications, and the Lille score
- Nutrition and supportive care
- Early transplant selection and alcohol use disorder drugs
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
- MELD score
- Lille model (alcohol-associated hepatitis)
- Maddrey discriminant function
- Child-Pugh score