Liver & intrahepatic bile ducts

Acute and chronic hepatitis

Hepatitis (acute and chronic)-general


Editorial Board Member: Wei Chen, M.D., Ph.D.
Deputy Editor-in-Chief: Catherine E. Hagen, M.D.
Maitreyi Rohit, M.B.B.S., M.S.
Rifat Mannan, M.B.B.S., M.D.

Last author update: 22 July 2022
Last staff update: 9 August 2022

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PubMed Search: Acute and chronic hepatitis liver

See Also: Acute hepatitis-general

Maitreyi Rohit, M.B.B.S., M.S.
Rifat Mannan, M.B.B.S., M.D.
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Cite this page: Rohit M, Mannan R. Hepatitis (acute and chronic)-general. PathologyOutlines.com website. https://www.pathologyoutlines.com/topic/liverhepatitisgeneral.html. Accessed April 18th, 2024.
Definition / general
  • Acute hepatitis:
    • Active hepatocellular damage and necrosis caused most often due to viral infection, autoimmune disease or adverse drug reaction
    • Histologically characterized by lobular disarray and variable hepatocyte necrosis
    • Usually self limited duration of < 6 months
  • Chronic hepatitis:
    • Persistent and progressive inflammation and injury of hepatocytes
    • Histologically characterized by portal based chronic inflammation
    • Elevated liver enzymes for > 6 months' duration
Essential features
  • Hepatitis can be acute or chronic
  • Variable etiology
  • Morphologically characterized by lobular inflammation and necrosis, portal inflammation, interface hepatitis and fibrosis / cirrhosis
ICD coding
  • ICD-10:
    • B16.0 - acute hepatitis B with delta agent with hepatic coma
    • B17.1 - acute hepatitis C
    • B17.9 - acute viral hepatitis, unspecified
    • B18 - chronic viral hepatitis
    • B18.9 - chronic viral hepatitis, unspecified
    • B18.8 - other chronic viral hepatitis
Sites
  • Liver parenchyma
Pathophysiology
  • Inflammation of hepatocytes is caused by many factors, such as viruses, autoimmune disorders, drugs and alcohol
  • Inflammatory cells along with proinflammatory cytokines can cause hepatocyte degeneration and necrosis; can induce stellate cell activation resulting in fibrosis and even progressing to cirrhosis overtime (Alcohol Alcohol 2019;54:408, Cold Spring Harb Perspect Med 2018;8:a031708)
Etiology
Clinical features
  • Acute hepatitis:
    • Nonspecific constitutional symptoms: fever, fatigue, malaise (World J Gastroenterol 2021;27:1691)
      • Jaundice
      • Nausea, vomiting, weight loss, abdominal pain
      • May present with signs and symptoms of liver failure
  • Chronic hepatitis:
    • Asymptomatic or nonspecific constitutional symptoms
Diagnosis
  • Clinical history and physical examination for specific signs and symptoms
  • Laboratory evaluation
  • Biopsy for grade and stage in chronic hepatitis
Laboratory
Radiology description
  • Acute hepatitis (Radiopaedia: Acute hepatitis [Accessed 20 June 2022]):
    • Ultrasound features:
      • Hepatomegaly is the most sensitive sign
      • Gallbladder wall thickening (most often seen in hepatitis A)
      • Periportal edema
      • Accentuated brightness of portal vein radicle walls
      • Overall echotexture is decreased
      • Color / spectral doppler is normal
    • CT - not a first line imaging modality:
      • Hepatomegaly
      • Decreased attenuation around portal system and hepatic hilum
      • Diffusely decreased parenchymal attenuation on noncontrast CT
      • Periportal or hepatoduodenal lymphadenopathy
    • MRI findings are nonspecific and often used to exclude other etiologies of abnormal liver function studies
  • Chronic hepatitis (Radiopaedia: Cirrhosis [Accessed 20 June 2022]):
    • Ultrasound:
      • Surface nodularity
      • Overall coarse and heterogenous echotexture
      • Segmental hypertrophy / atrophy
      • Signs of portal hypertension
      • Splenomegaly
      • Fatty change
      • Ascites
    • CT / MRI - insensitive in early cirrhosis:
      • Surface and parenchymal nodularity
      • Fatty change
      • In advanced cirrhosis, nodular margin and lobar hypertrophy / atrophy may be seen
      • Signs of portal hypertension
      • Upper abdominal lymphadenopathy in advanced disease
Radiology images

Images hosted on other servers:

