eMedicine Specialties > Gastroenterology > Liver

Alcoholic Fatty Liver

Mohammad K Ismail, MD, Assistant Professor, Department of Internal Medicine and Gastroenterology, University of Tennessee at Memphis
Caroline Riely, MD, Professor, Departments of Medicine and Pediatrics, University of Tennessee Health Science Center

Updated: Sep 15, 2008

Introduction

Background

Pathologic changes observed in patients with alcohol-induced liver disease can be divided into the following 3 groups: alcoholic fatty liver (simple steatosis), alcoholic hepatitis, and alcohol-related cirrhosis. Alcoholic fatty liver is an early and reversible consequence of excessive alcohol consumption.

See related CME at Advances in Alcoholic Liver Disease and NAFLD.

Pathophysiology

The amount of fatty acid in the liver depends on the balance between the processes of delivery and removal. Fatty liver develops in every individual who consumes more than 60 g/d of alcohol. Many mechanisms of ethanol-induced fatty liver have been proposed. Increased hepatic levels of glycerol 3-phosphate (3-GP) following ethanol ingestion are related to an increase in the ratio of nicotinamide adenine dinucleotide, reduced form, (NADH) to nicotinamide adenine dinucleotide (NAD) in the liver. Increasing concentration of 3-GP results in enhanced esterification of fatty acids.

An increased level of free fatty acids also has been incriminated in the pathogenesis of fatty liver. Large amounts of alcohol enhance lipolysis because of the direct stimulatory effect on the adrenal and pituitary axis. In addition, chronic ingestion of ethanol inhibits the oxidation of fatty acids in the liver and the release of very low-density lipoprotein (VLDL) into the blood. All of these mechanisms favor steatosis. Centrilobular localization of steatosis results from decreased energy stores from relative hypoxia and a shift in lipid metabolism, along with a shift in the redox reaction caused by the preferential oxidation of alcohol in the central zone.

Advancement in the understanding of the pathogenesis of alcoholic steatosis provided some novel insights, including the role of peroxisome proliferator-activated receptor alpha, which is crucial for the regulation of hepatic fatty acid metabolism. Its blockade, in animal models, along with ethanol consumption, contributes to the development of alcoholic fatty liver. In addition, induction of adiponectin, a hormone secreted by adipocytes, has been implicated in the protective action of saturated fat against the development of alcoholic fatty liver in mice.

Recent developments in the understanding of the pathogenesis of fatty liver provided the findings described below.

The role of the early growth response-1 (EGr-1) transcription factor is thought to be essential for ethanol-induced fatty liver injury in mice. Hepatocyte death by apoptosis occurs in alcoholic fatty liver and has been demonstrated in rats and mice after ethanol feeding. This may be related to mitochondrial proteins that regulate apoptosis and necrosis and that are shown to be induced in mouse fatty liver models.

Serum leptin, a cytokine-type peptide hormone mainly produced by adipocytes, may play an important role in the pathogenesis of steatosis. Steatosis occurs with decreased leptin action, whether due to leptin deficiency or resistance. In a recent study in patients with alcoholic liver disease, serum leptin was noted to be independently correlated with the grade of steatosis.

Recent data from both animal studies and clinical studies support the role of proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha) in the early stage of fatty liver as well as alcoholic steatohepatitis.

Frequency

United States

Approximately 15.3 million people in United States abuse or depend on alcohol. Fatty liver develops in 90-100% of patients with heavy alcohol use.

International

One observational study from northern Italy demonstrated prevalence rates of steatosis in 46.4% of heavy drinkers (>60 g/d of alcohol) and in 94.5% of obese heavy drinkers.

Mortality/Morbidity

Simple steatosis rarely is fatal. With complete abstinence, histologic changes can return to normal within 2-4 weeks.
Continued alcohol consumption may result in more advanced forms of liver disease, either alcoholic hepatitis or cirrhosis.
A study from Denmark, which used the Danish National Registry, noted an increase in mortality among patients with a hospital discharge diagnosis of alcoholic fatty liver, which remained increased after censoring patients upon a diagnosis of cirrhosis.

Race

Very little data are available on racial differences in the incidence of alcoholic fatty liver. However, overall differences in alcoholic liver disease have been noted in various studies.

One study of 42,862 US adults showed differences in drinking patterns among different races. Whites were the most likely to drink, but blacks had the highest volume of intake and frequency of heavy drinking.
Another study showed a higher rate of cirrhosis among blacks.

