eMedicine Specialties > Gastroenterology > Liver

Alcoholic Hepatitis: Differential Diagnoses & Workup

Author: Anastasios A Mihas, MD, DMSc, FACP, FACG, Professor, Department of Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine; Consulting Staff, Virginia Commonwealth University Hospitals and Clinics; Chief of GI Clinical Research, Director of GI Outpatient Service, Associate Director of Hepatology, Hunter Holmes McGuire Veterans Affairs Medical Center
Coauthor(s): Patrick D Hung, MD, Senior Fellow, Department of Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine; Douglas M Heuman, MD, FACP, Director of Hepatology, McGuire Veterans Affairs Medical Center, Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine
Contributor Information and Disclosures

Updated: Jun 30, 2008

Differential Diagnoses

Hepatitis B
Hepatitis C
Pancreatitis, Chronic

Other Problems to Be Considered

Other common considerations in alcoholic patients with jaundice include chronic pancreatitis with biliary strictures and pancreaticobiliary neoplasms.

A disorder histologically resembling alcoholic hepatitis can occur in patients who do not use alcohol. This syndrome, termed nonalcoholic steatohepatitis (NASH), is being recognized with increasing frequency. It occurs most frequently in the setting of obesity, hyperlipidemia, or type 2 diabetes mellitus. It is also observed in the setting of chronic parenteral hyperalimentation and in individuals who undergo jejunoileal bypass surgery for treatment of obesity. In most cases, NASH is indolent; however, in some individuals, it may progress insidiously to cirrhosis. NASH is currently believed to be responsible for a large fraction of cases of what was previously termed cryptogenic cirrhosis. In most patients with NASH, the ratio of AST to alanine aminotransferase (ALT) is less than 1, unless cirrhosis is present.

Workup

Laboratory Studies

  • CBC count

    • A CBC count commonly reveals some degree of neutrophilic leukocytosis with bandemia. Usually, this is moderate; however, rarely, it is severe enough to provide a leukemoid picture.
    • Alcohol is a direct marrow suppressant, and moderate anemia may be observed. In addition, alcohol use characteristically produces a moderate increase in mean corpuscular volume.
    • Thrombocytosis may be observed as part of the inflammatory response; conversely, myelosuppression or portal hypertension with splenic sequestration may produce thrombocytopenia.
  • Liver enzyme levels

    • Liver enzyme levels exhibit a characteristic pattern. In most patients, the AST level is moderately elevated, while the ALT level is in the reference range or only mildly elevated. This is the opposite of what is observed in most other liver diseases. An AST/ALT ratio greater than 1 is almost universal in persons with alcoholic hepatitis. Even in severe disease, the elevations of aminotransferase levels are modest, and an AST level greater than 500 U/L should raise suspicion of an alternative diagnosis. An AST/ALT ratio greater than 1 may accompany cirrhosis of any cause and, therefore, is less diagnostically specific in the setting of cirrhosis.
    • Alkaline phosphatase level elevations are typically mild in persons with alcoholic hepatitis. Levels greater than 500 U/L occur in a small percentage of patients, but abnormalities of this magnitude suggest a coexisting infiltrative or biliary obstructive process.
    • The gamma-glutamyl transpeptidase level is elevated markedly by alcohol use. While a normal value helps to exclude alcohol as a cause of liver disease, an elevated level is of no value in distinguishing between simple alcoholism and alcoholic hepatitis.
  • Liver function tests

    • Common liver function tests include albumin level, PT, and bilirubin level.
    • Hypoalbuminemia occurs because of decreased hepatic synthetic function and coexisting PEM.
    • Hyperbilirubinemia is typically a mixture of unconjugated and conjugated bilirubin, with the latter predominating. Bilirubinuria is normally present in patients who are icteric.
    • Coagulopathy predominantly affects the extrinsic pathway of coagulation (measured by PT). It is usually unresponsive to vitamin K.
    • The severity of hyperbilirubinemia and coagulopathy reflects the severity of alcoholic hepatitis and is of prognostic value.
  • Serum biomarkers

