Introduction Alcohol is a common cause of chronic liver disease. Alcohol consumption is well-entrenched in the fabric of many cultures Less than 20% of heavy drinkers progress to advanced disease. Alcoholic liver disease presents as fatty liver, hepatitis or Laennec cirrhosis.
Epidemiology There is a rising incidence in developing countries Alcoholic liver disease does not occur below a threshold of 21units/wk in women and 28units/wk in men. Average alcohol consumption of an individual with cirrhosis is 160g/day for an average of 8 years. There is no clear cut relationship between dose and disease
Significant consumption Significant alcohol consumption varies with gender. More than 24g/day in males and more than 21g/day in females is significant.
Ethanol metabolism Alcohol is metabolized by two pathways: Alcohol and acetaldehyde dehydrogenases DHs increases generates NADH/NAD ratio Mixed function oxidase enzyme They generate free radicals Alcoholic effects on the liver Increased fatty acid synthesis Altered metabolism of proteins and CHOs Stimulates stellate cells
Pathogenesis 10-15% of heavy alcoholic drinkers develop liver disease. Why? Acetaldehyde-protein adducts Oxidative stress Gut permeability Cytokines-Endothelin
Pathology Fatty liver Lipogranuloma Macrovesicular steatosis Swiss cheese effect on haematoxylin and eosin stain Alcoholic hepatitis Neutrophil infiltration Mallory’s hyaline Pericellular fibrosis Cirrhosis Micronodular type Central hyaline sclerosis
Clinical features ALD is a spectrum. Fatty liver +/- symptom Abnormal LFTs Normal/large liver Alcoholic hepatitis Symptomatic Jaundice Malnutrition Hepatomegaly Features of portal hypertension