Sex

Women develop more severe alcoholic liver disease (ALD) more quickly and at lower doses of alcohol than men.
Increased susceptibility of females possibly is related to sex-dependent differences in the hepatic metabolism of alcohol, cytokine production, and the gastric metabolism of alcohol.

Age

The liver handles alcohol differently with age, and alcohol toxicity increases with age because of increased organ susceptibility. This is thought to be related to a mitochondrial transport defect with age as well as decreased function of the smooth endoplasmic reticulum and metabolism of CYP2E1-dependent microsomal ethanol oxidation.

Clinical

History

Alcohol-induced steatosis usually is asymptomatic in ambulatory patients.

Fatty liver occurs commonly after the ingestion of a moderate or large amount of alcohol, even for a short period of time.
A thorough clinical history, especially with regard to the amount of alcohol consumption, is essential to determining the role of alcohol in the etiology of the abnormal liver test results. History obtained from the family members may reveal past alcohol-related problems.
No specific test is available to rule out drug-related toxicity, but a good review of all concurrent and recent medications, including over-the-counter medications and alternative treatments, is essential in evaluating the possible causes of abnormal liver test results.
Severe fatty infiltration of the liver can result in symptoms of malaise, weakness, anorexia, nausea, and abdominal discomfort.
Jaundice is present in 15% of patients admitted to the hospital because of these symptoms of fatty infiltration of the liver.

Physical

Fatty liver may be present in the absence of any abnormalities noted on the physical examination.

Hepatomegaly is common in patients who are hospitalized, occurring in over 70% of persons with steatosis proven on biopsy.
Portal hypertension is rare in alcoholic steatosis.

Causes

Several risk factors may be cofactors required for the development of advanced ALD.
Minimum amounts of alcohol intake associated with an increased risk for developing ALD range from 40-80 g/d for 10-12 years.
Genetics play a role in alcohol consumption and alcoholism. In addition, early data suggested a genetic predisposition to the development of ALD mostly related to differences in major hepatic enzymes involved in the metabolism of alcohol—alcohol dehydrogenase (ADH), acetaldehyde dehydrogenase (ALDH), and cytochrome P-450 system (CYP4502E1).
Several studies demonstrate a high prevalence of hepatitis C virus (HCV) antibody in patients with ALD, as well as iron overload.
Obesity and dietary habits have been implicated in individual susceptibility to ALD.

Differential Diagnoses

Workup

Laboratory Studies

Abnormal levels of aminotransferases and bilirubin are found in about one third of hospitalized patients with alcohol-induced steatosis. In such patients, elevated bilirubin levels largely result from an increase in the indirect reacting fraction and may reflect alcohol-associated hemolysis.
Levels of aspartate aminotransferase (AST) usually are higher than alanine aminotransferase (ALT). The absolute values of serum AST and ALT almost always are less than 500 IU/L.
An increase in levels of glutamyl transpeptidase (GGT) may be related to alcohol use, but this study lacks specificity and sensitivity, and as many as 70% of people who abuse alcohol have normal values.
In rare instances, patients with alcoholic steatosis have severe cholestasis.
- Ballard et al (1961) described 5 patients with alcoholic steatosis presenting with jaundice.¹ Liver biopsy results in all 5 patients showed severe steatosis and marked cholestasis with little hepatic fibrosis. Hepatic failure characterized by progressive encephalopathy and coagulopathy developed and led to death in 2 of the patients.
- In a large cooperative study of ALD conducted by the Department of Veteran Affairs (VA), histologic cholestasis was observed in only 19% of patients with alcoholic steatosis.
Other laboratory findings in patients with alcohol liver disease are described below.
- Macrocytosis (increased mean cell volume) is common in patients with alcoholic liver disease, with a low sensitivity (27-52%) and a high specificity (85-91%).
- Serum carbohydrate-deficient transferrin (CDT) is a specific and sensitive test for alcoholism in patients with alcohol intake of more than 60 g/d.
- Hypertriglyceridemia, steatosis, and hemolysis (Zieve syndrome) may be associated with alcohol abuse.
Order viral serologies for hepatitis C, iron levels, and total iron-binding capacity (TIBC), and evaluate abnormal results from liver function tests as indicated.

Imaging Studies

Ultrasound, computed tomography scan, and MRI are useful in helping to establish a diagnosis of steatosis, as well as in finding evidence for portal hypertension; however, these tests can neither define its cause nor exclude associated steatohepatitis.
Fatty liver appears diffusely echogenic on ultrasound.
These imaging tests are also helpful in ruling out biliary dilation from other disorders, such as choledocholithiasis, in patients with cholestatic pattern of liver test result abnormalities.

