Alcoholic Hepatitis 07/11/2017

  • Risk Factors
    • Mean intake of 100g/day for 10-20 years
      • Standard drink of ETOH = 14g pure alcohol
        • 12oz beer
        • 5oz wine
        • 5 oz of 80 proof liquor (“Shot”)
    • Binge drinking
      • Men = 5 drinks in 1 sitting
      • Women = 4 drinks
  • Pathophysiology
    • Standard alcohol metabolism in cells
      • Alcohol dehydrogenase (ADH) plus cytochrome P-450 2E1 (CYP2E1) convert ethanol into acetaldehyde which is then converted to acetate
      • CYP2E1 releases reactive oxygen species leading to inflammation
      • NAD+ is used as oxidizing agent for ADH and is converted to NADH
        • Excess alcohol creates an imbalance of NAD/NADH
        • Excess NADH decreases oxidation of fatty acid oxidation
      • While acetate increases fatty acid synthesis
        • Both leading to steatosisAlcoholic hepatitis mechanism
  • Presentation
    • Pts often present between 40-50 years of age
    • Classic presenting features
      • Jaundice
      • Scleral icterus
      • Anorexia
      • Fever
      • Tender RUQ
      • Hepatomegaly
      • Abdominal distention due to ascites
      • Hepatic encephalopathy
      • Bruit can be appreciated over the liver due to increased hepatic blood flow


  • LFTs
    • Moderate elevations of AST and ALT
      • Usually less than 300, rarely higher than 500
      • AST:ALT ratio >2
        • ALT is less due to alcohol induced deficiency of Pyridoxal 5-phosphate, which is a coenzyme of ALT. Thus the ratio reflects the failure to appropriately increase the ALT, rather than an inappropriate increase in AST.
      • Elevated Tbili and Dbili
  • CBC
    • Leukocytosis (usually <20) with a neutrophil predominance
      • Extreme Leukemoid reaction (>50) is associated with a very poor prognosis.
    • Macrocytosis
      • Reflective of poor nutritional status
    • Thrombocytopenia
    • Coags
      • Elevated INR
  • Imaging (show pics!)
    • 1st choice: Abdominal ultrasound
      • It’s quick, easy, and relatively cheap
      • Will help rule out Budd-Chiari, abscess, obstruction, or neoplasm
      • Will show fatty changes in liver vs underlying cirrhosis
  • Maddrey Discriminant Function
    • DF >32 signifies severe alc hep and is associated with high short-term mortality
      • May benefit from glucocorticoid therapy
  • Treatment
    • 3 main things
      • Alcohol cessation
      • Nutritional support
      • Steroids
        • Contraindicated for:
          • GI Bleed
          • Infection
          • Renal failure
          • Pancreatitis
        • Check Lille Score on day 7 to evaluate response
          • >.45 is associated with 6-month survival of 25% –> ok to stop steroids
          • <.45 is associated with 85% survival
    • Pentoxyfilline –> little evidence!
      • The Steroids or Pentoxifylline for Alcoholic Hepatitis (STOPAH) trial was just published in the New England Journal in 2015.
        • They found a significant 28 day mortality benefit for prednisolone with an odds ratio of .61.
          • However, the mortality benefit was lost at 90 days and 1 year
        • On the other hand, pentoxifylline did not improve survival compared to placebo

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