Liver & intrahepatic bile ducts

Acute and chronic hepatitis

Chronic hepatitis


Editorial Board Member: Claudio Luchini, M.D., Ph.D.
Editor-in-Chief: Debra L. Zynger, M.D.
Kimberley J. Evason, M.D., Ph.D.

Last author update: 1 March 2023
Last staff update: 1 March 2023

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PubMed Search: Chronic hepatitis

Kimberley J. Evason, M.D., Ph.D.
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Cite this page: Evason KJ. Chronic hepatitis. PathologyOutlines.com website. https://www.pathologyoutlines.com/topic/liverchronichepgeneral.html. Accessed May 19th, 2024.
Definition / general
  • Liver injury occurring for at least 6 months as a result of hepatocyte based injury and inflammation, most commonly due to viral or autoimmune hepatitis (Am J Surg Pathol 1995;19:1409)
Essential features
Terminology
ICD coding
  • ICD-10:
    • B18.0 - chronic viral hepatitis B with delta agent
    • B18.1 - chronic viral hepatitis B without delta agent
    • B18.2 - chronic viral hepatitis C
    • B18.8 - other chronic viral hepatitis
    • B18.9 - chronic viral hepatitis, unspecified
    • K73.0 - chronic persistent hepatitis, not elsewhere classified
    • K73.1 - chronic lobular hepatitis, not elsewhere classified
    • K73.2 - chronic active hepatitis, not elsewhere classified
    • K73.8 - other chronic hepatitis, not elsewhere classified
    • K73.9 - chronic hepatitis, unspecified
Epidemiology
Sites
  • Liver parenchyma
Pathophysiology
  • Hepatocytes are injured by viral infection, drugs, deregulated inflammatory cells or abnormal accumulation of metabolites, leading to activation of hepatic stellate cells, which produce increased extracellular matrix resulting in fibrosis (Middle East J Dig Dis 2016;8:166, Physiol Rev 2008;88:125)
Clinical features
  • May lack symptoms until end stage (cirrhosis)
  • Associated signs and symptoms include (World J Gastroenterol 2022;28:5910):
    • General: fatigue (most common), malaise, mild discomfort in the right upper quadrant, anorexia
    • Impaired biliary tract function: jaundice, pruritus
    • Portal hypertension: gastroesophageal varices, ascites, edema, splenomegaly
    • Impaired hepatocyte metabolism: spider angiomata, hepatic encephalopathy, easy bleeding / bruising
Diagnosis
Laboratory
Radiology description
  • MRI and CT findings in cirrhosis
    • Surface and parenchymal nodularity
    • Hypertrophy of the caudate lobe and lateral segments of the left lobe
    • Atrophy of the posterior segments of the right lobe
  • Ultrasound findings in cirrhosis
Radiology images

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Nodular liver in patient with hepatitis B

Prognostic factors
Case reports
Treatment
Gross description
  • In cirrhosis, the liver is generally firm and demonstrates a micronodular or macronodular pattern
  • Color ranges from beefy red (normal) to dark green (cholestasis) or yellow (steatosis) (World J Gastroenterol 2016;22:1357)
Gross images

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Cirrhotic liver is diffusely nodular

Microscopic (histologic) description
  • Fibrosis
    • Required for pathologic diagnosis of chronic hepatitis in the absence of clinically confirmed chronic liver disease
    • Progressive fibrosis of the limiting plate leads to enlargement of portal tracts and stellate periportal fibrous extension
    • May lead to portal - portal or portal - central fibrous bridging, culminating in cirrhosis, which is usually micronodular (nodules < 3 mm in diameter) or mixed micronodular and macronodular type
  • Portal inflammation
    • Mononuclear infiltration of portal tracts (mostly CD4+ T lymphocytes with some plasma cells)
    • Lymphoid aggregates or follicles may be present (most common in hepatitis C infection)
  • Interface hepatitis
    • Previously called piecemeal necrosis
    • Hepatocyte apoptosis and inflammation at the stromal - parenchymal interface (interface of portal tract and lobule)
    • Mononuclear infiltrate (mostly CD8+ T lymphocytes)
  • Lobular hepatitis
    • Mononuclear infiltrate of the hepatic parenchyma (lobules)
    • Apoptotic / necrotic hepatocytes (Councilman bodies) in zones 2 and 3
  • Reference: Am J Surg Pathol 1995;19:1409
Microscopic (histologic) images

Contributed by Kimberley J. Evason, M.D., Ph.D.
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Chronic hepatitis C

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Fibrosis in chronic hepatitis C

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Cirrhosis (end stage)

Chronic hepatitis B and AIH

Chronic hepatitis B and AIH


Bridging fibrosis

Bridging fibrosis

Hereditary hemochromatosis

Hereditary hemochromatosis

Alpha-1 antitrypsin deficiency

Alpha-1 antitrypsin deficiency

Periportal fibrosis in A1AT

Periportal fibrosis in A1AT

Virtual slides

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Chronic hepatitis, autoimmune etiology

Autoimmune hepatitis, trichrome stain

Chronic hepatitis C

Chronic hepatitis C, trichrome stain

Positive stains
  • Trichrome stain can help with the assessment of the amount of scarring and fibrosis present (stage)
Sample pathology report
  • Liver, core biopsy:
    • Chronic hepatitis with mild portal and lobular necroinflammatory activity (grade 2, scale 0 - 4, Batts-Ludwig methodology) and periportal fibrosis (stage 2, scale 0 - 4, Batts-Ludwig methodology), consistent with clinical history of chronic hepatitis C
Differential diagnosis
  • Primary biliary cholangitis (PBC):
    • Can have portal based inflammation with interface activity and lobular activity
    • Florid duct lesions not seen in chronic hepatitis
    • Clinical history may include elevated alkaline phosphatase, gamma glutamyl transpeptidase, serum IgM and antimitochondrial autoantibodies
  • Lymphoma or leukemia infiltrating into the liver:
    • Can have portal lymphocytic inflammation
    • Lacks interface hepatitis and portal based fibrosis
    • May have monomorphism and marked atypia of the infiltrating cells
  • Chronic steatohepatitis:
    • Can have portal and lobular lymphocytic inflammation
    • Has steatosis / fat (may also be seen in chronic hepatitis)
    • Centrizonal, pericellular fibrosis not seen in chronic hepatitis
    • May be morphologically indistinguishable from chronic hepatitis at late stage (cirrhosis)
  • Active hepatitis with bridging necrosis:
    • Has portal inflammation with interface activity and lobular inflammation
    • Bridging necrosis can cause a nodular appearance from low power, mimicking bridging fibrosis or cirrhosis
    • Trichrome staining is paler in zones of dropout / necrosis than in fibrous areas
Board review style question #1

    An asymptomatic 35 year old woman has elevated serum aminotransferases (aspartate aminotransferase [AST] and alanine aminotransferase [ALT]). A liver biopsy was performed. What is the most likely underlying etiology of these findings?

  1. Alcoholic liver disease
  2. Infection with hepatitis C
  3. Oxaliplatin induced liver injury
  4. Tylenol overdose
  5. Valproic acid associated liver injury
Board review style answer #1
B. Infection with hepatitis C

Comment Here

Reference: Chronic hepatitis
Board review style question #2

    A liver biopsy from a 54 year old man is shown above. What feature, required for the pathologic diagnosis of chronic hepatitis, is shown in the image?

  1. Bridging necrosis
  2. Fibrosis
  3. Interface hepatitis
  4. Nodule formation
  5. Portal inflammation
Board review style answer #2
B. Fibrosis

Comment Here

Reference: Chronic hepatitis
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