Fatty Liver Workup

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

Laboratory Studies

No laboratory studies can help definitively establish a diagnosis of fatty liver or NASH.

Aminotransferases

The only abnormality may be an elevated aspartate aminotransferase (AST) or ALT level. These levels may be elevated as much as 10-fold. However, the AST and ALT levels may be normal in some patients with fatty liver or NASH.

In the absence of cirrhosis, an AST-to-ALT ratio of greater than 2 suggests alcohol use, whereas a ratio of less than 1 may occur in patients with NASH.

Alkaline phosphatase

This level can be elevated in some patients with NASH.

Usually, it is less than 2- to 3-times normal.

Lipids

Hyperlipidemia may be present.

Increased triglycerides are common in children and in patients with metabolic syndrome.

Iron studies

Elevations in serum ferritin, iron, and/or decreased transferrin saturation may occur in patients with NASH.

Although iron overload occurs in a small proportion of patients with NASH, these patients have more severe disease. An iron index score may be ordered on a liver biopsy specimen to evaluate for phlebotomy. Hemochromatosis gene testing is recommended when the ferritin is significantly elevated. Simply eliminating dietary iron has been shown to improve fatty liver.

Other

Before a diagnosis of NASH can be made, viral markers should be tested and viral infection excluded.

Autoimmune markers, such as antinuclear antibody (ANA) and anti–smooth muscle antibody (ASMA), are often slightly elevated in NASH.

Positive antibodies are associated with more severe fibrosis levels.

In the appropriate clinical setting, serum protein electrophoresis (SPEP) and anti–liver-kidney antibody may lead to a diagnosis of autoimmune liver disease.

Fasting insulin and glucose levels will alert the clinician to potential glucose intolerance and may lead to more effective therapies.

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Imaging Studies

Ultrasound

The liver is hyperechogenic or bright.

Steatosis is detected only when substantial (30% or more) fatty change is present.

Studies in patients who are about to undergo gastric bypass surgery reveal a 93% predictive value of NASH, with an accuracy of 76%.

Computed tomography

The mean CT (Hounsfield unit) number is lower in the liver than in the spleen.

CT scans may be used to monitor the course of the disease on successive scans.

Focal fatty lesions may be identified by dual-energy CT scans that demonstrate increased attenuation with increasing energy and no change in normals.

Magnetic resonance imaging

MRI may be useful for excluding fatty infiltration. Phase-contrast imaging correlates with the quantitative assessment of fatty infiltration across the entire range of liver disease.

Loss of intensity on T1-weighted images may be useful in identifying focal fat.

Other

Noninvasive studies, such as ultrasound, CT scan, and MRI, may identify the presence of a fatty liver. However, these imaging techniques cannot distinguish between benign steatosis and steatohepatitis. Benign steatosis may be focal or diffuse, whereas steatohepatitis is usually diffuse.

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Other Tests

  • Because fatty liver is common in the Western world and since NASH carries a 10% risk of cirrhosis, a simple blood test predictive of which patients would have worse disease is desirable. This has led to studies of databases, rat models, scoring systems, prospective studies, and novel uses for old markers of inflammation and scarring.[2, 10, 11, 12, 13]
  • The easily obtained NAFLD fibrosis score that consists of age, hyperglycemia, BMI, platelet count, albumin and AST/ALT ratio appears easy to use and promising to avoid excessive liver biopsies.[14]
  • Another promising tool has been reported. Kotronen et al developed a method for predicting NAFLD based on routinely available clinical and laboratory data.[15] Analysis of 470 subjects in whom liver fat content was measured with proton magnetic resonance spectroscopy revealed independent predictors of NAFLD were the presence of metabolic syndrome and type 2 diabetes, fasting serum insulin, fasting serum aspartate aminotransferase (AST), and the AST/alanine aminotransferase ratio[15] . Validation of the score demonstrated an area under the receiver operating characteristic curve of 0.86. The optimal cut-off point of -0.640 predicted increased liver fat content with a sensitivity of 86% and a specificity of 71%.
  • Other noninvasive commercial tests for fibrosis (eg, FIBROSpect, FibroSURE, FibroScan) have not yet been proven in the Western population for NASH; however, large studies are ongoing.
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Procedures

A liver biopsy and histopathologic examination are required to establish the diagnosis.

The diagnosis should be considered in all patients with unexplained elevations in serum aminotransferases (eg, with findings negative for viral markers or autoantibodies or with no history of alcohol use).

The Brunt classification is the standard used to report NAFLD and NASH biopsy specimens.[16]

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Histologic Findings

The diagnosis of fatty liver or NASH can be established only with a liver biopsy. Specific histologic findings include the following: (1) steatosis, which usually is macrovesicular but may be microvesicular or mixed; (2) inflammatory infiltrates consist of mixed neutrophilic and mononuclear cells, and portal infiltrates usually are not seen (unlike in hepatitis C); (3) ballooning degeneration; and (4) fibrosis. The first 3 findings are used to calculate the NAFLD activity score (0-8).

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Staging

The stage of disease is determined by the NAFLD activity score and the amount of fibrosis.

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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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