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Alcoholic Hepatitis

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overview of alcoholic hepatitis

overview of alcoholic hepatitis

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  • 1. Alcoholic Hepatitis Dr E M Said Gastroenterology Ward 11
  • 2.
    • Background
    • Spectrum of ALD
    • Alcoholic Hepatitis
    • Presentation
    • Investigation
    • Prognosis
    • management
  • 3. background
    • major cause of morbidity and mortality in the West
    • Per capita consumption has doubled between 1980-1995
    • Even though per capita consumption has plateaued in 1990s, recent surveys suggest drinking among females and the young continues to rise
    • Alcohol consumption in the UK accounts for:
      • 40,000 premature deaths per year
      • 1.3% of GP consultations
      • 12.5% of A&E attendances
      • 25% of ICU admissions
      • 30% of male and 15% of female admissions to general medical and surgical wards
  • 4. background
    • CMO's report 2001 stated a significant increase in liver cirrhosis and mortality rate in England and Wales (four- to eight-fold increase in males, three- to seven-fold increase females)
    • Alcoholic cirrhosis mortality rate:
      • 11/100,000 males
      • 6/100,000 females
    • Alcohol accounts for 50% of chronic liver disease
    • Economic cost: £10 billion per year
  • 5. Metabolism of Alcohol
    • Alcohol metabolism by the liver result in increase in the NADH/NAD ratio & change in the oxidation-reduction status with reduced intracelluar state.this lead to:
    • 1-Increase hepatic fatty acid production
    • 2-Impaired carbohydrate and protein metabolism
    • 3-Centrilobular necrosis of the hepatic acinus
    • The exact mechanism of alcohol hepatitis and cirrhosis is unknown.
  • 6.  
  • 7. Spectrum of alcoholic liver disease
    • The three most widely recognised forms of ALD are :
    • alcoholic fatty liver (steatosis).
    • acute alcoholic hepatitis.
    • alcoholic cirrhosis.
  • 8.  
  • 9. alcoholic fatty liver (steatosis )
    • appears to be the initial change and is the most common response to alcohol ingestion
    • The increased liver fat is derived from the diet, from free fatty acids mobilized from adipose tissue, and from lipid synthesized in the liver and inadequately degraded or excreted
    • may cause mild abnormalities of liver function tests, including elevated ALT
    • patients have an excellent prognosis if they abstain from alcohol.
  • 10.  
  • 11. alcoholic hepatitis
    • It is characterized by necrosis of hepatocytes, and deposition of Mallory hyaline bodies.
    • A polymorphonuclear reaction develops locally in response to the Mallory-containing and necrotic liver cells.
    • typically presents with jaundice, low grade fever, and tender hepatomegaly
    • Alcoholic hepatitis is often viewed as the intermediary step between fatty liver and cirrhosis
  • 12. alcoholic cirrhosis
    • represents end-stage disease
    • Classically of micronodular type
    • develop in 10 to 20% of those who are chronically heavy drinkers.
    • Although irreversible, patients may live many years with few obvious effects particularly with cessation of drinking
    • Decompensation of cirrhosis triggered by sepsis, bleeding, continued excessive drinking
  • 13.  
  • 14.
    • It is estimated ,that although 90-100% of heavy drinkers show evidence of fatty liver, only 10-35% develop alcoholic hepatitis and 8-20% develop cirrhosis
  • 15. Mechanisms of liver injury in Alcoholic hepatitis
    • Genetic factors
    • Malnutrition
    • Toxic effects on cell membranes
    • Hypermetabolic state of the hepatocyte
    • Generation of free radicals and oxidative injury
    • Formation of acetaldehyde adducts
    • Role of the immune system
    • Cytokines
    • Role of concomitant viral disease
  • 16. presentation
  • 17. INVESTIGATIONS
    • Laboratory findings
    • Ultrasonography
    • Liver biopsy
  • 18. laboratory findings in alcoholic hepatitis
    • Liver Function tests
    • Increased AST to ALT ratio (2 to 1) (below 400IU/L)
    • ALT usually < 100 IU/L
    • Increased Gamma-GT (variable)
    • Increased alkaline phosphatase (variable)
    • Note: AST has 50% sensitivity, 82% specificity for alcohol-induced liver injury. ALT has 35% sensitivity, 86% specificity for alcohol-induced liver injury.
    • Liver synthetic function (decrease after significant liver injury)
    • INR
    • Albumin
  • 19. laboratory findings in alcoholic hepatitis
    • Renal function (impaired in advanced ALD)
    • Urea/ creatinine
    • Haematological
