U.S. Department of Health

& Human Services 

National Institutes of Health 

National Institute on Alcohol Abuse 

and Alcoholism 

Number 64 January 2005 

ALCOHOLIC LIVER 

DISEASE 

The liver is one of the largest and most complex organs 

in the body. It stores vital energy and nutrients, manufactures proteins and enzymes necessary for good health, 

protects the body from disease, and breaks down (or 

metabolizes) and helps remove harmful toxins, like 

alcohol, from the body. 

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 (1). Patients 

“Because the liver is the chief organ responsible
 with alcoholic hepatitis 

who stop drinking may for metabolizing alcohol, it is especially 
 have a complete recovery 

from liver disease, or vulnerable to alcohol-related injury. they still may develop ” cirrhosis. 
“ Liver cirrhosis is a major cause of death


in the United States.”


Liver cirrhosis is a major cause of death in the United 

States (2,3). 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 (4). 

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 (5). 

Women are at higher risk than men for developing 

cirrhosis (6). 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 (7)—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 (8). 

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 (9). 

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 

(9), 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 (10,11). 

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 

(12,13). 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. 

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 

(14). In addition, many alcoholics suffer from malnutrition, which can lead to liver damage and impaired 

liver function (15). 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 

2

H C AND A

References 

(2) Coelho-Little, M.E.; 

19(5):1173–1176, 1995. 

C.L.; 

14:581–589, 1991. 

(5) Schiff, E., 

27(3):232–239, 2003. 

17(8):1031–1037, 2003. 

31(6):1207–1211, 2000. 

EPATITIS LCOHOL 

Hepatitis C is a liver disease caused by the hepatitis C virus (HCV). People usually become infected after 

coming in contact with blood from an infected person. Sharing needles or other equipment for injecting 

drugs is the most common way of spreading HCV. The disease also can be spread by sexual contact. About 

4 million people in the United States have HCV, and between 10,000 and 12,000 die each year (1). 

HCV infection is particularly common in alcoholics with liver disease (2–4). Heavy alcohol consumption 

accelerates patients’ progression from chronic HCV to cirrhosis (a condition in which fibrous scar tissue 

replaces healthy liver tissue) and liver cancer (specifically, hepatocellular carcinoma, the most common form 

of liver cancer) (5). Although fewer studies have examined the effects of moderate drinking on the course of 

liver disease in HCV patients, there is some indication that alcohol consumption in the moderate-to-heavy 

range may increase HCV-infected patients’ risk of developing liver fibrosis and cirrhosis (6). Research on 

whether gender has any effect on the connection between alcohol consumption and liver disease progression 

in HCV patients is very limited. 

Treatment Recommendations—Blood tests can diagnose HCV infection, either by detecting antibodies to the 

virus or by detecting the presence and quantity of the virus’s genetic material itself (7). There currently is no vaccine 

for hepatitis C. The standard treatment includes the use of antiviral treatment (interferon-alfa with ribavirin) (7). 

Strict abstinence from alcohol is important during treatment, as heavy drinking during treatment has been 

shown to hinder patients’ responses to therapy (8). In addition, depression, irritability, and anxiety—side 

effects that occur in 20 to 30 percent of patients who receive interferon treatment—may be especially difficult to manage in patients with a history of alcoholism, perhaps putting them at greater risk for relapsing to 

drinking (9). Thus, for treatment to be most successful, clinicians recommend that alcoholic patients 

abstain from drinking alcohol at least 6 months prior to beginning interferon therapy. Light-to-moderate 

drinkers can begin treatment immediately and do not need a period of abstinence before starting therapy. 

(1) National Institute of Diabetes and Digestive and Kidney Diseases. Chronic Hepatitis C: Current Disease Management. Online at: http://digestive.niddk.nih.gov/ddiseases/pubs/chronichepc/index.htm. Accessed 2003. Jeffers, L.J.; Bernstein, D.E.; et al. Hepatitis C virus in 

alcoholic patients with and without clinically apparent liver disease. Alcoholism: Clinical and Experimental Research (3) Mendenhall, 

Seeff, L.; Diehl, A.M.; et al. Antibodies to hepatitis B virus and hepatitis C virus in alcoholic hepatitis and cirrhosis: Their prevalence and clinical relevance. The VA Cooperative Study Group (No. 119). Hepatology (4) Takase, S.; Takada, N.; Sawada, M.; et al. Relationship between 

alcoholic liver disease and HCV infection. Alcohol and Alcoholism (Suppl. 1A):77–84, 1993. and Ozden, N. Hepatitis C and alcohol. Alcohol 

