Monday, November 12, 2012


Alcohol itself is a primary cause of liver damage, although associated malnutrition may be a contributory factor. In the absence of carbohydrate alcohol is more absorbed and more than 95% is metabolized in liver. Ethanol is oxidized to acetaldehyde by cytosolic alcohol dehydrogenase and also by cytochrome P450 system. Acetaldehyde is metabolized by aldehyde dehydrogenase in the mitochondria to acetate, which is in turn oxidized by peripheral tissue to CO2 and water. Acetaldehyde is the main culprit in tissue damage.

In alcoholic hepatitis there are 3 features

1.      Fatty liver (steatosis) occurs as in all individual as response to ethanol consumption but reverse with abstinence.

2.      Mallory bodies

3.      Megamitocohndira and creeping pericellular fibrosis.

Porphyria cutanea tarda is often associated with excessive alcohol consumption due to deficiency of uroporphyrinogen decarboxylase leading to high hepatic porphyrins, high level of uroporphyrinogen in liver and increased coproporphyrin in the faeces.

Biochemical abnormalitites:

Alcoholic steatosis: 

There is subclinical hyperbilirubinaemia and mild elevation of aminotransferases. Raised plasma GGT due to enzyme induction rather than injury.

Alcoholic hepatitis: 

There is deep prolonged jaundice, hepatic failure, leukocytosis, anaemia, elevated aminotransferases. However, AST is never above 10 times URL and ALT values are lower thus AST: ALT >2 along with increased GGT. Ratio <2 ratio suggest non alcoholic cause.

Use of laboratory test in clinical practice:

AST: ALT ratio of >2 and fall in GGT during hospital stay suggest liver disease is due to alcoholism in patient who denies alcohol consumption. Estimation of Desialylated transferrin (CDT) to total transferrin ratio is highly specific for alcohol abuse. Increase in GGT and MCV are reliable test to assess the risk of liver dysfunction in alcoholics.

A longitudional follow up study in assessing abnormal LFT or liver function by measuring GGT and MCV in alcoholics.

Non-alcoholic fatty liver disease (NAFLD)

This comprises a condition ranging from simple hepatic steatosis (excessive accumulation of fat in hepatocytes) to end-stage chronic liver disease, clearly associated with epidemic of obesity, diabetes (insulin resistance) and hypertriglyceridaemia. Steatosis is the adaptive response of the liver to insulin resistance and when this is associated with oxidative stress and inflammatory condition termed non-alcoholic steatohepatitis (NASH). This can lead to cirrhosis and hepatocellular carcinoma.   
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