Alcoholic hepatitis is a very common cause of liver injury. It is caused by excessive alcohol intake.
Typically there will be steatosis of the liver. In this pathological change, fat globules begin to accumulate in the cytoplasm of liver cells. this can be pretty harmless, and as a result, is not very specific for predicting if the liver will develop cirrhosis.
Mallory’s hyalin is an aggregate of filament found in the hepatocytes that, if present, indicate a risk of irreversible changes in hepatocytes, that may ultimately lead to cirrhosis. Mallory’s hyalin (aka Mallory bodies) is not specific for alcoholic liver disease, but is a sign of steatohepatitis
When we talk about alcohol, we are actually referring to ethanol.
Ethanol is oxidised to acetaldehyde. Acetaldehyde is then converted to acetate by the mitochondria of liver cells. The liver does 90% of this metabolism. Acetate is then released into the bloodstream and taken up by peripheral tissues where it is metabolised to carbon dioxide, fatty acids and water.
Alcohol dehydrogenases are present in many tissues around the body, and some people believe that the gastric mucosa itself is responsible for a lot of alcohol metabolism.
Also, alcoholic drinks often contain a lot of sugar – for example a typical pint of beer contains 250 calories! For this reason a lot of alcoholics will not lose weight despite severe malnutrition.
Long-term effects of alcohol use are all due to ethanol. The short term effects of alcohol use can often be due to other alcohols present in the drink, such as isoamyl alcohol.These additional alcohols are known as cogeners. Brandy and bourbon contain the highest percentage of cogeners.
10-30% of heavy drinkers will develop cirrhosis
50% will have fatty liver.
Nutritional factors are controversial, although it is possible that malnutrition and obestiy both contribute to liver damage.
High alcohol consumption combined with hep C infection also greatly increases the risk of hepatitis.
In males with hepatitis, average alcohol consumption was about 16 units/day over a period of 8 years. However, this is highly variable. In females, the corresponding figure was 11 units/day.
Approximately 1/3 of alcoholics have a parent who is an alcoholic.
The first sign is fatty liver. This occurs in most heavy drinkers at some time, but it is completely reversible upon cessation of alcohol.
The hepatocytes have to divert resources away from metabolising fats to metabolising alcohol. As a result, fat metabolism is altered resulting in fat deposits inside the cells. There are more fats released into the blood stream (fatty acids) and within the hepatocytes, there is increased synthesis of triglycerides and fatty acids.
Acetaldehyde is a product of alcohol metabolism. It binds to liver cell proteins, and causes hepatocytes injury, leading to inflammation. This inflammation can be a causatory factor in cirrhosis. It is likely that this produces Mallory’s sign.
Alcohol stimulates collagen synthesis by fibroblasts as well as fibroblast proliferation.
Ultimately, the fibrosing process will end up linking hepatic veins to portal veins, and in these places, cell regeneration occurs, and nodules form – this is the start of the process of cirrhosis.
Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio
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