Research & Health (6) Hézode, C.; Lonjon, I.; Roudot-Thoraval, F.; et al. Impact of moderate alcohol consumption on histological 

activity and fibrosis in patients with chronic hepatitis C, and specific influence of steatosis: A prospective study. Alimentary Pharmacology and Therapeutics 

(7) National Institutes of Health. National Institutes of Health Consensus Development Conference statement: Management of 

hepatitis C: 2002—June 10–12, 2002. Hepatology 36(5 Suppl. 1):S3–20, 2002. (8) Mochida, S.; Ohnishi, K.; Matsuo, S.; et al. Effect of alcohol intake on 

the efficacy of interferon therapy in patients with chronic hepatitis C as evaluated by multivariate logistic regression analysis. Alcoholism: Clinical and 

Experimental Research 20(Suppl. 9):371A–377A, 1996. (9) Zdilar, D.; Franco-Bronson, K.; Buchler, N.; et al. Hepatitis C, interferon alfa, and depression. 

Hepatology 

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 (15). 

In addition to dietary supplements, alcoholics with 

moderate malnutrition might benefit from treatment 

with anabolic steroids (16). 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. 

Emerging Therapies—Studies using animals are helping researchers find other dietary supplements that may 

help in the treatment of liver disease. For example, eating 

certain healthy fats (called medium-chain triglycerides, 

or MCTs) may help to reduce the buildup of harmful 

3

fats in the liver (17,18). MCTs generally are available 

only in health food stores as a dietary supplement. 

Oxidative stress plays a major role in the development 

of alcoholic liver disease. Oxidative stress occurs when 

harmful oxygen molecules, or free radicals, form in 

the body. These molecules are highly charged and very 

unstable. They cause cellular changes in their effort to 

pair with the nearest available molecule, injuring cells 

and modifying their function. Antioxidants can help 

prevent this free radical damage. 

An important antioxidant, glutathione, or GSH, cannot be used as a supplement because this substance 

cannot directly enter the cells threatened by oxidative 

stress. However, researchers are using a precursor compound, the molecule S-adenosylmethionine (SAMe), 

which can enter the cells and then break down to form 

the helpful antioxidant. When SAMe was given to 

patients with alcoholic cirrhosis in a clinical trial, they 

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. 

were significantly less likely to die or require a liver 

transplant within the next 2 years, compared with 

patients who had received an inactive substance (that 

is, a placebo) (19). Moreover, the study detected virtually no harmful side effects of SAMe treatment. Thus, 

this approach appears to hold promise for the treatment of patients with ALD (20). 

Pharmacological Therapy—No FDA-approved therapy exists for either alcoholic cirrhosis or alcoholic hepatitis. However, several drugs have been used “off label,” 

including pentoxifylline (PTX) and corticosteroids. 

PTX was shown to be effective in patients with severe 

alcoholic hepatitis. Akriviadis and colleagues (21) treated 49 patients with PTX and 52 patients with placebo 

(vitamin B12) for 4 weeks and found that PTX improved 

survival: 12 PTX patients died (24.5 percent), compared with 24 placebo patients (46 percent). 

Although corticosteroids are the most extensively studied 

form of therapy for alcoholic hepatitis, their usefulness 

may be only short-term. Mathurin and colleagues (22) 

reported significantly improved survival at 28 days (85 

percent vs. 65 percent) in severely ill alcoholic hepatitis 

patients, but this survival advantage did not extend 

much longer than a year. Most investigators agree that 

if corticosteroids are used, they should be reserved for 

patients with the most severe liver disease. In addition, 

steroids have well-documented side effects, including 

increasing the risk of infection, which already is substantial in patients with alcoholic hepatitis (9). 

Transplantation 

Liver transplantation currently is the only definitive 

treatment for severe (end stage) liver failure. A total 

of 41,734 liver transplants using organs from cadavers 

were performed in the United States between 1992 

and 2001 (23). Of these, 12.5 percent were performed 

in patients with ALD, and 5.8 percent were performed 

in patients with ALD and a concurrent infection with 

the hepatitis C virus (HCV), making ALD the second 

most frequent reason (after HCV infection alone) for 

transplantation (24). 

ALD patients must undergo a thorough evaluation to 

determine whether they are suitable candidates for 

transplant. This screening addresses any coexisting 

medical problems, such as heart damage, cancer, pancreatitis, and osteoporosis, which might influence the 

outcome of the transplant. It includes a psychological 

evaluation to identify those patients who are most 

likely to remain abstinent and comply with the strict 

medical regimen that follows the procedure (24). 