Procedures

Liver biopsy is an important component in the diagnostic evaluation in patients with suspected alcoholic liver disease.
Liver biopsy is the most sensitive and specific means of evaluating the degree of liver cell injury and hepatic fibrosis.
Several reasons justify obtaining a liver biopsy in patients with ALD. Reasons include confirming the diagnosis, excluding other unsuspected causes of liver disease, assessing the extent of liver damage, and defining prognosis.
When deciding to perform a biopsy, consider the strength of the clinical diagnosis and the role that the biopsy findings would have in guiding therapeutic options.

Histologic Findings

Histologically, fatty liver is characterized by fat accumulation, which is most prominent in the pericentral (centrilobular) zone. Macrovesicular steatosis is the rule; hepatocytes containing one or more large fat droplets displace the nucleus to an eccentric position. Occasional lipid release from rupture of distended hepatocytes may produce a mild localized inflammatory response (lipogranulomas) composed predominantly of macrophages and occasional lymphocytes. Although infiltration of liver with inflammatory cells is not prominent in patients with steatosis alone, in some instances, fibrosis around terminal venules (ie, perivenular fibrosis) and/or hepatocytes (ie, pericellular fibrosis) has been noted. Early changes observed with the electron microscope include accumulation of membrane-bound fat droplets, proliferation of smooth endoplasmic reticulum, and gradual distortion of mitochondria. Microvesicular steatosis also is being recognized with increasing frequency.

Alcoholic foamy degeneration (microvesicular fatty change) was the term used by Uchida et al (1983) to describe a clinical syndrome in people with chronic alcoholism.² The syndrome is characterized by jaundice and hyperlipidemia and is associated with striking microvesicular steatosis and abundant giant mitochondria observed on liver biopsy.

Treatment

Medical Care

No specific medical treatment is needed for patients with alcoholic fatty liver. Steatosis usually resolves within 2 weeks of discontinuing alcohol.
Abstinence and adequate diet are the mainstays in therapy for alcohol-induced steatosis.
Bed rest has no proven benefit.
Anabolic steroids may be detrimental.
Management of patients with alcoholism and fatty liver often requires recognition and treatment of alcohol withdrawal.
These patients may have deficiencies of vitamins, minerals, and trace elements. Adequate replacement of these deficiencies should be a part of management.
Although alcohol-induced hyperhomocysteinemia (which has been associated with endoplasmic reticulum stress leading to apoptosis and up-regulation of lipid synthesis) and its correction by betaine have been studied in animal models, no definite role of the use of betaine in alcoholic fatty liver in humans is available.

Consultations

Offer alcohol rehabilitation to all patients, with an understanding of the addictive problem of alcoholism.
Counsel patients on the detrimental effects of alcohol on the current liver problem and the likely progression to a more advanced form of liver disease with continued alcohol use.

Diet

No specific dietary restrictions are needed in patients with simple steatosis.
Protein-calorie malnutrition is a common finding for patients with ALD and is associated with major complications observed with cirrhosis. Consequently, recognizing and understanding the significance of malnutrition in these patients is very important.

Medication

No drug therapy is indicated for patients with alcoholic fatty liver unless the patient has alcoholic hepatitis.

Follow-up

Further Outpatient Care

Provide follow-up care for patients in an outpatient facility.
Determination of blood alcohol at every outpatient visit often is helpful in determining patient's compliance with abstinence.

Deterrence/Prevention

Almost all authorities agree that abstinence from alcohol improves survival and is the cornerstone of long-term management of patients with ALD.
Emphasize abstinence from alcohol early and continuously to optimize its beneficial effects. Abstinence improves histology, decreases portal hypertension, and decreases, but does not eliminate, development of cirrhosis.
Emphasize alcohol rehabilitation.

Complications

Continued alcohol consumption may result in a more advanced form of liver disease, either alcoholic hepatitis or cirrhosis.
In a study from Denmark, using a population-based National Registry, investigators noted an increased mortality and an increased cancer risk, particularly liver cancer, among patients discharged with a diagnosis of alcoholic fatty liver.

Prognosis

Alcoholic steatosis usually is considered a benign lesion with a favorable prognosis once alcohol consumption is discontinued.
Several prognostic factors have been described in the literature that may indicate advancement to more severe lesions in patients who continue to drink.