    • Mild anaemia (usually macrocytic)
    • Thrombocytopenia
    • Other abnormalities
    • Hyperuricaemia
    • Hypertriglyceridaemia
    • Raised IgA
    • Hyperglycaemia
  • 20. Exclusion of other causes of liver disease:
    • Alpha-1 antitrypsin genotype
    • Serum caeruloplasmin/ serum copper
    • Iron studies
    • Autoantibodies (including LKM (Liver kidney microsomal)/ AMA (anti-mitochondrial)/ ANCA (anti-nuclear))
    • Immunoglobulins/ complement
    • Hepatitis serology (HBsAg/HbCAb/HCVAb)
  • 21. Ultrasonography
    • Preferred study as inexpensive ,noninvasive and widely available
    • The liver appears enlarged and diffusely hyperechoic.
    • Helpful in excluding gallstones ,bile duct obstruction and hepatic or biliary neoplasm.
  • 22. Liver biopsy
    • Accurate assessment of severity of liver damage
    • Consider in patients in whom diagnosis is uncertain
    • A stestosis
    • B black arrows
    • Mallory bodies
    • C pericellular fibrosis
    • D satellitosis
    • Degeneration of hepatocytes
  • 23. PROGNOSIS
    • Alcoholic hepatitis carries a significant mortality
    • The most established tool for predicting survival in alcoholic hepatitis is Maddrey's discriminant function (MDF)
    • An MDF ≥32 indicates a poor prognosis with a risk of mortality around 35%.
  • 24. PROGNOSIS
    • Others factors that correlate with poor prognosis include :
    • older age,
    • impaired renal function,
    • encephalopathy,
    • rise in the white blood cell count in the first 2 weeks of hospitalization
    • Nearly 2/3 of patients with severe alcoholic hepatitis will die in the hospital
  • 25. management
    • General measures:
    • Stop drinking
    • Treat withdrawal symptoms
    • Thiamine/multivitamins
    • Bed rest
    • High protein diet
    • Treat decompansaton
  • 26. THERAPY
    • Evidence
    • support use of:
    • 1-corticosteroids
    • 2-pentoxifylline
    • 3-nutritional support
    • Insufficient
    • evidence:
    • 1-Anabolic steroids
    • 2-Malotilate
    • 3-Etanercept
    • 4-Infliximab
    • Therapeutic agents for alcoholic hepatitis:
    Evidence not supporting use: 1-Propylthiouracil 2-Insulin and glucagon 3-Colchicine
  • 27. Corticosteroids
    • Steroid effects are mediated through a decrease in immune mediated injury, inhibition of cytokine production and activation, as well as suppression of extracellular matrix protein expression.
    • should not be started until a sepsis screen has excluded infection
    • Meta-analysis of three randomised trials showed an improvement in 28 day survival, but benefit was not seen at later time points
    • The side effects of corticosteroids are justified only in patients with severe alcoholic hepatitis (MDF >32).
  • 28.
    • Randomized, controlled trials using prednisolone 40 mg/d (or an equivalent) for 28 days have shown an increase in both short-term (30 and 60 day) and long-term (1 year) survival in a subgroup of patients with severe alcoholic hepatitis
  • 29. Pentoxifylline
    • Pentoxifylline inhibits tumor necrosis factor (TNF)- production.
    • showed promise in one randomised controlled trial of patients with an MDF ≥32 who were not treated by steroids
    • associated with a marked reduction in the incidence of hepatorenal syndrome and improved 28 day mortality with no significant side effects
    • No trial has assessed combination therapy with steroids and pentoxifylline
  • 30.
    • A recent randomized, controlled study in severe alcoholic hepatitis used pentoxifylline 400mg thrice daily (mean duration, 21 days), to show a short-term survival benefit of 22% (absolute risk reduction)
  • 31. Nutritional support
    • Energy expenditure increased up to 60% in AH
    • Severe negative nitrogen balance occurs in AH
    • Nutritional status correlates with survival in moderate and severe AH
    • 1-1.5g/Kg/day protein is required to achieve neutral balance in cirrhotics. This requirement increases significantly in AH
    • Total enteral nutrition is recommended in patients admitted with AH. Studies have shown a decreased mortality rate in patients receiving enteral feeding.
    • Oral supplementation is ineffective due to anorexia and poor compliance due to encephalopathy and insufficient protein-calorie content to meet metabolic demands
  • 32. In summary…
    • Common condition, high mortality
    • Diagnosis :history of alcohol intake, physical finings,imaging,lab results and exclusion of other conditions
    • Treatment:steroids,after exclusion of sepsis,pentoxifylline and nutrition support.
  • 33.  
  • 34. Thank you
    • Questions?

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