Fatty Liver 

  • Author: Dawn Sears, MD; Chief Editor: Julian Katz, MD   more...
 
Updated: Jun 24, 2011
 

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, high triglyceride levels, or a high fat diet.

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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.

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Epidemiology

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.

A study by Bhala et al evaluated mortality in a group of 500 patients with chronic hepatitis C or NASH. The study found that patients with hepatitis C were more likely to die due to liver-related disease. However, when comparing NASH with hepatitis C, long-term mortality was equal. This is due to increased cardiovascular causes of death found in patients with NASH.[4]

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. Hispanics in general do not have higher rates of NASH compared with Caucasians, unless diabetes is also present.[5]

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.[6]

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.[7, 8, 9]
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Contributor Information and Disclosures
Author

Dawn Sears, MD  Associate Professor of Internal Medicine, Division of Gastroenterology and Hepatology, Scott and White Memorial Hospital

Dawn Sears, MD is a member of the following medical societies: American Association for the Study of Liver Diseases and American College of Gastroenterology

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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.

Alex J Mechaber, MD, FACP  Senior 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

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 & Ethics, American Trauma Society, Association of American Medical Colleges, and Physicians for Social Responsibility

Disclosure: Nothing to disclose.

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