Skip Navigation
 
 
 
 
 
Print This Page
Share this page: More
 

FAQs about Alcoholic Liver Disease

What is alcoholic liver disease (ALD)?
ALDis the development of liver damage as a result of heavy alcohol consumption. This damage may occur in three patterns: fatty liver (an abnormal accumulation of fat in the structural cells of the liver), alcoholic hepatitis (inflammation of the liver caused by the toxic effect of alcohol) and cirrhosis (progressive destruction and regeneration of liver cells with fibrotic connective tissue).

What causes ALD?
Heavy alcohol consumption (20-40 grams of ethanol per day) is the major cause of ALD.

There is emerging evidence that heredity may influence the development of ALD. The genetic basis is yet unknown, but advances in molecular biology have aided the study of patients with ALD and may identify the specific genes that increase susceptibility.

Other risk factors for ALD include nutrition and environmental variables. It has been demonstrated that high-calorie, high-protein diets improve the clinical signs and symptoms of ALD even in patients who continue to drink more than 60 grams of ethanol per day.

What is the incidence of ALD?
There is a 7 percent incidence of alcoholism in the United States. Alcohol dependence and/or abuse rates are higher in white males than in women, although women develop ALD more rapidly than men with the same quantity and duration of alcohol consumption. Black men, although not in the highest incidence rates of alcoholism, tend to have a higher rate of cirrhosis.  

What are the symptoms of ALD?
Some patients with ALD may be asymptomatic while others may present with a wide range of symptoms such as nausea, dry retching, diarrhea, anorexia, right upper quadrant pain, prominent vascular spiders, liver enlargement and tenderness. Others may seek medical attention because of the effects of alcoholism that may include accidents, violent behavior, depression, tremors, poor work performance or inappropriate social behaviors.  

What is "fatty liver"?
Fatty liver is an abnormal accumulation of fat (small or large droplets) in the cytoplasm of liver cells and may often be accompanied by fibrosis. Fatty liver is present in approximately 90 to 100 percent of heavy drinkers (who consume more than 80 grams of alcohol per day over a five-year period). Palpable liver enlargement is also characteristic of fatty liver and is present in about 90 percent of these patients. Conditions other than heavy alcohol consumption may also cause fatty liver.

What is alcoholic hepatitis and how is it diagnosed?
Alcoholic hepatitis is an inflammation of the liver characterized by necrosis and fibrotic scarring. The definitive diagnosis of alcoholic hepatitis is made by liver biopsy. Other considerations in diagnosis include a history of chronic or current heavy alcohol consumption, an enlarged liver and blood enzyme analysis. Patients with alcoholic hepatitis may present with anorexia, nausea, jaundice and weight loss.

Alcoholic hepatitis has a variable prognosis, dependent upon on the severity and the presence or absence of cirrhosis. About 10 to 15 percent of patients with alcoholic hepatitis have fulminant disease with a high mortality rate. Another 5 to 10 percent develop a prolonged illness resulting in death.  

What is alcoholic cirrhosis?
Alcoholic cirrhosis is a liver disease, characterized by widespread destruction and regeneration of liver tissue with marked increase in fibrotic connective tissue. The regenerated liver tissue forms nodules and permanently alters the structure of the liver. The scarring and increased connective tissue results in impairment of liver function. Continued necrosis (death) and fibrosis result in a progressive deterioration and ultimately end-stage liver disease.  

Which tests and/or procedures are performed to diagnose ALD?
Blood tests are useful in the determination of ALD. Blood tests can establish alcohol as the cause of the disease but cannot determine the seriousness of the illness. Aminotransferase abnormalities are usually indicative of ALD. These are AST, ALT and AST/ALT ratios. There is increased serum activity of gamma glutamyl transpeptidase (GGTP) in chronic alcohol users. Sixty percent of alcoholics have elevated GGTP in combination with elevated AST levels. Serum electrolytes, mean corpuscular volume (MCV) and serum uric acid levels are also indicative of ALD in combination with results from other tests. Prothrombin time (ability of the blood to clot) may be indicative of mild hepatic disease, but may be present in hepatic failure.

Liver biopsy is not always necessary to confirm the diagnosis of ALD, but is the most sensitive measure of disease stage and is useful in predicting the disease course.

Abdominal ultrasound and CT scanning may also be performed. Abdominal ultrasound is useful in the assessment of fatty content of the liver. CT scanning detects cirrhosis, portal hypertension and tumors. 

What is a liver biopsy and will such a procedure require hospitalization?
A liver biopsy is usually performed as an outpatient in a hospital or a GI clinic. The patient is instructed to have nothing by mouth for at least six hours prior to the procedure. After a sedative and local anesthetic is administered, a needle is inserted through the skin and into the body of the liver. Small pieces of liver tissue are extracted for microscopic examination. A pressure dressing is applied to the site. The patient is monitored for signs and symptoms of bleeding during and usually discharged within 3 to 6 hours.  

