Excessive alcohol consumption is a global healthcare problem. The liver sustains the greatest degree of tissue injury by heavy drinking as it is the primary site of alcohol (ethanol) metabolism.
Chronic and excessive alcohol consumption produces a wide spectrum of liver injuries, the most characteristic of which are steatosis, hepatitis, and fibrosis / cirrhosis.
Spectrum of Alcoholic Liver Disease:
Heavy alcohol consumption produces a wide spectrum of hepatic injury. Steatosis is the earliest, most common response that develops in more than 90 per cent of the alcoholics who consume 4 to 5 standard drinks per day over 4 -5 years. A standard drink is the amount of alcoholic beverage that contains approximately 14 grams of pure alcohol. However, steatosis also develops after binge drinking.
A “binge” is the consumption of 4 to 5 drinks in 2 hours or less, which is very commonly being observed among youngsters these days. A word of caution for all the people partying out — watch your liver.
Alcoholic hepatitis is a more severe, inflammatory type of liver injury which in turn progresses to fibrosis and if alcohol consumption is continued, it eventually leads to cirrhosis. In an estimate by the World Health Organization, 50 per cent of all deaths caused by cirrhosis were attributable to alcohol abuse.
Factors Affecting Liver Injury In Alcoholics:
Pattern of Consumption and Beverage Type -The most important factors determining the progression of liver disease are the beverage type consumed, the amount and pattern of drinking (occasional, regular or binges). Intake of 40 to 80 grams ethanol/day by males and of 20 to 40 grams/day by females for 8-10 years in the western population and even earlier in the Indian scenario is a general predictor of more severe cases of alcoholic liver disease, including alcoholic steatohepatitis, fibrosis, and cirrhosis.
Gender -It is shown that women are more susceptible to alcohol-related liver damage than men.
Age - Older individuals above 65 years of age are more vulnerable to and show greater degrees of ethanol-induced impairments than younger people.
Genetics -Both genetic and epigenetic influences govern the initiation and progression of ALD. Genome-wide association studies have identified specific genetic markers for ALD.
Nutritional factors -A diet rich in unsaturated fatty acids such as linoleic acid leads to liver damage.
Drugs -Alcohol and other drugs (like pain killers, particularly acetaminophen) interact to enhance the hepatotoxic effects of alcohol.
Obesity -People with a high body mass index who consume alcohol are at a higher risk of liver damage.
Smoking - Cigarette smoking adversely affects the liver functions and is associated with a higher risk of alcoholic cirrhosis in humans.
Viral Infections - Alcoholics with a co-existent hepatitis C (HCV) and hepatitis B (HBV) viral infections show a rapid progression to fibrosis, cirrhosis, and even hepatocellular carcinoma.
Treatment of Alcoholic Liver Disease:
Abstinence: Abstinence from alcohol not only resolves alcoholic steatosis but also improves survival in cirrhotic patients.
Corticosteroids: Steroids have been the most widely used form of therapy, especially for severe alcoholic hepatitis, only to be given under specialist care.
High-calorie diet: All patients with severe alcoholic hepatitis and cirrhosis are malnourished. They require very specific high-calorie intensive feeding.
Newer therapies: Therapies like Fecal microbiota transplantation and Granulocyte colony-stimulating factors are being used to treat alcoholic hepatitis.
Liver transplantation: For the patients who develop liver failure; decompensated cirrhosis liver transplantation is the cure.