Clinical presentation and course
The disease is distinguished by strict cyclicity, featuring pre-icteric and icteric periods in its clinical course. When assessing the probability of infection, a thorough epidemiological history is of paramount importance to identify direct and indirect risk factors for transmission.
Laboratory diagnostics: non-specific changes
In acute viral hepatitis (AVH), characteristic alterations are observed in clinical and biochemical blood tests:
- Complete blood count: leukocyte count is normal or decreased (leukopenia); the formula shows relative or absolute lymphomonocytosis. ESR is typically slowed. Thrombocytopenia and anemia may be noted.
- Cytolysis syndrome: an early and highly informative sign, manifested by an increase in serum transaminases (ALT and AST), with ALT activity exceeding AST in moderately severe cases.
- Cholestasis syndrome: elevated alkaline phosphatase (ALP) and gamma-glutamyl transpeptidase (GGT).
- Pigment metabolism: elevation of bilirubin (predominantly the conjugated fraction). Clinically, this is expressed as dark urine and pale, clay-colored stools (acholia).
- Severity assessment: an early decrease in prothrombin index (PTI) indicates a severe course and impaired liver function.
Specific (etiological) diagnostics
Laboratory verification methods are used to confirm the diagnosis:
- ELISA (enzyme-linked immunosorbent assay): the baseline method for detecting specific antibodies (IgM to HAV). Differentiation of immunoglobulin classes (IgM, IgG) allows determination of the stage of the process (acute phase, past infection).
- Differential diagnosis: performed to rule out other viral infections (HBV, HCV, HDV, HEV, herpesvirus group) using ELISA and PCR.
Principles of differential diagnosis of jaundice
Jaundice is classified into pre-hepatic, hepatocellular, and post-hepatic. Viral hepatitis causes hepatocellular jaundice, which pathogenetically combines cytolysis and cholestasis syndromes against a background of hyperbilirubinemia.
Hepatitis A must be differentiated from other conditions causing liver damage:
- Infectious mononucleosis (EBV): gradual onset, fever, tonsillitis, lymphadenopathy, atypical mononuclear cells in the blood (>12%).
- Leptospirosis: contact with rodents/water bodies, myalgia (calf pain), neutrophilic leukocytosis, kidney damage (AKI).
- Toxic and alcoholic hepatitis: neutrophilic leukocytosis, AST > ALT elevation in alcoholic hepatitis, onset of AKI in toxic poisoning.
- Drug-induced liver injury: absence of a pre-icteric period, eosinophilia.
- Wilson's disease: low ALP levels, decreased ceruloplasmin, Kayser-Fleischer rings.
Briefly: answers to topical questions
What clinical variants of the course are characteristic of the pre-icteric period of hepatitis A?
The pre-icteric period of viral hepatitis A is described in the cited sources as follows:
- typically — acute onset with febrile fever, intoxication, and dyspeptic syndromes;
- objectively, hepatomegaly, tenderness/sensitivity of the liver edge, and possible splenomegaly may be detected;
- already in this period, a significant increase in aminotransferase activity (ALT, AST) is recorded;
- atypically, in 2–5% of cases, the prodromal period can be asymptomatic or mild, and then jaundice becomes the first manifestation.
What are the main mechanisms and routes of transmission of the hepatitis A virus?
The primary mechanism of transmission of the hepatitis A virus is fecal-oral, which predisposes the infection to epidemic spread.
The realization of the fecal-oral mechanism includes the following transmission routes:
- waterborne;
- foodborne;
- contact-household.
Risk factors within the incubation period include staying in endemic areas, contact with infected individuals, drinking unboiled water from questionable sources, or eating unwashed vegetables and fruits.
What is the duration of the incubation period in viral hepatitis A?
The incubation period for viral hepatitis A ranges from 7 to 50 days. On average, this latent stage of the infectious process lasts from 2 to 4 weeks. During this time, the virus, having entered the body enterally, settles in the tissues of the gastrointestinal tract, after which it reaches the liver via the portal vein system to begin active replication.
Class and exam questions
What changes in the complete blood count are typical for viral hepatitis?
Leukopenia (or normal leukocyte count), lymphomonocytosis, and delayed ESR.
How to differentiate cytolysis syndrome in viral versus alcoholic hepatitis?
In viral hepatitis (moderate severity), ALT is higher than AST, whereas in acute alcoholic hepatitis, an elevation of AST predominates.
What is a predictor of a severe course of hepatitis?
Early and pronounced decrease in prothrombin index (PTI), indicating suppressed protein-synthetic function of the liver.
What else to study on this topic
- Acute bacterial hepatitis: yersiniosis and leptospirosis
- Alcoholic hepatitis: icteric, cholestatic, and fulminant forms
- Drug-induced liver injury and their clinical syndromes
- Autoimmune hepatitis: serological types and criteria
- Extrahepatic manifestations in viral hepatitis (cytotoxic and immune complex mechanisms)
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