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GI & hepatology

Alcohol-related liver disease

Spectrum: steatosis → AH → cirrhosis. Harmful drinking: ≥3/d men, ≥2/d women (or binge). AUDIT-C screen.

Maggie Selesky5 min6 questions1 trials

Spectrum — steatosis to hepatitis to cirrhosis

Women more susceptible than men. Pattern (daily + binge), obesity, diabetes, PNPLA3, α1-antitrypsin, smoking, HCV/MASLD raise risk; coffee lowers it (: ; ACG: ). Harmful drinking: men ≥3 drinks/d or ≥21/week; women ≥2/d or ≥14/week. AUDIT-C everyone.

ALD is a ladder
  1. 1

    Steatosis

    Usually asymptomatic; mild AST > ALT and GGT. 90% after >60 g/d for 2 weeks. Reverses with 4–6 weeks of abstinence. 20–40% → fibrosis → 8–20% cirrhosis → 20–40% decompensation/ACLF; HCC in 3–10% of cirrhotics.

  2. 2

    Steatohepatitis / AH

    Histologic correlate of alcohol-associated hepatitis. Can appear at any fibrosis stage. 40–50% already fibrotic; >75% headed toward cirrhosis.

  3. 3

    Cirrhosis

    Architectural distortion and portal hypertension. 5-year liver mortality ~25%. Treatment of the disease is cessation of alcohol.

  • Counsel with the 5 As (ask, advise, assess, assist, arrange). Pharmacotherapy: baclofen, acamprosate, naltrexone, gabapentin, topiramate. Avoid disulfiram in liver disease.
  • AH can generate acute portal hypertension (varices, ascites, HE) without established cirrhosis because the liver is swollen.

Alcohol-associated hepatitis — diagnose, then score

Jaundice within 8 weeks of ongoing heavy use (women >3, men >4 standard drinks/day for >6 months), <60 days of abstinence before jaundice, AST 50–400 with AST/ALT >1.5, total bilirubin >3. Often leukocytosis <20k (PMN-predominant) and a rising INR. Tender hepatomegaly, anorexia, fever, malaise.

  • Exclude viral hepatitis, APAP, ischemia, AIH, Budd-Chiari, biliary obstruction, and decompensated cirrhosis (superimposed in 10–20%). HAV/HBV/HCV, APAP level, Doppler US, ± ANA/ASMA/IgG/AMA.
  • Transjugular biopsy if atypical (AST/ALT >400), uncertain drinking history, jaundice >3 months, or competing toxin/ischemia.
  • Screen infection even if SIRS is ‘just inflammation’ — 12–26% of severe AH are infected on arrival.
ScoreJobPartsCut
Maddrey DFWho might benefit from steroidsPT, control PT, bilirubin≥32 = severe; 1-month mortality 30–50% ()
MELDAdmission and 90-day deathBili, INR, Cr, Na>20: admit, GI for steroids; 3-month mortality ~20% ()
LilleIs the steroid working?Age, albumin, PT, Cr, serial bili days 0/4/7≥0.45 at day 4 or 7 = nonresponse → stop ()

STOPAH, nutrition, early transplant

If MDF ≥32 or MELD 20–50 and no steroid contraindication (uncontrolled diabetes, UGIB, infection, Cr >2.5, / multi-organ failure, untreated HBV/HCV/DILI/HCC/pancreatitis/HIV/TB): prednisolone 40 mg daily (methylprednisolone 32 mg IV). (): possible 28-day mortality signal, none at 90 days, more infection. Pentoxifylline does not death.

  • Lille ≥0.45 → stop steroids. Lille <0.45 → complete 28 days then a 2–4 week taper.
  • NAC with steroids × 5 days may lower 1-month mortality, not 3- or 6-month (). Large volume load.
  • Hold beta-blockers if MDF ≥32 (↑ AKI; ).
  • Nutrition is disease-modifying: 35 kcal/kg/d and 1.2–1.5 g/kg protein; thiamine, folate, MVI, B6, B12, zinc. Low intake predicts infection (). Tube-feed if <21 kcal/kg/d.
  • G-CSF and fecal transplant are experimental. Nonresponders: early transplant discussion or palliation (especially ≥3 organ failures).