eMedicine Specialties > Gastroenterology > Liver

Fatty Liver

Author: Dawn Sears, MD, Assistant Professor of Internal Medicine, Division of Gastroenterology and Hepatology, Scott and White Memorial Hospital
Contributor Information and Disclosures

Updated: Jan 5, 2010

Introduction

Background

Fatty liver disease can range from fatty liver alone (steatosis) to fatty liver associated with inflammation (steatohepatitis). This condition can occur with the use of alcohol (alcohol-related fatty liver) or in the absence of alcohol (nonalcoholic fatty liver disease [NAFLD]).

Fatty liver disease is now the most common cause for elevated liver function tests in the United States. This is mainly due to the ongoing obesity epidemic in the United States.

Fatty liver can be associated with the use of alcohol. This may occur with as little as 10 oz of alcohol ingested per week. Identical lesions also can be caused by other diseases or toxins.

If steatohepatitis is present but a history of alcohol use is not, the condition is termed nonalcoholic steatohepatitis (NASH). Fatty change in the liver results from excessive accumulation of lipids within hepatocytes. Simple fatty liver is believed to be benign, but NASH can progress to cirrhosis and can be associated with hepatocellular carcinoma. The main risk factors for simple fatty liver (NAFLD) and NASH are obesity, diabetes, and high triglyceride levels.

Pathophysiology

Fatty liver is the accumulation of triglycerides and other fats in the liver cells. In some patients, this may be accompanied by hepatic inflammation and liver cell death (steatohepatitis).

Potential pathophysiological mechanisms include the following: (1) decreased mitochondrial fatty acid beta-oxidation, (2) increased endogenous fatty acid synthesis or enhanced delivery of fatty acids to the liver, and (3) deficient incorporation or export of triglycerides as very low-density lipoprotein.

Frequency

United States

Steatosis affects approximately 25-35% of the general population. Steatohepatitis may be related to alcohol-induced hepatic damage or may be unrelated to alcohol (ie, NASH). NASH has been detected in 1.2-9% of patients undergoing routine liver biopsy. NAFLD is found in over 80% of patients who are obese. Over 50% of patients undergoing bariatric surgery have NASH.

International

Danish and Australian studies show less intense disease progression than studies in the United States. Asian studies reveal NASH and NAFLD at lower body mass indexes (BMIs).1,2,3

Mortality/Morbidity

A natural history study from Olmsted County, Minnesota, revealed that 10% more patients with NAFLD died versus control subjects over a 10-year period. Malignancy and heart disease were the top 2 causes of death. Liver-related disease was the third cause of death (13%), as compared to the 13th cause of death (<1%) for control subjects.

  • Steatosis was once believed to be a benign condition, with rare progression to chronic liver disease. Steatohepatitis may progress to liver fibrosis and cirrhosis and may result in liver-related morbidity and mortality.
  • Fibrosis or cirrhosis in the liver is present in 15-50% of patients with NASH. Approximately 30% of patients with fibrosis develop cirrhosis after 10 years. Many cases of cryptogenic cirrhosis may represent so-called burnt-out NASH because a high proportion is associated with obesity, type II diabetes, or hyperlipidemia.
  • Some patients with drug-induced fatty liver present dramatically with the rapid evolution of hepatic failure. Some patients with inborn errors of metabolism, such as tyrosinemia, may rapidly progress to cirrhosis.

Race

Fatty liver has been found across all races, but most of the research and the highest prevalence appear in the Caucasian race.

A small study evaluating fatty liver disease in the Indian population found its association with the nonobese and its recovery with simple lifestyle habits.3  However, obesity, when present, was a significant risk factor for NASH in Indians as well as in Koreans.2

Interestingly, and as supported in the author’s clinical practice, Asian patients often develop NAFLD and NASH at normal BMIs, but BMIs on the higher range for a patient’s ethnicity. A diagnosis of cirrhosis in an 80-year-old, 5-foot, 110-lb Asian female, with a BMI of 21, is not unusual.

Mutations for hemochromatosis appear to put Caucasians at a higher risk of more advanced fibrosis.4

Sex

  • As many as 75% of patients in initial reported studies were females.
  • In more recent studies, 50% of patients are females.

