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Infectious Diseases · Viral Hepatitis and HIV

Laboratory diagnosis of hepatitis

Hepatitis viralis acuta

Laboratory diagnosis of acute viral hepatitis is based on identifying liver damage syndromes and specific pathogen markers. The baseline panel includes a biochemical blood test to assess hepatocyte function, as well as ELISA and PCR for precise etiological verification.

Cytolytic syndromeA sharp increase in ALT and AST precedes the clinical symptoms of the disease.
ELISA and PCRThe basis of etiological diagnosis, searching for antibodies and viral nucleic acids.
Severity predictorA drop in the prothrombin index indicates depression of liver function.
HemogramLeukopenia and lymphomonocytosis are typical, ESR is decreased or normal.
4 min readFor medical studentsUpdated 10.10.2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesPending instructor review

Basic clinical and laboratory syndromes

Acute viral hepatitis is characterized by strict cyclicity with a sequence of pre-icteric and icteric periods. The diagnostic process begins with assessing the epidemiological history and identifying the leading syndromes.

  • Hemogram changes: The complete blood count has low diagnostic value, but reflects the overall viral load. A normal leukocyte count or leukopenia (neutropenia) is typical, with a shift in the formula toward relative or absolute lymphomonocytosis. ESR is usually decreased or within the normal range.
  • Disorder of pigment metabolism: During the icteric period, bile pigments are detected in the urinalysis (urine visually darkens), and stool becomes discolored (acholic).
  • Biochemical markers:
  • Cytolytic syndrome: Has the highest diagnostic value, as biochemical changes precede the clinical picture. It manifests as a sharp increase in serum transaminases (ALT and AST increase by 10–20 times or more). In moderate severity, ALT activity exceeds AST.
  • Cholestatic syndrome: Indicates impaired bile outflow. The direct (conjugated) fraction of bilirubin predominates in the blood, and the activity of excretory enzymes—alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT)—increases. An increase in the levels of cholesterol, $\beta$-lipoproteins, and bile acids is also characteristic.
  • Impairment of protein-synthetic function: An early and pronounced decrease in the prothrombin index (PTI) and serum albumin is a reliable laboratory predictor of severe disease.

Specific etiological verification

To confirm the diagnosis, methods aimed at finding markers of specific viruses (A, B, C, D, E) are used.

  • Enzyme-linked immunosorbent assay (ELISA): The baseline method of early diagnosis, detecting specific antigens and antibodies with mandatory differentiation of immunoglobulin classes.
  • Hepatitis A: Anti-HAV IgM serve as a marker of the acute phase (appearing at the end of the incubation period and circulating for 3–6 months). Anti-HAV IgG is a marker of past infection and immunity, persisting practically for life.
  • Hepatitis E: The search is aimed at early anti-HEV IgM antibodies. An important diagnostic feature is the high risk of false-negative results, as these antibodies persist in the blood for a very short time.
  • Polymerase chain reaction (PCR): Used to detect nucleic acids (HBV DNA, HCV RNA, HDV, HAV, HEV). The goals of PCR include confirming active viral replication, assessing disease prognosis, and monitoring the effectiveness of antiviral therapy.
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Laboratory profile of atypical forms and clinical variants

The severity of laboratory changes depends on the clinical form of the disease. The diagnostic logic ranges from minimal symptoms to their complete absence:

  • Anicteric form: Jaundice is absent, but fermentemia (elevated liver enzymes) is recorded.
  • Subclinical form: Complete absence of external manifestations. The diagnosis is based solely on biochemical changes (increase in ALT and AST) and the detection of serological markers.
  • Inapparent form: Absolute absence of clinical and biochemical signs (transaminases are normal). Verification is possible only upon detecting specific virus markers.
  • Cholestatic variant: Characterized by the development of bilirubin-transaminase dissociation. In this phenomenon, a pronounced increase in the bilirubin level is not accompanied by a proportional increase in transaminase activity.

Severity assessment and diagnosis structure

Laboratory data play a key role in formulating the final clinical diagnosis.

The severity of the disease is determined by the severity of intoxication, the presence of hemorrhagic syndrome, and signs of acute liver failure (ALF). Special attention is paid to pregnant women (especially in the III trimester) with suspected hepatitis E, as they are prone to a fulminant course with a high risk of complications.

The detailed diagnosis must indicate: nosology and form, severity degree, presence of complications (e.g., acute liver failure), background conditions (gestational age), and clear laboratory justification. The justification is supported by the results of specific tests indicating the method, date, analysis number, and detected marker (e.g., ELISA: anti-HEV IgM "+").

How to memorize

To remember hepatitis A markers: IgM — "Momentary" (acute) infection, IgG — "Years" (lifelong immunity).

Class and exam questions

What hemogram changes are typical for acute viral hepatitis?

A normal leukocyte count or leukopenia, relative lymphomonocytosis, and decreased (or normal) ESR are typical.

What is bilirubin-transaminase dissociation?

This is a laboratory phenomenon in the cholestatic variant of the disease, when a pronounced increase in bilirubin is not accompanied by a proportional increase in transaminase activity.

Which parameter indicates severe hepatitis?

An early predictor of severe disease is a decrease in the prothrombin index (PTI) and albumin, which indicates depression of the protein-synthetic function of the liver.

What is the special feature of serological diagnosis of hepatitis E?

Acute phase anti-HEV IgM antibodies persist in the blood for a very short time, which creates a high risk of obtaining false-negative ELISA results.

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What else to study on this topic

  • Topographic classification and differential diagnosis of jaundice.
  • Clinical and epidemiological features of hepatitis E in pregnant women.
  • Classification of acute viral hepatitis by cyclicity and duration.
  • Rules for formulating a detailed clinical diagnosis in viral hepatitis.
  • Latent and inapparent forms: subtleties of differential diagnosis.

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