Acute hepatitis

Author: Prof. Dr. med. Peter Altmeyer

All authors of this article

Last updated on: 28.12.2020

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Acute hepatitis; acute liver inflammation

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Acute viral hepatitis is a common, globally spread disease with a diffuse inflammation of the liver caused by primarily hepatotropic viruses with different transmission paths and epidemiologies. A distinction is made between concomitant hepatitis in systemic viral diseases, e.g. EBV, cytomegalovirus, herpes virus (see below). All viral hepatitides have, independent of the pathogen, clinical, biochemical and laboratory characteristics in common.

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The known types of hepatitis virus and their incidence in % of the world population:

  • Hepatitis-A (HAV), most common acute viral hepatitis
  • Hepatitis-B (HBV), 5% of virus carriers
  • Hepatitis C (HCV), 3% of virus carriers
  • Hepatitis-D (HDV), 5% of HB virus carriers
  • Hepatitis-E (HEV), special endemic risk areas

routes of infection:

  • Faeco-oral: drinking water and food, especially in countries with low hygiene standards (hepatitis A and E)
  • Praenteral: hospital staff, dialysis patients, i.v. drug users, tattooed people (hepatitis B, C and D)
  • Sexual, perinatal: hepatitis B, more rarely C and D
  • Note: Hepatitis D virus infection is a so-called simultaneous (5%) or superinfection (>90%), and is linked to the presence of hepatitis B virus.

Obligation to report: in case of suspicion of infection or death.

Clinical features
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Incubation period: The virus multiplies and spreads without causing clinical symptoms. (Incubation periods: HAV: 2-6week; HBV: 1-6 months; HCB: 1-6 months; HDV: 1-6 months; HEV: 3-6 weeks).

Prodromal or preicteric phase: occurrence of non-specific symptoms such as subfebrile temperatures, loss of appetite, feeling sick, nausea and vomiting, a newly developed aversion to cigarettes and fats (fat intolerance), often pain in the right upper abdomen. Urticaria and arthralgia are common, especially in HBV infection (frequent misdiagnosis: flu-like infection). Possible arthralgias and volatile exanthema, immune complex formation of HBsAG and anti-HBs in HBV. Remark: Frequently (60-70%) asymptomatic course.

Icteric phase (anicteric courses are frequent) 2-4 weeks: After 3-10 days darkening of the urine, followed by icterus. Although icterus increasingly (climax of icterus after 7-14 days) significant improvement of general condition. Hepatomegaly, liver pressure pain, liver edges remain soft and smooth. Low splenomegaly in 15-20% of patients.

Aniqueric hepatitis: more frequent in patients with HCV and in children with HAV than the icteric form of hepatitis. Typically manifests as a flu-like disease and is usually not recognized as such.

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BSG↑; CRP↑; Liver function tests: Bilirubin mostly elevated: 2-3mg/dl; increase in transaminases (500-3,000U/l); GPT>GOT (GOT/GPT = so-called de Ritis Quotient <1); cholestasis parameters ↑. Possibly only a slight increase of the gamma-GT. Furthermore: determination of prothrombin time or INR; increase of serum iron, possibly increase of gamma globulin fraction in electrophoresis. Blood count: possibly lymphocytosis. Virus serology to determine virus type and antigen/antibody status. This includes HBsAg (in 90% of cases of hepatitis B, always positive in hepatitis D)

Liver values increase early during the prodromal phase, reach their peak before the icterus is at its maximum and then slowly decrease during the convalescence phase. Bilirubin excretion in urine usually precedes the icterus. Hyperbilirubinemia is differently pronounced in acute viral hepatitis. However, their differentiation has no clinical benefit. Alkaline phosphatase is usually only moderately elevated, strong elevations suggest the suspicion of extrahepatic cholestasis and trigger imaging procedures (e.g. sonography).

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Liver biopsy: It is generally not necessary as long as the diagnosis is largely confirmed. Usually: complete histological regeneration. Exception: extensive bridge necrosis with destruction of whole acini destroyed ("bridging necrosis").

Histological signs of acute hepatitis:

  • Inflammatory infiltration of the portal and periportal fields with lymphocytes, plasma cells, histiocytes
  • Proliferation of v. Kupffer's star cells
  • Single cell necroses and Councilman corpuscles (= necrotic cell residues)
  • Ballooned liver cells
  • Accumulation of ceroid pigment and iron in phagocytes in the declining stage of hepatitis.

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Medical history (risk factors, travel history)


Laboratory constellation (transaminases: GPT>GOT, for cholestatic course: AP↑, gamma GT↑; for icteric course: bilirubin elevation; serological tests to identify the virus. In the case of a fulminant course: strongly decreased synthesis performance (Quick and albumin in serum and Cholinesterase↓↓)

Differential diagnosis
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Concomitant hepatitis in other infectious diseases
:Viral infections

  • Herpes viruses (EBV, CMV, in immunosuppressed patients also HSV and VZV)
  • Coxsackieviruses
  • Rare viruses such as (note: take travel history): arboviruses (yellow fever, denque fever, rift valley fever,) arenaviruses (Lassa fever, South American hemorrhagic fever), Marburg virus, Ebola virus.

Bacterial infections:

  • Brucellosis, Q fever (Coxiella burnetii).
  • Leptospirosis (e.g. Weil's disease with hepatitis and nephritis, jaundice, haematuria, albuminuria, etc.).

