Alcoholic Liver Disease

by National Institute of Health

Because the liver is the chief organ responsible for metabolizing alcohol, it is especially vulnerable to alcohol-related injury. Even as few as three drinks at one time may have toxic effects on the liver when combined with certain over-the-counter medications, such as those containing acetaminophen.

This issue of Alcohol Alert examines the diagnosis and treatment of alcoholic liver disease (ALD), a serious and potentially fatal consequence of drinking alcohol. Another disorder, hepatitis C, also featured here, often is found in patients with ALD.

Ald - From Steatosis To Cirrhosis

ALD includes three conditions: fatty liver, alcoholic hepatitis, and cirrhosis. Heavy drinking for as little as a few days can lead to "fatty" liver, or steatosis - the earliest stage of alcoholic liver disease and the most common alcohol-induced liver disorder. Steatosis is marked by an excessive buildup of fat inside liver cells. This condition can be reversed, however, when drinking stops.

Drinking heavily for longer periods may lead to a more severe, and potentially fatal condition, alcoholic hepatitis - an inflammation of the liver. Symptoms include nausea, lack of appetite, vomiting, fever, abdominal pain and tenderness, jaundice, and, sometimes, mental confusion. Scientists believe that if drinking continues, in some patients this inflammation eventually leads to alcoholic cirrhosis, in which healthy liver cells are replaced by scar tissue (fibrosis), leaving the liver unable to perform its vital functions.

The presence of alcoholic hepatitis is a red flag that cirrhosis may soon follow: Up to 70 percent of all alcoholic hepatitis patients eventually may go on to develop cirrhosis. Patients with alcoholic hepatitis who stop drinking may have a complete recovery from liver disease, or they still may develop cirrhosis.

Liver cirrhosis is a major cause of death in the United States. In 2000, it was the 12th leading cause of death. Cirrhosis mortality rates vary substantially among age groups: They are very low among young people but increase considerably in middle age. In fact, cirrhosis is the fourth leading cause of death in people ages 45-54.

Other factors besides alcohol also may influence ALD development, including demographic and biological factors such as ethnic and racial background, gender, age, education, income, employment, and a family history of drinking problems.

Women are at higher risk than men for developing cirrhosis. This higher risk may be the result of differences in the way alcohol is absorbed and broken down. When a woman drinks, the alcohol in her bloodstream reaches a higher level than a man's even if both are drinking the same amount. The chemicals involved in breaking down alcohol also differ between men and women. For example, women's stomachs may contain less of a key enzyme (alcohol dehydrogenase) needed for the initial breakdown of alcohol. This means that a woman breaks down alcohol at a slower rate, exposing her liver to higher blood alcohol concentrations for longer periods of time -a situation that is potentially toxic to the liver. Differences in how a woman's body breaks down and removes alcohol also may be linked to how much and how often she drinks, the fact that estrogen is present in her body, and even her liver size.

Diagnosis

Diagnosing ALD is a challenge. A history of heavy alcohol use along with certain physical signs and positive laboratory tests for liver disease are the best indicators of disease. Alcohol dependence is not necessarily a prerequisite for ALD, and ALD can be difficult to diagnose because patients often minimize or deny their alcohol abuse. Even more confounding is the fact that physical exams and lab findings may not specifically point to ALD.

Diagnosis typically relies on laboratory tests of three liver enzymes: gamma-glutamyltransferase (GGT), aspartate aminotransferase (AST), and alanine aminotransferase (ALT). Liver disease is the most likely diagnosis if the AST level is more than twice that of ALT, a ratio some studies have found in more than 80 percent of alcoholic liver disease patients. An elevated level of the liver enzyme GGT is another gauge of heavy alcohol use and liver injury. Of the three enzymes, GGT is the best indicator of excessive alcohol consumption, but GGT is present in many organs and is increased by other drugs as well, so high GGT levels do not necessarily mean the patient is abusing alcohol.

Treatment

Treatment strategies for ALD include lifestyle changes to reduce alcohol consumption, cigarette smoking, and obesity; nutritional therapy; pharmacological therapy; and possibly liver transplantation (in case of cirrhosis).

Lifestyle Changes

Abstinence from alcohol is vital to prevent further liver injury, scarring, and possibly liver cancer; it appears to benefit patients at each stage of the disease. Although only a few studies have looked specifically at the effects of abstinence on the progression of ALD, virtually every one has shown that abstaining from alcohol is beneficial.

Many people who drink alcohol also smoke cigarettes, and European studies have found scarring of the liver occurs more rapidly in ALD patients who smoked. Obesity is another factor associated with liver disease - specifically, the development of fatty liver and nonalcoholic steatohepatitis, a disorder similar to alcoholic hepatitis. Thus, stopping smoking and maintaining a healthy weight are two more measures patients can take to reduce or prevent further liver injury.

Treatment for Alcoholic Liver Disease

• Lifestyle modification (decreasing alcohol use, stopping smoking, losing weight).
• Appropriate nutritional, vitamin supplementation.
• Use of pentoxifylline or prednisone for alcoholic hepatitis.
• Complementary and alternative medicine (e.g., SAMe) for cirrhosis.
• Transplantation in selected abstinent patients with severe disease.

Nutritional Treatment

Although alcoholic beverages contain calories, research suggests that under certain conditions these calories do not have as much value for the body as those derived from other nutrients. In addition, many alcoholics suffer from malnutrition, which can lead to liver damage and impaired liver function. Many drinkers take in less than the recommended daily amount of carbohydrates, proteins, fats, vitamins (A, C, and B, especially thiamine [B1]), and minerals (such as calcium and iron).

To prevent these deficiencies, clinicians should provide alcoholics with a balanced diet. Dietary supplements may prevent or relieve some of alcohol's harmful effects. For example, brain damage resulting from a lack of vitamin B1, which can lead to conditions such as Wernicke-Korsakoff syndrome, can be reversed to some extent. Because vitamin B1 generally can be administered safely, clinicians often recommend that all alcoholics undergoing treatment receive 50 milligrams of thiamine per day (either by injection if the patients are hospitalized or by mouth). Alcoholics also should receive supplements of vitamins B2 (riboflavin) and B6 (pyridoxine) in dosages found in standard multivitamins. Vitamin A, however, can be toxic when combined with alcohol and should be given only to those alcoholics who have a well-documented deficiency and who can stop or significantly reduce their drinking.

In addition to dietary supplements, alcoholics with moderate malnutrition might benefit from treatment with anabolic steroids. These compounds, which are derived from the male hormone testosterone, can be used in the short term to promote overall body "buildup" and, therefore, may help the alcoholic better recover from malnutrition.

About the Author

NIH is the nation's medical research agency - making important medical discoveries that improve health and save lives. The National Institutes of Health (NIH), a part of the U.S. Department of Health and Human Services, is the primary Federal agency for conducting and supporting medical research.