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Propaedeutics · Liver, Biliary Tract, and Spleen

Acute viral hepatitis

Hepatitis viralis acuta

Acute viral hepatitis is a group of acute infectious liver diseases of viral etiology. The underlying pathology is diffuse inflammation of the liver tissue, accompanied by cytolytic syndrome and jaundice.

PathogensHepatitis A, B, C, D, and E viruses
Underlying pathologyDiffuse inflammation of the liver tissue
Incubation periodFrom 2 weeks (A, E) to 6 months (B, C, D)
Risk of chronicityHighest in hepatitis C (up to 85%)
4 min readFor medical studentsUpdated 09/24/2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Classification and transmission routes

All pathogens are divided into two large groups depending on their mechanism of entry into the body:

  1. Enteral hepatitis (A and E). Transmitted via the fecal-oral route. Hepatitis A virus has the greatest epidemiological significance in this group.
  2. Parenteral hepatitis (B, C, D). The main route of transmission is bloodborne (injections, transfusions, dental and surgical procedures, hemodialysis, tattooing, intravenous drug use). Sexual transmission is also possible (particularly characteristic of hepatitis B virus) and, exceptionally, the fecal-oral route. Hepatitis C is noted for a high risk of transition to a chronic form.

Clinical course

The disease proceeds cyclically, with a sequential change of stages:

  • Incubation period. Lasts 2–5 weeks for enteral viruses and 1 to 6 months for parenteral ones.
  • Prodromal (pre-jaundiced) period. Characterized by asthenovegetative manifestations (fatigue, weakness), dyspepsia (decreased appetite), and musculoskeletal syndrome (myalgia, arthralgia).
  • Period of manifest illness (jaundiced). Occurs 4–10 days after the onset of malaise. Manifests as parenchymatous jaundice, pain in the right upper quadrant, enlargement of the liver and spleen (hepatosplenomegaly). The color of excreta changes: urine darkens («beer-colored» urine), while stool becomes discolored (acholic stool).

In severe cases, complications may develop: cholestasis syndrome (severe pruritus, elevated alkaline phosphatase) and hepatocellular failure (decreased albumin and prothrombin, hemorrhages, hepatic encephalopathy, hepatorenal syndrome).

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Laboratory diagnostics

Diagnosis requires a comprehensive approach including medical history, clinical presentation, and laboratory tests.

Blood biochemistry:

  • Cytolytic syndrome: elevated ALT and AST.
  • Pigment metabolism: hyperbilirubinemia (elevation of both direct and indirect fractions).
  • Cholestasis syndrome: elevated GGT and a moderate increase of alkaline phosphatase against the background of high bilirubin levels.
  • Decreased leukocyte count in the complete blood count.

Serology and PCR:

  • Hepatitis A: early marker — anti-HAV-IgM.
  • Hepatitis B (DNA virus): acute phase — HBsAg; seroconversion stage — anti-HBc, followed by anti-HBs.
  • Hepatitis C: detection of IgM antibodies and viral RNA.
  • Hepatitis D: IgM antibodies (correlate with the disappearance of HBsAg).
  • Hepatitis E: method of exclusion + specific antibodies.
  • PCR is used to confirm the diagnosis and determine the type of the pathogen's nucleic acid.

Principles of treatment and prognosis

The basis of therapy is bed rest and a sparing diet (exclusion of fried and spicy foods, restriction of protein if there is a risk of encephalopathy). Oral detoxification is performed with a 5% glucose solution. Intravenous infusions (glucose, Hemodez) and hemostasis correction (vitamin K, fresh frozen plasma in case of a drop in the prothrombin index) are prescribed according to strict indications.

Prognosis and work capacity assessment:

  • Hepatitis A: favorable prognosis, recovery in 2–3 months. Disability leave — from 14 days after discharge. Follow-up dispensary observation — from 1 to 3 months. An effective vaccine is available.
  • Hepatitis B: chronicity in 10–15% of patients.
  • Hepatitis C: chronicity in 50–85%.

In parenteral hepatitis (B and C), disability leave is 30 days after discharge, and dispensary follow-up lasts 6–12 months.

Briefly: answers to topical questions

What clinical and laboratory signs indicate the development of hepatocellular failure?

Signs of hepatocellular failure include:

  • Decreased synthetic function of the liver: drop in albumin and prothrombin levels.
  • Hemorrhagic syndrome: decreased synthesis of clotting factors (II, V, VII, X).
  • Edematous-ascitic syndrome: decrease in oncotic pressure due to a drop in albumin synthesis.
  • Hepatic encephalopathy: associated with the retention and accumulation of nitrogenous compounds, with ammonia playing a key role; the ultimate result is edema and functional disorders of brain astroglia.
  • Hepatorenal syndrome.
  • Intoxication syndrome: accumulation of toxic products of intestinal origin.

What diet (Pevzner diet number) is prescribed in the treatment of acute viral hepatitis?

In viral hepatitis, Diet No. 5 according to the Pevzner dietary system is prescribed.

Basic therapy for acute viral hepatitis includes:

  • exclusion of spicy and fried foods;
  • in acute hepatitis B — exclusion of fried, smoked, pickled foods, and refractory fats;
  • absolute ban on alcohol in acute hepatitis B;
  • restriction of protein in case of a risk of hepatic encephalopathy.

What extrahepatic (systemic) manifestations are characteristic of acute hepatitis B?

For hepatitis with a parenteral mechanism of infection, including hepatitis B, the prodromal period is characterized by:

  • arthralgic syndrome;
  • exanthematous syndrome.

Their development is caused by immune complex reactions: circulating immune complexes damage the microvasculature of the skin, mucous membranes, and synovial membranes of the joints.

Class and exam questions

What is the difference in transmission routes between hepatitis A and B?

Hepatitis A virus is transmitted predominantly enterally (fecal-oral route), whereas hepatitis B virus is transmitted parenterally (via blood and other biological fluids).

How do urine and stool color change during the icteric period?

Urine becomes dark (acquires a «beer-like» color), while stool becomes discolored (acholia develops).

Which markers indicate the acute phase of hepatitis B?

In the acute phase (from week 6 to week 24), the surface antigen HBsAg is detected in the blood.

What are the signs of hepatocellular insufficiency?

Decreased synthesis of albumin and prothrombin, development of hemorrhagic syndrome, hepatic encephalopathy, and hepatorenal syndrome.

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What else to study on this topic

  • Pathogenesis of cytolytic and cholestatic syndromes
  • Clinical and diagnostic features of hepatitis E
  • Dynamics of serological markers in hepatitis B
  • Mechanisms of hepatic encephalopathy development
  • Indications and contraindications for infusion therapy

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