Alcoholic Liver Disease (ALD)
Discuss the spectrum of ALD?
The spectrum of alcohol-related liver injury is often grouped into three histological stages of ALD: fatty liver or simple steatosis, alcoholic hepatitis, and chronic hepatitis with hepatic fibrosis or cirrhosis.
Fatty liver- develops in the majority with alcohol consumption of > 60g/day (8 g is 1 unit) of alcohol, but may also occur in individuals who drink less. Fatty liver is usually asymptomatic and self limited, and may be completely reversible with abstinence after about 4-6 weeks. However, progression to fibrosis and cirrhosis occurs in 5%-15% of patients despite abstinence.
A subset of patients with ALD will develop severe alcoholic hepatitis (AH), which has a substantially worse short-term prognosis (discussed separately)
Discuss conversion of alcohol in units?
Grams of alcohol consumed= percentage of alcohol X specific gravity of alcohol (0.79g/ml) X volume consumed
A unit is defined as the equivalent of 8 g of ethanol
Discuss alcohol as a hepatotoxin?
Unlike many other hepatotoxins, the likelihood of developing progressive liver disease is not completely dose-dependent, because it occurs in only a subset of patients. The risk of developing cirrhosis increases with the ingestion of >60-80 g/day of alcohol for 10 years or longer in men, and >20 g/day in women. Yet, even drinking at these levels, only 6%-41% develop cirrhosis. Thus liver disease should not be presumed to be alcoholic in nature in a person with excess alcohol intake
Based on epidemiological evidence, a suggested “safe” limit of alcohol intake had been 21
units per week in men and 14 units per week in women who have no other chronic liver disease (where).
Discuss the diagnosis of ALD?
- The diagnosis of ALD is based on a combination of features, including a history of significant alcohol intake, clinical evidence of liver disease, and supporting laboratory abnormalities.
- No single laboratory marker definitively establishes alcohol to be the aetiology of liver disease.
- A combination of raised GGT and mean corpuscular volume may improve the sensitivity for diagnosing alcohol abuse.
- Levels of AST more than 500 IU/L or an ALT) >200 IU/L are uncommonly seen with alcoholic hepatitis. In about 70% of patients, the AST/ALT ratio is higher than 2, but this may be of greater value in patients without cirrhosis. Ratios greater than 3 are highly suggestive of ALD.
- Physical exam findings more commonly observed in ALD are parotid enlargement, Dupuytren’s contracture, and especially those signs associated with feminization
- Other alcohol related diseases like cardiomyopathy, skeletal muscle wasting, pancreatic dysfunction, and alcoholic neurotoxicity may co exist and evidence of these must be sought during the clinical examination, so that appropriate treatment may be provided.
Discuss the treatment of ALD?
Abstinence is the most important therapeutic intervention. It has been shown to improve the histology, decrease progression to cirrhosis, and to improve survival at all stages in patients with ALD. The improvement can be relatively rapid, and in 66% of patients abstaining
from alcohol, significant improvement was observed in 3 months.
Discuss the management of recidivism?
Recidivism is a major risk in all patients at any time following abstinence. Options:
Disulfiram- little evidence that disulfiram enhances abstinence, and based on its poor tolerability, its use has been largely supplanted by newer agents.
Naltrexone- is a pure opioid antagonist and controls the craving for alcohol. A Cochrane systematic review concluded that short-term treatment with naltrexone lowers the risk of relapse.
Acamprosate- has been shown to reduce withdrawal symptoms, including alcohol craving. Its effect is more pronounced in maintaining rather than inducing remission when used in combination with counselling and support. In detoxified alcoholics, it has been shown to
decrease the rate of relapse, maintain abstinence, and decrease severity of relapse when it occurs.
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