A study from England, for example, followed the cases of 88 patients with fatty liver for a mean of 10.5 years. Of these, 9 developed cirrhosis and 7 developed fibrosis. All but 1 of these 16 patients continued to use alcohol.
Histologic predictors of progression at the time of fatty liver included the presence of mixed macrovesicular/microvesicular fat and giant mitochondria.
Patients with alcoholic fatty liver have a high risk for development of cirrhosis and an increased mortality with the severity of steatosis in the index liver biopsy.
The presence of histologic cholestasis in association with alcoholic steatosis did not appear to be of prognostic significance in determining the risk of progression to cirrhosis.

Patient Education

Patient handouts are available for alcohol-related liver disease. These can be provided during inpatient or outpatient visit.
Patient family and social support play a central role in the patient's abstinence from alcohol.
Some important addresses and Web sites are provided below.
- Alcoholics Anonymous
  World Services, Inc
  PO Box 459
  New York, NY 10163
  Phone: 212-870-3400
  Web site: http://www.alcoholics-anonymous.org
- National Institute on Alcohol Abuse and Alcoholism
  5635 Fishers Lane, MSC 9304
  Bethesda, Maryland 20892-9304
  Web site: http://www.niaaa.nih.gov
- National Clearinghouse for Alcohol and Drug Information
  PO Box 2345
  Rockville, MD 20847-2345
  Phone: 800-729-6686
  Web site: http://ncadi.samhsa.gov/ (offers many publications on alcohol and substance abuse)
- National Council on Alcoholism and Drug Dependence, Inc
  22 Cortlandt Street, Suite 801
  New York, NY 10007-3128
  Phone: 800-NCA-CALL or 212-269-7797
  Web site: http://www.ncadd.org
For excellent patient education resources, visit eMedicine's Mental Health and Behavior Center, Liver, Gallbladder, and Pancreas Center, and Hepatitis Center. Also, see eMedicine's patient education articles Alcoholism, Hepatitis A, Hepatitis B, Hepatitis C, and Cirrhosis.

Miscellaneous

Medicolegal Pitfalls

Failure to consider differential diagnosis
Failure to be aware of the rare complication of severe fatty liver, as death has been reported from this benign disease

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Keywords

alcoholic fatty liver, alcoholic steatosis, alcoholism, fatty liver, alcohol-related fatty liver, alcoholic liver disease, alcohol-related liver disease, simple steatosis, alcohol-related steatosis, fatty acids, alcoholic complications, alcohol-induced steatosis, alcohol-induced fatty liver

Contributor Information and Disclosures

Author

Mohammad K Ismail, MD, Assistant Professor, Department of Internal Medicine and Gastroenterology, University of Tennessee at Memphis
Mohammad K Ismail, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Caroline Riely, MD, Professor, Departments of Medicine and Pediatrics, University of Tennessee Health Science Center
Caroline Riely, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Federation for Medical Research, American Gastroenterological Association, North American Society for Pediatric Gastroenterology and Nutrition, and Society of Obstetric Medicine
Disclosure: Nothing to disclose.

Medical Editor

Ann Ouyang, MBBS, Professor, Department of Internal Medicine, Pennsylvania State University College of Medicine; Attending Physician, Division of Gastroenterology and Hepatology, Milton S Hershey Medical Center
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

James L Achord, MD, Professor Emeritus, Department of Medicine, Division of Digestive Diseases, University of Mississippi School of Medicine
James L Achord, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Medical Association, American Society for Gastrointestinal Endoscopy, Mississippi State Medical Association, New York Academy of Sciences, Sigma Xi, and Southern Medical Association
Disclosure: Nothing to disclose.

CME Editor

Alex J Mechaber, MD, FACP, Associate Dean for Undergraduate Medical Education, Associate Professor of Medicine, University of Miami Miller School of Medicine
Alex J Mechaber, MD, FACP is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, and Society of General Internal Medicine
Disclosure: Nothing to disclose.

Chief Editor

Julian Katz, MD, Clinical Professor of Medicine, Drexel University College of Medicine; Consulting Staff, Department of Medicine, Section of Gastroenterology and Hepatology, Hospital of the Medical College of Pennsylvania
Julian Katz, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, American Geriatrics Society, American Medical Association, American Society for Gastrointestinal Endoscopy, American Society of Law Medicine and Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility
Disclosure: Nothing to disclose.

Further Reading