For transplantation to be successful in alcoholic 

patients it is essential that they remain abstinent after 

the surgery and comply with a demanding medical 

regimen (e.g., consistently take the necessary antirejection medications). Routinely conducting psychiatric 

evaluations before patients are included on the list of 

candidates for transplantation helps to identify those 

who may not be able to meet these criteria (24). 

Because of the shortage of donated organs, transplantation to patients with alcoholic liver disease remains controversial, mainly out of concern that the transplanted 

liver could be “wasted” if a patient relapses to drinking 

and damages the new liver as well. Yet the relapse rates 

in patients following transplant are lower than in patients 

undergoing alcoholism treatment, and serious relapses 

4

that adversely affect the transplanted liver or the patient 

are uncommon. In contrast, patients who receive a 

transplant because of an infection with hepatitis B or C 

viruses typically experience disease recurrence and are 

more likely to lose the transplanted liver because of 

recurrence of these infections (24). 

Another concern is that patients with ALD will not be 

able to comply with the antirejection medication regimen, but this has not been supported by research. 

Liver rejection rates are similar for patients transplanted for ALD and those transplanted for other types of 

liver disease, indicating comparable rates of compliance with the antirejection medications. Finally, it was 

believed that ALD patients would use more resources, 

thereby incurring higher costs than non-ALD patients, 

but again this assumption has not been corroborated 

by research evidence (25). 

In contrast to these negative assumptions on the use of 

liver transplants in ALD patients, many clinicians contend 

that ALD is, in fact, an excellent reason for liver transplantation. The overall improvement in patients with 

ALD after transplant, including higher productivity and 

better quality of life, supports considering these patients 

for liver transplants. Moreover, the long-term costs of 

transplantation and subsequent management of the alcoholic patient may well be lower than the costs of managing alcoholism and ALD without transplantation (26). 

Summary 

The liver is one of the largest organs in the body. It performs many of the vital functions necessary for maintaining good health. The liver is remarkably resilient in 

responding to disease and infection and, in fact, under 

certain circumstances, can even generate whole new sections of itself to replace those that are diseased. 

Alcohol is a toxin that is especially harmful to the 

liver, and alcoholic liver disease—particularly cirrhosis—is one of the leading causes of alcohol-related 

death. Not everyone who drinks heavily will develop 

ALD. Other factors besides alcohol also influence 

development of the disease, including demographic, 

biological, and environmental factors. Nevertheless, 

stopping drinking can help to alleviate or even reverse 

ALD, especially in the early stages of disease. 

Treatment for ALD includes making lifestyle changes, 

such as stopping or decreasing alcohol use, stopping 

smoking, and maintaining a healthy weight. Health care 

providers may prescribe medications, such as pentoxifylline or prednisone, in cases of alcoholic hepatitis. 

And patients may want to seek nutritional supplements or complementary and alternative medicine, 

such as SAMe for cirrhosis. Severe ALD is best treated 

with transplantation in selected abstinent patients. 

References 

(1) Bird, G.L., and Williams, R. Factors determining cirrhosis in alcoholic liver disease. Molecular Aspects of Medicine 10(2):97–105, 1988. (2) Yoon, Y.-H.; Yi, H.; 

Grant, B.F.; et al. Surveillance Report No. 60: Liver Cirrhosis Mortality in the United 

States, 1970–99. Washington, DC: National Institute on Alcohol Abuse and 

Alcoholism, 2002. (3) Minino, A.; Arias, E.; Kochanek, K.D.; et al. Deaths: Final 

data for 2000. National Vital Statistics Reports 50:1–107, 2002. (4) Mann, R.E.; 

Smart, R.G.; and Govoni, R. The epidemiology of alcoholic liver disease. Alcohol 

Research & Health 27(3):209–219, 2003. (5) Jones-Webb, R. Drinking patterns and 

problems among African-Americans: Recent findings. Alcohol Health & Research 

World 22(4):260–264, 1998. (6) Tuyns, A.J., and Péquignot, G. Greater risk of 

ascitic cirrhosis in females in relation to alcohol consumption. International Journal 

of Epidemiology 13:53–57, 1984. (7) Frezza, M.; Di Padova, C.; Pozzato, G.; et al. 

High blood alcohol levels in women: The role of decreased gastric alcohol dehydrogenase activity and first-pass metabolism. New England Journal of Medicine 

322:95–99, 1990. (8) Ramchandani, V.A.; Bosron, W.F.; and Li, T.K. Research 

advances in ethanol metabolism. Pathologie Biologie 49:676–682, 2001. (9) Marsano, 

L.S.; Mendez, C.; Hill, D.; et al. Diagnosis and treatment of alcoholic liver disease 

and its complications. Alcohol Research & Health 27(3):247–256, 2003. (10) Powell, 

W.J., Jr., and Klatskin, G. Duration of survival in patients with Laennec’s cirrhosis. 