Acute viral hepatitis with gallbladder wall thickening

Hepatic cirrhosis with portal hypertension

Case reports
Treatment
  • Based on the underlying etiology
Gross description
  • Acute hepatitis:
    • Liver is homogenously enlarged and congested, stretching Glisson capsule
    • Necrosis and collapse of the liver lobules maybe seen
    • Surface is usually reddish brown
    • In cholestatic cases, a spectrum of brown to green may be seen
  • Chronic hepatitis:
    • Nonspecific in early stages
    • Can be enlarged with yellow (fatty change in steatosis) to green (in cholestasis)
    • In advanced stages the liver is cirrhotic with a firm, nodular appearance; they can have a micronodular or macronodular pattern (World J Gastroenterol 2016;22:1357)
Gross images

Images hosted on other servers:

Viral hepatitis with necrosis and lobular collapse

Macronodular cirrhosis of liver

Micronodular cirrhosis of liver with fatty change

Microscopic (histologic) description
  • Histological features are broad ranging and can vary based on etiology
  • Acute hepatitis:
    • Predominantly lobular injury pattern
  • Chronic hepatitis:
  • Lobular inflammation and necrosis:
    • Necrosis may be spotty, confluent or bridging
    • Apoptotic bodies (acidophilic bodies / Councilman bodies)
    • Ballooned hepatocytes (Alcohol Alcohol 2019;54:408)
    • Canalicular cholestasis
  • Portal inflammation (World J Gastroenterol 2016;22:1357):
    • Viral hepatitis: primarily composed of lymphocytes, admixed plasma cells, histiocytes; lymphoid follicles are common in hepatitis C
    • Autoimmune hepatitis: prominent plasma cell infiltrate with interface activity
    • Drug induced: variable histology, mixed inflammatory cells, often rich in eosinophils
  • Interface hepatitis (piecemeal necrosis) (Gut Liver 2020;14:430):
    • Destruction of hepatocytes in the interface with inflammation extending into the adjacent liver parenchyma
  • Fibrosis / cirrhosis (varying degrees, depending on stage of the disease)
Microscopic (histologic) images

Contributed by Rifat Mannan, M.B.B.S., M.D., Alexander Boyd, M.B.Ch.B., Owen Cain, M.B.Ch.B.,
Abhishek Chauhan, Ph.D. and Gwilym J. Webb, M.B.Ch.B., M.A.

Lymphoid aggregate: hepatitis C

Acute hepatitis histopathology

Chronic hepatitis B

Interface hepatitis

Nonalcoholic fatty liver disease

Alpha-1 antitrypsin deficiency

Virtual slides

Images hosted on other servers:

Autoimmune hepatitis

Chronic hepatitis C

Positive stains
Videos

Histopathology of liver in viral hepatitis

Histopathology of liver in chronic hepatitis

Sample pathology report
  • Liver, needle biopsy:
    • Chronic hepatitis B, with mild portal fibrosis (see comment)
    • Histologic grade: A1 (METAVIR system)
    • Histologic stage: 1/4 (Scheuer system)
    • Comment: The patient's clinical history of hepatitis B virus infection (HBV DNA positive by report) is noted.
Differential diagnosis
  • Primary biliary cholangitis, primary sclerosing cholangitis:
    • Cholestasis with bile duct damage or loss
    • Portal inflammation without interface hepatitis
    • Alkaline phosphatase is elevated more than transaminases
  • Lymphoma / leukemia:
    • Portal tract inflammation with severe interface activity
    • Infiltrates comprised of atypical lymphocytes
    • Gene rearrangement studies and immunohistochemistry can help with diagnosis
  • Graft rejection:
    • Liver transplant patients
    • Portal inflammation with mixed inflammatory cells, including eosinophils
    • Lymphocytic cholangitis with duct damage, endothelialitis
Board review style question #1

An asymptomatic 50 year old woman presented with elevated transaminases (aspartate aminotransferase and alanine aminotransferase) on routine laboratory tests. The image above is a micrograph of the liver biopsy. What are the predominant inflammatory cells seen and what could be the underlying etiology?

  1. Lymphocytic predominance seen in viral hepatitis
  2. Lymphoid follicles seen in chronic hepatitis C infection
  3. Mixed inflammatory cells with eosinophils seen in drug induced hepatitis
  4. Plasma cell predominance seen in autoimmune hepatitis
Board review style answer #1
D. Plasma cell predominance seen in autoimmune hepatitis

Comment Here

Reference: Hepatitis (acute and chronic)-general
Board review style question #2
A 45 year old woman presented with jaundice, vomiting and abdominal pain. Elevated transaminases were found on laboratory testing. Patient is diagnosed with acute viral hepatitis. What would be the microscopic findings in this patient?

  1. Bile duct proliferation with extensive fibrosis and brown, green plugs
  2. Lobular disarray with interface hepatitis and plasma cell rich portal inflammation
  3. Lobular inflammation with confluent necrosis and balloon degeneration
  4. Necrosis of hepatocytes with atypical lymphocytic infiltration
Board review style answer #2
C. Lobular inflammation with confluent necrosis and balloon degeneration

Comment Here

Reference: Hepatitis (acute and chronic)-general
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