    • Ash test: The diagnostic value of serum biomarkers, such as the Ash test (ie, the 6 components of the FibroTest-ActiTest plus AST), was tested and validated in 275 patients with alcoholic hepatitis. Both the sensitivity and the specificity of the Ash test in predicting alcoholic steatohepatitis were impressive (0.80 and 0.84, respectively).51
    • Carbohydrate-deficient transferrin (CDT): CDT is perhaps the most reliable marker of chronic alcoholism, irrespective of the presence of liver disease.35 Recently, serum CDT has been proposed as a reliable biomarker in the differentiation of NASH from alcoholic hepatitis.42
    • C-reactive protein (CRP): Recent studies have indicated that serum CRP is an accurate marker of alcoholic hepatitis (ie, sensitivity, 41%; specificity, 99%; positive predictive value [PPV], 98%; negative predictive value [NPV], 88%).54
  • Electrolyte panel

    • Electrolyte disorders may reflect the effects of vomiting, portal hypertension with decreased circulating volume, alcoholic ketoacidosis, or respiratory alkalosis.
    • Hypophosphatemia and hypomagnesemia are common consequences of coexistent malnutrition.
  • Screening blood tests to exclude other conditions (appropriate in any patient with alcoholic hepatitis)

    • Hepatitis B surface antigen detects hepatitis B.
    • Anti–hepatitis C virus by enzyme-linked immunosorbent assay detects hepatitis C.
    • Ferritin and transferrin saturation detect hemochromatosis.
    • Marked elevation of aminotransferase levels should raise concern for viral hepatitis or drug hepatotoxicity. In particular, people who are alcoholics may develop severe liver necrosis from standard therapeutic doses of acetaminophen.
    • Rapid deterioration of liver function should raise the possibility of hepatocellular carcinoma, which can be tested for by determination of alpha-fetoprotein levels.
    • Jaundice with fever can be caused by gallstones producing cholangitis and is suggested by a disproportionate elevation of the alkaline phosphatase level.

Imaging Studies

  • Imaging studies are rarely required for the diagnosis of alcoholic hepatitis, but they can be useful in excluding other causes of liver disease.
  • Ultrasonography
    • In general, real-time ultrasonography is the preferred study because it is inexpensive, noninvasive, and widely available. It provides a good evaluation of the liver and other viscera, and it permits guided liver biopsy.
    • On ultrasonograms, the liver in patients with alcoholic hepatitis appears enlarged and diffusely hyperechoic.
    • Features suggestive of coexistent portal hypertension and/or cirrhosis include the presence of varices, splenomegaly, and ascites.
    • Ultrasonography is also helpful in excluding gallstones, bile duct obstruction, and hepatic or biliary neoplasms. Jaundice with fever can be caused by gallstones producing cholangitis; ultrasonographic examination of the abdomen is usually sufficient to exclude this possibility. However, if stones are found or fever persists, cholangiography may be necessary.
    • Rapid deterioration of liver function should raise the possibility of hepatocellular carcinoma, which can be tested for by performing imaging studies (eg, ultrasonography, CT scanning, MRI) of the liver.
  • Other imaging tests
    • Similar and complementary information can be obtained by CT scanning or MRI of the abdomen.
    • These imaging studies are more expensive and are usually required only in atypical cases. They are more sensitive and accurate if cancer is suspected.

Procedures

  • Liver biopsy: This is not always required in the evaluation of alcoholic hepatitis, but it may be useful in establishing the diagnosis, in determining the presence or absence of cirrhosis, and in excluding other causes of liver disease.
  • Percutaneous liver biopsy
    • Percutaneous biopsy can be performed at the bedside by an experienced practitioner, usually a gastroenterologist or a hepatologist.
    • Real-time ultrasonographic guidance may be desirable to optimize biopsy site selection and to reduce the risk of complications.
    • Usually, a biopsy should be avoided in the presence of severe thrombocytopenia or coagulopathy because of the risk of serious (possibly fatal) hemorrhage.
  • Transjugular liver biopsy
    • If biopsy information is considered essential and the risk of percutaneous biopsy appears excessive, an alternative approach is to perform a biopsy angiographically via a catheter passed into the hepatic vein under fluoroscopic guidance. In principle, the risk of hemorrhage should be reduced because the puncture site is contained within the venous system.
    • At the time of transjugular liver biopsy, the angiographer can determine the transhepatic venous pressure gradient.
    • In alcoholic hepatitis and cirrhosis, the pressure measurement obtained with a catheter wedged retrograde in a branch of the hepatic vein accurately reflects the portal venous pressure.

