What is Alcohol liver disease
Alcohol ingestion affects the liver, nervous system, cardiovascular system, gastrointestinal system, muscles and the reproductive system. There is also an increased risk of cancer of the mouth, pharynx, food pipe, and liver associated with prolonged alcohol abuse.
The liver bears the greatest brunt of alcoholic injury leading to 3 distinctive, but overlapping forms of liver disease:
- Fatty change (hepatic steatosis)
- Acute alcoholic hepatitis
Daily ingestion of 80 gm or more of ethanol poses a significant risk for serious liver damage while a daily intake of 160 gm or more for 10-20 years is consistently associated with severe liver injury. Only 10-15% of chronic alcoholics, however, develop cirrhosis. Women are more prone to hepatic injury and this may be related to reduce breakdown of alcohol and differences in body composition, possibly a genetic susceptibility. No genetic markers are known that can identify susceptible individuals.
The relation between fatty change or alcoholic hepatitis and progression to cirrhosis is not yet clear with cirrhosis developing without preceding evidence of fatty change or hepatitis in some individuals. In the absence of a clear understanding of the different factors responsible for liver injury, no safe upper limit for alcohol intake can be stated.
Types of Alcoholic Liver Disease
This is an acute, reversible effect of alcohol ingestion and, in chronic alcoholism, may lead to a massive enlargement of the liver. This occurs because of increased breakdown of fat in the body causing more fatty acids to be delivered to the liver; excess lipid biosynthesis in the liver; reduced fat breakdown by the liver; and decreased transport of fat out of the liver.
Acute alcoholic hepatitis:
This liver injury is also potentially reversible. It is caused by the direct toxic effect of alcohol and is due to injury to the liver cell; reduced protective chemicals in the liver cells; increased production of toxic substances within the liver; and stimulation of the immune system. Reduced oxygen supply within the liver also contributes to the injury. If alcohol ingestion is continued, about 10-15% of patients from this stage will develop cirrhosis of liver. This occurs acutely, usually after a bout of heavy drinking. Patient may have minimal symptoms or may come in a fulminate liver failure. The usual symptoms, however, are malaise, loss of appetite, weight loss, fever, liver pain and jaundice. Each bout of hepatitis carries a risk of death of 10%-20% and repeated episodes lead to cirrhosis in 1/3rd of patients in a few years.
This stage is characterized by a hard, shrunken liver and is a serious, potentially fatal condition. The patient has weakness, wasting of muscles, fluid in the abdominal cavity (ascites), bleeding in the intestinal tract and coma. Jaundice, ascites, portal hypertension and other features like grossly bloated abdomen and wasting of extremities clinically manifest this state.
The causes of death include hepatic coma, profuse intestinal bleeding, unremitting infection, involving kidney failure and cancer of the liver.
In case of fatty change the patient is usually asymptomatic with only a mild liver enlargement. Blood tests may be normal or there may be a mild increase in bilirubin and alkaline phosphatase enzyme.
In case of acute alcoholic hepatitis, blood tests reveal elevated bilirubin level, increase in alkaline phosphatase and rise in white cell count.
Blood tests are grossly abnormal and biopsy of liver may be indicated in case of cirrhosis.
Stopping alcohol and a well balanced diet helps reverse the liver injury in case of fatty change.
In case of acute alcoholic hepatitis total abstinence from alcohol and proper nutrition usually allow it to improve slowly. In some cases, however, it progresses to cirrhosis despite stopping alcohol.
There is no treatment for cirrhosis. Liver transplant is the only available option.