eMedicine Specialties > Gastroenterology > Liver

Alcoholic Fatty Liver: Differential Diagnoses & Workup

Author: Mohammad K Ismail, MD, Assistant Professor, Department of Internal Medicine and Gastroenterology, University of Tennessee at Memphis
Coauthor(s): Caroline Riely, MD, Professor, Departments of Medicine and Pediatrics, University of Tennessee Health Science Center
Contributor Information and Disclosures

Updated: Sep 15, 2008

Differential Diagnoses

Other Problems to Be Considered

Steatosis can be observed on histology in the following conditions:
Nonalcoholic steatohepatitis (NASH)
Drug-induced liver disease (valproic acid, tetracycline, antiviral agents such as zidovudine)
Acute fatty liver of pregnancy
Metabolic liver disease and inborn errors of metabolism, such as defects in mitochondrial beta-oxidation
Reye syndrome

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.

More on Alcoholic Fatty Liver

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

References

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Further Reading

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.

 
 
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