Liver & intrahepatic bile ducts

Acute and chronic hepatitis

Acute hepatitis-general

Topic Completed: 1 December 2014

Minor changes: 17 March 2021

Copyright: 2002-2021,, Inc.

PubMed Search: Acute hepatitis general[TI]

Rifat Mannan, M.D.
Songyang Yuan, M.D., Ph.D.
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Cite this page: Mannan, A.A.S.R. Acute hepatitis-general. website. Accessed December 2nd, 2021.
Definition / general
  • Active hepatocellular damage and necrosis, usually with a lobular inflammatory response, less than 6 months duration
  • Clinically defined as significant elevation (at least 2x upper normal reference range) of serum ALT or AST in a patient with no previous history of liver disease
  • Mechanisms of acute hepatitis include direct toxin induced necrosis (i.e. acetominophen) or immune mediated damage (i.e. viral hepatitis)
  • Associated with disease ranging from subclinical to self limited symptomatic to fulminant hepatic failure
  • Usually is self limited with recovery within 1 - 2 months from onset of symptoms but in "prolonged resolving" cases, lasts > 6 months and regresses slowly thereafter
  • Viral hepatitis:
    • Most common cause, accounting for 72% of cases of acute hepatitis
    • Majority due to hepatitis A and hepatitis B viruses
    • Acute infection due to hepatitis C virus is usually subclinical
    • Infection with hepatitis D virus usually occurs in intravenous drug users, either as a superinfection or coinfection with HBV
    • Acute hepatitis due to hepatitis E virus / HEV usually occurs in endemic regions, such as Central and Southeast Asia, North and West Africa and Mexico
  • Other causes:
Clinical features
  • Most patients are asymptomatic or subclinical and remain undiagnosed
  • In more severe cases, fatigue, abdominal pain, nausea and vomiting, muscle aches or jaundice may be present
  • Liver transaminases ALT and AST are classically elevated 20 - 100x
  • Careful review of drug / toxin history is often helpful
  • Serologic tests for hepatitis A, B or C infection and autoimmune hepatitis should be performed routinely
Microscopic (histologic) description
  • Usually not biopsied
  • Biopsies may be indicated if clinical suspicion of:
    • Second independent hepatic insult (i.e. an underlying chronic liver disease)
    • Unusual infectious process in immunocompromised patients
  • For all forms of acute hepatitis, histology is characterized by "lobular disarray," which includes:
    • Ballooning degeneration
    • Spotty necrosis
    • Predominantly sinusoidal and lobular mononuclear cell infiltrate (with occasional neutrophils and eosinophils)
    • Kupffer cell hyperplasia
    • Scattered apoptotic bodies
    • Canalicular cholestasis
    • Hepatocellular regeneration
  • Prolonged resolving:
    • Necrosis subsides and phagocytic activity predominates during regression
    • Mild portal inflammation is present and clumps of Kupffer cells are often seen
    • Ductular reaction is seen in severe cases
    • Cholestasis may persist after inflammation and necrosis have subsided
    • There are no dense bundles of collagen and elastic fibers
Microscopic (histologic) images

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Resolving hepatitis

Additional references
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