Trends in alcohol use suggest that less Australians are drinking alcohol on a daily basis. However, the number of Australians drinking at a potentially harmful level remains stable with an estimated one in five adults.

Effects of alcohol are dose-related

Alcohol related liver disease (ALD) is a common consequence of excessive alcohol consumption. The spectrum of ALD often mirrors the total consumption of alcohol. Mild abnormalities in LFTs and hepatic steatosis are frequently observed in those with heavy or binge-style alcohol use. As alcohol frequency, volume and dependence increases to extremely heavy alcohol use, alcoholic hepatitis, cirrhosis and hepatocellular carcinoma (HCC) become more frequent. Cessation of alcohol consumption may reverse alcoholic steatosis and hepatitis and prevent progression of cirrhosis.

Not all individuals who drink at hazardous levels develop ALD. The risk of alcohol related cirrhosis increases in men who drink 60-80g and women who drink more than 20g/alcohol per day over 10 years with between 6 and 41% developing cirrhosis. In those who drink more than 30g/alcohol per day the risk of developing any form of ALD is 23.6 times more than non-drinkers (and cirrhosis 13.7 times more likely to develop). Sex, race and co-existent risk factors for liver disease also influence the development of ALD. Individuals consuming less than 20g of ethanol per day do not develop ALD.

Diagnosis may be difficult

Diagnosis of ALD can be difficult with patients frequently underestimating or denying alcohol intake and physicians lacking reliable clinical screening tools and reliable diagnostic tests. Elevations in GGT, MCV and an AST/ALT ratio greater than two are highly suggestive of alcohol abuse. Carbohydrate deficient transferrin has been useful in detecting heavy alcohol use though sensitivity and specificity is poor. Imaging and histopathology is useful to stage ALD though this can rarely differentiate ALD from other causes of liver disease. The exception is alcoholic hepatitis which has characteristic histopathological findings.

Alcohol cessation is the only treatment for ALD. It is important to identify those with alcohol-dependence as they will likely benefit from additional support and strategies to maintain abstinence. Baclofen, disulfarim and naltrexone have all been used to assist in maintaining abstinence. Though liver disease is a contraindication to disulfarim and naltrexone, these medications are likely to be safe and useful in experienced centres. A subset of those with severe alcoholic hepatitis may benefit from corticosteroids in a specialized unit. Those with cirrhosis require HCC surveillance and management of complications including variceal bleeding, ascites and encephalopathy.

Key Points

  • Alcohol is a frequent cause of liver disease.
  • Elevated GGT, MCV and AST:ALT>2 are highly suggestive of ALD
  • Alcohol abstinence may reverse steatosis and hepatitis
  • Cirrhosis is not generally reversible but progression may be halted by abstinence
  • Pharmacological therapies are likely to be safe and useful in assisting with alcohol abstinence

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