eMedicine Specialties > Gastroenterology > Liver

Hepatitis B: Differential Diagnoses & Workup

Author: Nikolaos T Pyrsopoulos, MD, PhD, FACP, Chief of Hepatology, Medical Director of Liver Transplantation, Florida Hospital; Associate Professor of Medicine, University of Central Florida College of Medicine
Coauthor(s): K Rajender Reddy, MD, FACP, FACG, Professor, Department of Medicine, Division of Hepatology, University of Miami School of Medicine
Contributor Information and Disclosures

Updated: Jun 19, 2009

Differential Diagnoses

Alcoholic Hepatitis
Hepatitis C
Autoimmune Hepatitis
Hepatitis D
Cholangitis
Hepatitis E
Cirrhosis
Hepatitis, Viral
Hemochromatosis
Primary Sclerosing Cholangitis
Hepatic Carcinoma, Primary
Wilson Disease
Hepatitis A

Other Problems to Be Considered

Congestive heart failure
Drug hepatotoxicity

Workup

Laboratory Studies

  • Acute hepatitis B disease
    • High levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), at a range of 1000-2000 IU/mL, is the hallmark of this disease, although values 100 times more than the upper limit of normal (ULN) can be identified. Higher values are found in patients with icteric hepatitis. ALT levels are usually higher than AST levels.
    • Alkaline phosphatase (ALP) levels may be elevated, but they are usually not more than 3 times the upper limit of normal.
    • Albumin levels can be slightly low, and serum iron levels may be elevated. In the preicteric period (ie, before the appearance of jaundice), leukopenia (ie, granulocytopenia) and lymphocytosis are the most common hematologic abnormalities and are accompanied by an increase in the erythrocyte sedimentation rate (ESR).
    • Anemia due to a shortened red blood cell survival period is an infrequent finding, although hemolysis may be noted. Thrombocytopenia is a rare finding.
    • Patients with severe hepatitis experience a prolongation of the prothrombin time (PT).
    • Several viral markers can be identified in the serum and the liver. HBsAg (Australian antigen) and HBeAg (marker of infectivity) are the first markers that can be identified in the serum. HBcAb (IgM) follows.
    • For patients who recover, seroconversion to HBsAb and HBeAb is observed, and the HBcAb is of the IgG class. Patients with persistent HBsAg for longer than 6 months develop chronic hepatitis.
  • Chronic inactive hepatitis B disease
    • Healthy carriers have normal AST and ALT levels, and the markers of infectivity (ie, HBeAg, HBV DNA) may be negative.
    • HBsAg, HBcAb of IgG type, and HBeAb are also present in the serum.
  • Chronic active hepatitis B disease
    • Patients have mild to moderate elevation of the aminotransferases (less than or equal to 5 times the ULN). The ALT levels are usually higher than the AST levels. Extremely high levels of ALT can be observed during exacerbation or reactivation of the disease, and they can be accompanied by impaired synthetic function of the liver (ie, decreased albumin levels, increased bilirubin levels, and prolonged PT). Hepatitis B virus (HBV) DNA levels are high during this phase. HBsAg and HBcAb of IgG or IgM type (in case of reactivation) are identified in the serum.
    • If the AST levels are higher than the ALT levels, the diagnosis of cirrhosis must be excluded. Hyperglobulinemia is another finding, predominantly with an elevation of the IgG globulins. Tissue-nonspecific antibodies, such as antismooth muscle antibodies (ASMAs) (20-25%) or antinuclear antibodies (ANAs) (10-20%), can be identified. Tissue-specific antibodies, such as antibodies against the thyroid gland (10-20%), can also be found. Mildly elevated levels of rheumatoid factor (RF) are usually present.
  • Cirrhosis
    • In early stages, findings of chronic viral hepatitis can be found.
    • Later on, as the disease progresses, low albumin levels, hyperbilirubinemia, prolonged PT, low platelet count and white blood cell count, and AST levels higher than ALT levels can be identified.
    • ALP levels and gamma-glutamyl transpeptidase (GGT) can be slightly elevated.

Imaging Studies

  • Acute hepatitis B disease
    • Performing abdominal ultrasonography, computed tomography (CT) scanning, or magnetic resonance imaging (MRI) is important to help exclude biliary obstruction.
    • Nonspecific findings include increased echogenicity of the liver parenchyma.
  • Chronic hepatitis B disease
    • Nonspecific findings may include increased echogenicity of the liver parenchyma.
  • Cirrhosis
    • Findings include coarse echogenicity of the liver, with a nodular appearance, and findings compatible with portal hypertension (eg, varices, splenomegaly, ascites, pleural effusion [ie, hepatic hydrothorax]).
    • Lesions can be detected and may be very difficult to evaluate because they can be mistaken for regenerating nodules. For these cases, highly sophisticated techniques, such as MRI with superparamagnetic iron oxide (ferumoxides), should be considered. Ferumoxides (negative contrast material) are phagocytosed by the reticuloendothelial cells of the normal liver, producing predominant T2 imaging on MRI. Therefore, a marked decrease of the signal in the normal liver parenchyma occurs, effectively permitting the identification of tumors.

Procedures

  • Liver biopsy, percutaneous or laparoscopic, is the standard procedure to assess the severity of disease for patients with features of chronic active liver disease (ie, abnormal aminotransferase levels and detectable levels of HBV DNA). See images below for examples.

  • Liver biopsy with trichrome stain showing stage 3...