How is ALD treated?
The most important aspect of treatment in ALD is the immediate and total abstinence from alcohol. It is also critical that the patient’s nutritional intake is adjusted to maintain a high-calorie, high-protein diet.
This does not need to be accomplished within the confines of a hospital, although efforts to enroll these patients in a detoxification program are clearly justified.

Hospitalization may be necessary for those patients who have extrahepatic complications or those with risks factors associated with acute liver-related mortality. Drugs may be used to treat the symptoms of withdrawal. Proteins and vitamin dietary supplements are prescribed. Vitamin B and K are administered. Potassium, magnesium and zinc are administered to those patients with decompensated liver disease.

Corticosteroids are prescribed for severely ill patients. This group of patients, with a high risk of mortality, has been found to have high levels of circulating pro-inflammatory cytokines. These are blocked by steroids, which have an anti-inflammatory effect. Pentoxifylline prevents worsening of renal function in patients with severe alcoholic hepatitis.

Orthotopic liver transplantation improves survival rates in decompensated liver cirrhosis. Currently, ALD is the single most common indication for transplantation in adults in the United States. However, considering the scarcity of donors and the financial expenditure, most transplant centers require a documented period of abstinence from alcohol (usually six to 12 months).

What are the complications of ALD?
Complications of ALD are usually caused by the systemic complications of hepatic injury. These include portal hypertension, an obstruction of the normal blood flow through the liver and reduction in functional hepatocyte mass. These conditions may occur in those with alcoholic hepatitis or alcoholic cirrhosis and in other non-alcohol related liver diseases.

Portal hypertension results in an elevation in pressure throughout the vascular tree above the portal vein. This elevation in pressure may cause the formation of ascites (accumulation of serous fluid in the abdomen) and increased blood flow through alternative pathways resulting in the development of varices and hypersplenism. Spontaneous bacterial peritonitis may occur in the acutely ill cirrhotic patient.

Reduction in functional liver mass causes hepatic encephalopathy (mental dysfunction caused by an accumulation of nitrogenous wastes in the blood and brain), coagulopathy (dysfunctional clotting mechanism due to decreased synthesis of clotting factors) and hypoalbuminemia (decreased synthesis and hepatic secretion of albumin, a protein responsible for maintaining serum osmotic pressure). When albumin content is decreased, the water tends to move out of serum into the tissues (edema or swelling) or into the peritoneal space (area surrounding organs in the abdomen) or ascites.  

How are the complications of ADL treated?
The treatment for ascites is salt restriction and careful diuresis (fluid removal through the use of drugs that cause the patient to excrete large volumes of urine). Paracentesis (aspiration [removal] of fluid from the abdominal cavity) is reserved for symptomatic patients with tense ascites (respiratory distress, abdominal pain and early satiety).

Spontaneous bacterial peritonitis is treated with third-generation cephalosporins after analyzing paracentesis fluid.

Therapy for variceal bleeding includes prompt fluid replacement and medication to lower portal pressure. Endoscopic therapy may be employed to stop bleeding. Pitressin is a medication used for gastric varices while esophageal varices are usually managed by endoscopic variceal banding and/or sclerotherapy (intravariceal injection of a sclerosing agent). If endoscopic management fails then tamponade with a Sengstaken-Blakemore tube (a temporizing measure) or fluoroscopic embolization of the feeding vessel is done. Porto-systemic shunts can be placed to decrease the blood flow through the varices. Devascularization can be performed to eliminate the feeding variceal veins.

Hepatic encephalopathy is treated by correcting the precipitating event and by the administration of lactulose (a compound sugar that promotes the elimination of ammonia and amines). Neomycin (an antibiotic) may also be administered. It works by killing the intestinal bacteria that degrade proteins to ammonia and amines. Lactulose is not absorbed by the intestines.

Coagulopathy is treated by administration of subcutaneous vitamin K. Treatment of malnutrition and alcohol abstinence is used in conjunction with vitamin K therapy. Patients may be transfused with fresh frozen plasma as a temporary measure. Liver transplantation may ultimately be the only way to correct this problem.

Hypoalbuminemia can be treated with IV albumin replacement. Although this is a short-term, expensive treatment, it can help mobilize ascites and increase serum albumin. The recommended treatment for hypoalbuminemia is good nutrition and abstinence from alcohol. In chronic alcoholics with end-stage liver disease, liver transplantation is the only therapy.  

What lifestyle changes will I need to make?
The most important lifestyle change is total abstinence from alcohol. Disulfiram or naltrexone may be prescribed (drugs that help the patient abstain from drinking). They should be used in combination with extensive counseling. Good nutritional support is also important. Hepatic improvement may occur if alcohol consumption is reduced when accompanied by nutritional supplementation.

 

Employee Intranet

 

Traveling for care?

blue suitcase

Whether crossing the country or the globe, we make it easy to access world-class care at Johns Hopkins.

Maryland 410-933-7495
U.S. 1-410-464-6713 (toll free)
International +1-410-614-6424

 

 

 
 
 
 
 

© The Johns Hopkins University, The Johns Hopkins Hospital, and Johns Hopkins Health System. All rights reserved.

Privacy Policy and Disclaimer