Alcoholic liver disease (ALD) is a serious and potentially fatal consequence of alcohol use. The diagnosis of ALD is based on drinking history, physical signs and symptoms, and laboratory tests. Treatment strategies for ALD include lifestyle changes to reduce alcohol consumption, cigarette smoking, and obesity; nutrition therapy; and pharmacological therapy. The diagnosis and management of the complications of ALD are important for alleviating the symptoms of the disease, improving quality of life, and decreasing mortality.

The liver is one of the largest and most complex organs in the body. It performs multiple functions, including the production of proteins and enzymes, detoxification, metabolic functions, and the regulation of cholesterol and blood clotting. Because the liver is primarily responsible for alcohol metabolism, it is especially vulnerable to alcohol-related injury.

Alcoholic liver disease (ALD) is a serious and potentially fatal consequence of drinking alcohol. ALD encompasses three conditions: fatty liver, alcoholic hepatitis, and cirrhosis. Fatty liver (steatosis), the most common alcohol-induced liver disorder, is marked by the excessive accumulation of fat inside the liver cells. Alcoholic hepatitis is inflammation and more severe injury of the liver, in which the body's immune system responds to and causes liver damage. In cirrhosis, normal liver cells are replaced by scar tissue (fibrosis), and consequently the liver is unable to perform many of its usual functions.

Cirrhosis and alcoholic hepatitis often coexist and cause substantial morbidity and mortality. For example, studies from the Department of Veterans Affairs (VA) demonstrate that patients with both cirrhosis and alcoholic hepatitis have a death rate of greater than 60 percent over a 4-year period, with most of the deaths occurring in the first year. Thus, the mortality rate for ALD is greater than that of many common types of cancer such as colon, breast, and prostate. This article examines the issues of diagnosing and treating ALD and the complications of this disease.

Diagnosis of Alcoholic Liver Disease (ALD)

The diagnosis of ALD is established by a history of habitual alcohol intake of sufficient duration and quantity, together with physical signs and laboratory evidence of liver disease. Alcohol dependence is not a prerequisite for the development of ALD, and ALD can be difficult to diagnose because patients frequently minimize or deny alcohol abuse. In addition, there may be no evidence of ALD from the physical exam, and laboratory abnormalities may not specifically point to ALD.

Ambulatory patients with alcoholic fatty liver often are asymptomatic. Patients with alcoholic hepatitis may be asymptomatic, have only enlarged liver (hepatomegaly), or have full-blown alcoholic hepatitis with tender hepatomegaly, jaundice, fever, accumulation of fluid in the abdominal cavity (ascites), nervous system effects such as confusion and personality change (hepatic encephalopathy), anorexia, and fatigue. Other signs may include high white blood cell counts resembling those seen in leukemia (leukemoid reactions) and the rapid deterioration of kidney function (hepatorenal syndrome). Even in the absence of cirrhosis, the main vein that brings blood from the intestine and stomach into the liver (the portal vein) may come under increased pressure because of scarring of the liver, resulting in portal vein hypertension.

Ten to 20 percent of patients with alcoholic hepatitis develop cirrhosis, and up to 70 percent of alcoholic hepatitis patients go on to develop cirrhosis each year. Women are at higher risk for developing cirrhosis, as are people who continue drinking or have severe alcoholic hepatitis. Some patients with alcoholic hepatitis who abstain still may develop cirrhosis, but others will have complete clinical and histologic recovery.

Patients with early stage alcoholic cirrhosis with no complications (well-compensated) may be asymptomatic and have normal physical exams and normal routine blood tests of liver function and injury. In other patients, alcoholic fatty liver or alcoholic hepatitis often coexist and may be accompanied by hepatomegaly, an enlarged spleen (splenomegaly), or both. In cirrhotics with severe alcoholic hepatitis, hepatomegaly or splenomegaly may be the dominant feature; in other patients, the signs and symptoms of portal vein hypertension (ascites and engorged veins [varices] in the esophagus) may predominate. As the disease advances, the liver decreases in size, the left hepatic lobe becomes more prominent, and the entire liver has a hard and nodular consistency. Splenomegaly of varying degrees is frequent.

Tags: Alcoholism

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