Histologic Findings

In alcoholic hepatitis, injury is characteristically most prominent in centrilobular (perivenular) areas (zone 3 of Rappaport). Hepatocytes exhibit ballooning with necrosis. Focal accumulation of polymorphonuclear leukocytes is noted in areas of injury (see Media file 3).  Lymphocytes may also be present, especially in portal tracts.

Ropy eosinophilic hyaline inclusions termed Mallory bodies may be observed in the perinuclear cytoplasm. With electron microscopy, Mallory bodies may be observed to be composed of fibril clumps that histochemically are identifiable as intermediate filaments. Mallory bodies are characteristic of alcoholic hepatitis, but they are not always present in this disease, and, occasionally, they can be observed in a variety of other disorders.

Macrovesicular steatosis, perivenular fibrosis, and frank cirrhosis commonly coexist with alcoholic hepatitis.

More on Alcoholic Hepatitis

Overview: Alcoholic Hepatitis
Differential Diagnoses & Workup: Alcoholic Hepatitis
Treatment & Medication: Alcoholic Hepatitis
Follow-up: Alcoholic Hepatitis
Multimedia: Alcoholic Hepatitis
References
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Further Reading

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Keywords

alcoholic steatohepatitis, alcoholic steatonecrosis, sclerosing hyaline necrosis, subacute alcoholic cirrhosis, florid alcoholic cirrhosis, fatty liver with hepatic failure, acute hepatic insufficiency of patients with chronic alcoholism, steatosis, cirrhosis, alcoholism, alcoholic cirrhosis, alcoholic liver disease, chronic alcoholism, alcohol-induced cirrhosis, alcohol-induced hepatitis, hepatomegaly, portal hypertension, ascites, variceal hemorrhage, hepatic encephalopathy, Mallory hyaline inclusions, protein-energy malnutrition, PEM, giant mitochondria, megamitochondria, hepatitis C infection, acetaminophen-alcohol interactions, jaundice, coagulopathy, delirium tremens, respiratory alkalosis, scleral icterus, splenomegaly, flapping tremor, spider angiomata, gynecomastia, heavy intake of ethanol

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Contributor Information and Disclosures

Author

Anastasios A Mihas, MD, DMSc, FACP, FACG, Professor, Department of Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine; Consulting Staff, Virginia Commonwealth University Hospitals and Clinics; Chief of GI Clinical Research, Director of GI Outpatient Service, Associate Director of Hepatology, Hunter Holmes McGuire Veterans Affairs Medical Center
Anastasios A Mihas, MD, DMSc, FACP, FACG 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 Clinical Research, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy, Gastroenterology Research Group, Sigma Xi, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

Coauthor(s)

Patrick D Hung, MD, Senior Fellow, Department of Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine
Disclosure: Nothing to disclose.

Douglas M Heuman, MD, FACP, Director of Hepatology, McGuire Veterans Affairs Medical Center, Professor, Department of Internal Medicine, Division of Gastroenterology, Virginia Commonwealth University School of Medicine
Douglas M Heuman, MD, FACP is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Physicians, and American Gastroenterological Association
Disclosure: Nothing to disclose.

Medical Editor

George Y Wu, MD, PhD, Professor, Department of Medicine, Director, Hepatology Section, Herman Lopata Chair in Hepatitis Research, University of Connecticut School of Medicine
George Y Wu, MD, PhD is a member of the following medical societies: American Association for the Study of Liver Diseases, American Gastroenterological Association, American Medical Association, American Society for Clinical Investigation, and Association of American Physicians
Disclosure: Humana Press Consulting fee Consulting; Novartis Consulting fee Review panel membership

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, Assistant Dean for Medical Curriculum, Associate Professor of Medicine, Division of General Internal 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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