Alcoholic Hepatitis (1)

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Presentation transcript:

Alcoholic Hepatitis (1) C.L.I.P.S. Patient Characteristics Usually more than 100g alcohol intake daily. Often for more than 20 years, but can develop with much shorter history Patients may have recently stopped drinking (usually due to illness) or increased drinking (often in response to social stressors) Signs and Symptoms Jaundice, anorexia, fever, RUQ pain, ascites or encephalopathy May be found incidentally with minimal symptoms Laboratory Analysis AST/ALT elevation in 2:1 fashion, usually less than 300. Elevated serum bilirubin (direct and indirect) Elevated INR Leukocytosis (sometimes extremely elevated leukemoid reaction). Infection must be ruled out before you can blame leukocytosis on hepatitis Diagnosis Above laboratory findings in setting of alcoholism Rule out other causes of acute hepatitis DF > 32 is severe alcoholic hepatitis -- Ddx for acute hepatitis: -APAP toxicity -NASH -Viral Hepatitis -Ischemic Hepatitis -Budd-Chiari -HELLP -Wilson disease -Autoimmune -A1 antitrypsin deficiency -Toxin induced (mushrooms) Updated 5/17 P. Boyne

Alcoholic Hepatitis (2) C.L.I.P.S. Treatment Non severe alcoholic hepatitis (DF<32). Alcohol abstinence and counseling and nutritional support Severe alcoholic hepatitis (DF>32). Prednisolone 40mg daily for 28 days plus 2 week taper plus alcohol cessation and nutritional support. Discontinue beta blockers if taking. Lactulose if encephalopathic If contraindications to steroids, can consider pentoxifylline (Trental) but recent large study showed this was no better than placebo Liver transplant. Rarely done as AH implies recent alcohol use Mortality Non-severe AH: <10% 1 month mortality Severe AH: 25-45% 1 month mortality MELD >11 may be as effective as DF>32 at predicting mortality. Lille score (performed on day 7 of therapy) may show response to glucocorticoids. Lille>0.45 suggests poor response to steroids and 75% 6 month mortality. Lille score alone probably shouldn’t be used to discontinue treatment Cause of death Hepatic failure, GI bleeding, infection/sepsis, hepatorenal syndrome Why is prednisolone preferred over prednisone? This bypasses the “first-pass” hepatic metabolism in a poorly functioning liver where inactive prednisone is converted to active prednisolone