Parasitic infections:

  • Malaria, amoebiasis, echinococcosis, schistosomiasis, liver fluke infestation among others.

Drug- and toxin-induced hepatitis

Other liver diseases:

  • Autoimmune hepatitis (AIH), primary biliary cirrhosis, hereditary metabolic diseases, hepatic sarcoidosis, tumors. Alcoholic hepatitis: drinking history, slowly developing symptoms with signs of chronic alcohol abuse. Transaminases rarely exceed 300 I.U./l even in severe cases. In unclear situations, clarification of viral serology, if necessary liver biopsy to differentiate between alcoholic and viral hepatitis.

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Virus persistencies (virus carriers):

HBV: healthy adults: 5%, newborns >90%, immunocompromised: 50%

HCV: symptomatic icteric patients with acute HCV infection: 50% (with INF therapy <5%); asymptomatic HCV infections usually become chronic.

HDV: with superinfection of an HBsAg carrier: >90%.

HDV/HBV simultaneous infection as with HBV infection

HEV: Chronic courses with virus persistence possible in immunocompromised patients

Protracted and recurrent hepatitis (course > 3 months): in some patients recurrent hepatitis (characterized by recurrent disease manifestations, e.g. transaminase elevations during the convalescence phase)

Cholestatic hepatitis: manifestations of cholestasis may develop during the icteric phase, usually disappearing spontaneously. If it persists, it causes prolonged icterus, increased alkaline phosphatase and pruritus, despite the general regression of the inflammation.

Fulminant hepatitis: acute fulminant life-threatening hepatitis (HAV:0.2%; HBV: 1%; HDV: >2%; HEV: up to 3%, in pregnant women up to 20%). Triad: icterus, coagulation disorder, somnolence.

Primary hepatocellular carcinoma (HCC): risk increases in chronic viral hepatitis with the level of viral load and the development of liver cirrhosis (especially in chronic hepatitis B)

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Antiviral therapy:

Acute hepatitis B: therapy only if liver function is impaired (see below Hepatitis B virus infection).

Acute hepatitis C: Directly acting antiviral substances (see below Hepatitis C virus infection)

General measures:

Prevention: Since all forms of treatment have only a limited effect, prevention is of great importance.

Good personal hygiene reduces the risk of transmission, especially faecal-oral transmission as in HAV and HEV. Blood and other body fluids (e.g., saliva, seminal fluid) from patients with acute HBV and HCV and stool from patients with hepatitis A must be considered infectious. Protective measures are recommended.

The risk of posttransfusion hepatitis is minimized by avoiding unnecessary transfusions and testing all blood donors for HBsAg and anti-HCV. This screening has reduced the incidence of posttransfusion hepatitis to about 1:100,000 units of transfused blood.

Immunoprophylaxis: This consists of active immunization using vaccines and passive immunization.

Vaccines for hepatitis A and hepatitis B are available. Routine vaccination against hepatitis A and B is recommended for all children and adults at high risk. Available HAV/HBV vaccine (Twinrix®). Dos.: 3x1 dose i.m. (M. deltoideus) at time points 0,1,6 months.

HEV: Recombinant hepatitis E vaccine has been successfully tested. 3Doses at time points 0,1,6 months confer 90% vaccine protection.

HDV: An HDV vaccine does not exist. However, genetically engineered vaccine from the surface antigen (HBsAg) protects against HBV infection and HDV simultaneous infection. This also reduces the incidence of hepatocellular carcinoma. Preparations: HB-Vax Pro®, Engerix®: 3x1 dose i.m. (to be injected into the M. deltoides at time points 0,1,6).

Vaccines for immunoprophylaxis of HCV do not exist. The ability of HCV to alter its genome complicates vaccine development.

Standard immunoglobulins prevent or reduce the severity of HAV infection and should be given to family members and close contacts of patients. Hepatitis B immunoglobulin HBIG (hyperimmunoglobulin) is unlikely to prevent infection, but it prevents or attenuates the clinical presentation.

General therapy
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No specific treatment mitigates the course of acute viral hepatitis. Alcohol should be avoided, intensification of liver damage. Restrictions in diet or physical activity including often prescribed bed rest have no scientific basis.

Most patients can safely resume work after the icterus has subsided, even if the transaminases are still elevated. In cholestatic hepatitis, the administration of colestyramine (8 g p.o. 1 to 2 times/day) can reduce itching.

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Duration of acute viral hepatitis: about 6-8 weeks after onset of symptoms. With hepatitis A usually shorter. Spontaneous cure in the majority of cases:

Spontaneous cure rates of acute viral hepatitis in adults

  • HAV infection: almost 100%.
  • HBV infection: approx. 95% (5% virus persistence = chronic hepatitis)
  • HDV simultaneous infection with HBV: spontaneous cure rates as with HBV.
  • HDV superinfection of an HBs-Ag carrier: low spontaneous cure rate.
  • HCV infection: symptomatic (icteric) patients have a 50% chance of spontaneous recovery. Asymptomatic (anikteric) infections are usually chronic (80%). With antiviral therapy, healing is successful in >95% of cases.


Please ask your physician for a reliable diagnosis. This website is only meant as a reference.


Last updated on: 28.12.2020