    Liver biopsy with trichrome stain showing stage 3 fibrosis in a patient with hepatitis B.

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    Liver biopsy with trichrome stain showing stage 3...

    Liver biopsy with trichrome stain showing stage 3 fibrosis in a patient with hepatitis B.


  • Liver biopsy with hematoxylin stain showing stage...

    Liver biopsy with hematoxylin stain showing stage 4 fibrosis (ie, cirrhosis) in a patient with hepatitis B.

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    Liver biopsy with hematoxylin stain showing stage...

    Liver biopsy with hematoxylin stain showing stage 4 fibrosis (ie, cirrhosis) in a patient with hepatitis B.

Histologic Findings

Although liver biopsy is not indicated for patients with acute hepatitis B disease, the findings are predominantly lobular, with degenerative and regenerative hepatocellular changes as well as accompanying inflammation. Necrosis may be predominantly centrilobular.

Ground-glass cells are seen in approximately 50-75% of livers affected by chronic hepatitis B virus (HBV) infection, and they stain positive for HBsAg (see image below). Immunohistochemical staining of the specimen can help identify the presence of HBsAg or HBcAg (ie, chronic infection).

Liver biopsy specimen showing ground-glass appear...

Liver biopsy specimen showing ground-glass appearance of hepatocytes in a patient with hepatitis B.

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Liver biopsy specimen showing ground-glass appear...

Liver biopsy specimen showing ground-glass appearance of hepatocytes in a patient with hepatitis B.


Staging

  • Liver damage is graded according to the inflammatory component and is described as follows:
    • Grade 0 – Portal inflammation only, no activity
    • Grade 1 – Minimal portal inflammation and patchy lymphocytic necrosis, with minimal lobular inflammation and spotty necrosis
    • Grade 2 – Mild portal inflammation and lymphocytic necrosis involving some or all portal tracts, with mild hepatocellular damage
    • Grade 3 – Moderate portal inflammation and lymphocytic necrosis involving all portal tracts, with noticeable lobular inflammation and hepatocellular change
    • Grade 4 – Severe portal inflammation and severe lymphocytic bridging necrosis, with severe lobular inflammation and prominent diffuse hepatocellular damage
  • Liver damage staging (ie, fibrosis) is described as follows:
    • Stage 0 – No fibrosis
    • Stage 1 – Portal fibrosis
    • Stage 2 – Periportal fibrosis
    • Stage 3 – Septal, bridging fibrosis (see image below)

    • Liver biopsy with trichrome stain showing stage 3...

      Liver biopsy with trichrome stain showing stage 3 fibrosis in a patient with hepatitis B.

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      Liver biopsy with trichrome stain showing stage 3...

      Liver biopsy with trichrome stain showing stage 3 fibrosis in a patient with hepatitis B.

    • Stage 4 – Cirrhosis (see image below)

    • Liver biopsy with hematoxylin stain showing stage...

      Liver biopsy with hematoxylin stain showing stage 4 fibrosis (ie, cirrhosis) in a patient with hepatitis B.

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      Liver biopsy with hematoxylin stain showing stage...

      Liver biopsy with hematoxylin stain showing stage 4 fibrosis (ie, cirrhosis) in a patient with hepatitis B.

More on Hepatitis B

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

Additional resources on hepatitis B are available at Medscape’s Hepatitis B Resource Center.

Clinical Trials

National Guideline Clearinghouse

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Keywords

hepatitis B, hepatitis, HBV, hepatitis B infection, viral hepatitis, hepatitis B virus, chronic hepatitis, acute hepatitis, cirrhosis, fulminant hepatitis, hepatocellular carcinoma, HCC, extrahepatic manifestations, hepatitis D virus, HDV, delta virus, hepatitis C virus, HCV, hepatitis B surface antigen, HBsAg, Australia antigen, hepatitis B surface antibody, HBsAb, orthohepadnavirus, hepadnaviridae infection,

liver transplantation, liver transplant, OLT, interferon-alpha, IFN-a, peginterferon-alfa 2a, pegylated IFN-a 2a, lamivudine, adefovir dipivoxil, entecavir, telbivudine, tenofovir

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Contributor Information and Disclosures

Author

Nikolaos T Pyrsopoulos, MD, PhD, FACP, Chief of Hepatology, Medical Director of Liver Transplantation, Florida Hospital; Associate Professor of Medicine, University of Central Florida College of Medicine
Nikolaos T Pyrsopoulos, MD, PhD, FACP 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 Liver Foundation, American Medical Association, American Society of Gastrointestinal Endoscopy, American Society of Transplantation, International Liver Transplantation Society, and Transplantation Society
Disclosure: Gilead Sciences Honoraria Speaking and teaching; Schering-Plough Honoraria Speaking and teaching; Roche Honoraria Speaking and teaching

Coauthor(s)

K Rajender Reddy, MD, FACP, FACG, Professor, Department of Medicine, Division of Hepatology, University of Miami School of Medicine
K Rajender Reddy, MD, 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 Gastroenterological Association, American Society for Gastrointestinal Endoscopy, and Florida Medical 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: eMedicine Salary Employment

Managing Editor

Oscar S Brann, MD, FACP, Associate Clinical Professor, Department of Medicine, University of California at San Diego; Consulting Staff, Mecklenburg Medical Group
Oscar S Brann, MD, FACP is a member of the following medical societies: American Gastroenterological 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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