Influence of alcohol withdrawal, and possible effects of recent changes in general 

management of the disease. American Journal of Medicine 44(3):406–420, 1968. (11) 

Merkel, C.; Marchesini, G.; Fabbri, A.; et al. The course of galactose elimination 

capacity in patients with alcoholic cirrhosis: Possible use as a surrogate marker for 

death. Hepatology 24(4):820–823, 1996. (12) Klatsky, A.L., and Armstrong, M.A. 

Alcohol, smoking, coffee, and cirrhosis. American Journal of Epidemiology 

136(10):1248–1257, 1992. (13) Corrao, G.; Lepore, A.R.; Torchio, P.; et al. The 

effect of drinking coffee and smoking cigarettes on the risk of cirrhosis associated with 

alcohol consumption. A case-control study. European Journal of Epidemiology 

10(6):657–664, 1994. (14) Pirola, R.C., and Lieber, C.S. The energy cost of the 

metabolism of drugs including ethanol. Pharmacology 7:185–196, 1972. (15) Lieber, 

C.S. Relationships between nutrition, alcohol use, and liver disease. Alcohol Research 

& Health 27(3):220–231, 2003. (16) Mendenhall, C.; Roselle, G.A.; Gartside, P.; et 

al. Relationship of protein calorie malnutrition to alcoholic liver disease: A reexamination of data from two Veterans Administration Cooperative Studies. Alcoholism: 

Clinical and Experimental Research 19(3):635–641, 1995. (17) Nanji, A.A.; Yang, 

E.K.; Fogt, F.; et al. Medium-chain triglycerides and vitamin E reduce the severity of 

established experimental alcoholic liver disease. Journal of Pharmacology and 

Experimental Therapeutics 277:1694–1700, 1996. (18) Nanji, A.A.; Jokelainen, K.; 

Tipoe, G.L.; et al. Dietary saturated fatty acids reverse inflammatory and fibrotic 

changes in rat liver despite continued ethanol administration. Journal of 

Pharmacology and Experimental Therapeutics 299:638–644, 2001. (19) Mato, J.M.; 

Camara, J.; Fernandez de Paz, J.; et al. S-adenosylmethionine in alcoholic liver cirrhosis: A randomized, placebo-controlled, double-blind multicenter clinical trial. 

Journal of Hepatology 30(6):1081–1089, 1999. (20) Lieber, C.S. S-adenosylmethionine (SAMe): Its role in the treatment of liver disorders. American Journal of Clinical 

Nutrition 76:1183S–1187S, 2002. (21) Akriviadis, E.; Botla, R.; Briggs, W.; et al. 

Pentoxifylline improves short-term survival in severe acute alcoholic hepatitis: A doubleblind, placebo-controlled trial. Gastroenterology 119(6):1637–1648, 2000. (22) 

Mathurin, P.; Mendenhall, C.L.; Carithers, R.L., Jr.; et al. Corticosteroids improve 

short-term survival in patients with severe alcoholic hepatitis (AH): Individual data 

analysis of the last three randomized placebo controlled double blind trials of corticosteroids in severe AH. Journal of Hepatology 36(4):480–487, 2002. (23) United 

Network for Organ Sharing (UNOS). Public data from UNOS/OPTN scientific 

registry. Accessed December 2002. Available at http://www.unos.org. (24) 

Anantharaju, A., and Van Thiel, D.H. Liver transplantation for alcoholic liver disease. Alcohol Research & Health 27(3):257–269, 2003. (25) Campbell, D.A., Jr., and 

Lucey, M.R. Liver transplantation for alcoholic cirrhosis. In: Busuttil, R.W., and 

Klintmalm, G.B., eds. Transplantation of the Liver, 1st ed. Philadelphia: W.B. 

Saunders, 1996. pp. 145–150. (26) Keeffe, E.B. Comorbidities of alcoholic liver 

disease that affect outcome of orthotopic liver transplantation. Liver 

Transplantation and Surgery 3:251–257, 1997. 

5

Alcohol Research & Health, 

Alcohol Research & Health 

Back issues of Alcohol Research & Health and 

▲ 

R e s o u r c e s 

Source material for this Alcohol Alert originally 

appeared in the journal 

“Alcoholic Liver Disease: Part I, An Overview” 

and “Alcoholic Liver Disease: Part II, Mechanisms 

of Injury” (Vol. 27, Nos. 3 and 4, 2003). 

is the quarterly, 

peer–reviewed journal published by the National 

Institute on Alcohol Abuse and Alcoholism. Each 

issue provides in-depth focus on a topic in the 

field of alcohol research. 

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