Age

  • Fatty liver occurs in all age groups.
  • NAFLD is the most common liver disease among adolescents in the United States. Older age often is predictive of more severe grading of fibrosis.
  • NASH is the third most common cause of chronic liver disease in adults in the United States (after hepatitis C and alcohol). It is now probably the leading reason for mild elevations of transaminases.
  • NASH has recurred within 6 months after pediatric or adult liver transplant.5,6,7

Clinical

History

  • Most patients with fatty liver are asymptomatic. However, if questioned, more than 50% of patients with fatty liver or NASH report persistent fatigue, malaise, or upper abdominal discomfort.
  • Symptoms of liver disease, such as ascites, edema, and jaundice, may arise in patients with cirrhosis due to progressive NASH. Laboratory abnormalities during blood donations or life insurance physical examinations often reveal elevated alanine aminotransferase (ALT) levels and ultimately lead to the diagnosis of fatty liver disease.

Physical

  • Hepatomegaly is common.
  • Splenomegaly and stigmata of portal hypertension (eg, ascites, edema, spider angiomas, varices, gynecomastia, menstrual disorders) may occur in patients with cirrhosis.
  • Patients with drug-induced fatty liver may present with rapid fulminant liver failure.
  • In patients who abuse alcohol, extrahepatic effects, such as skeletal muscle wasting, cardiomyopathy, pancreatitis, or peripheral neuropathy, may be present.

Causes

The most common association with fatty liver disease is metabolic syndrome. This includes carrying the diagnosis of type II diabetes, obesity, and/or hypertriglyceridemia. Other factors, such as drugs (eg, amiodarone, tamoxifen, methotrexate), alcohol, metabolic abnormalities (eg, galactosemia, glycogen storage diseases, homocystinuria, tyrosinemia), nutritional status (eg, overnutrition, severe malnutrition, total parenteral nutrition [TPN], starvation diet), or other health problems (eg, celiac sprue, Wilson disease) may contribute to fatty liver disease. There are reports of lean NASH families.

More on Fatty Liver

Overview: Fatty Liver
Differential Diagnoses & Workup: Fatty Liver
Treatment & Medication: Fatty Liver
Follow-up: Fatty Liver
References
Further Reading
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References

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  2. Park JW, Jeong G, Kim SJ, et al. Predictors reflecting the pathological severity of non-alcoholic fatty liver disease: comprehensive study of clinical and immunohistochemical findings in younger Asian patients. J Gastroenterol Hepatol. Apr 2007;22(4):491-7. [Medline].

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Further Reading

Related eMedicine Topics

Clinical Trials
Clinical Guidelines

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Keywords

fatty liver, fatty liver disease, NAFLD, FLD, steatosis, hepatic steatosis, steatohepatitis, alcohol-related fatty liver, alcoholic steatohepatitis, nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, NASH, liver fibrosis, cirrhosis, hyperlipidemia, protein-calorie malnutrition, abetalipoproteinemia,

galactosemia, glycogen storage disorder, hereditary fructose intolerance, homocystinuria, hypobetalipoproteinemia, Refsum disease, systemic carnitine deficiency, tyrosinemia, Weber-Christian disease, Wilson disease, variceal bleeding, encephalopathy, starvation, jejunoileal bypass, total parenteral nutrition, rapid weight loss

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Contributor Information and Disclosures

Author

Dawn Sears, MD, Assistant Professor of Internal Medicine, Division of Gastroenterology and Hepatology, Scott and White Memorial Hospital
Disclosure: Nothing to disclose.

Medical Editor

John Gunn Lee, MD, Director of Pancreaticobiliary Service, Associate Professor, Department of Internal Medicine, Division of Gastroenterology, University of California at Irvine School of Medicine
John Gunn Lee, MD is a member of the following medical societies: American College of Gastroenterology, American College of Physicians, American Gastroenterological Association, and American Society for Gastrointestinal Endoscopy
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Simmy Bank, MD, Chair, Professor, Department of Internal Medicine, Division of Gastroenterology, Long Island Jewish Hospital, Albert Einstein College of Medicine
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.

 
 
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