Etiology and Epidemiology
The causative agent belongs to the family Hepadnaviridae (genus Orthohepadnavirus). Its genome is a circular double-stranded DNA with a characteristic defect: one strand is shorter than the other. The virus demonstrates extreme resistance to temperature fluctuations and most disinfection methods.
The source of infection includes patients with any form of the disease, but the main epidemiological threat is posed by silent carriers.
Main transmission routes:
- Parenteral: natural and artificial (medical procedures, blood transfusions).
- Sexual.
- Vertical: transmission from mother to fetus (transplacentally or intrapartum), which is especially common in the third trimester. The risk is directly proportional to the concentration of HBsAg in the mother's blood.
Immunopathogenesis
Once the virus reaches the liver via the bloodstream, it does not kill hepatocytes directly. The leading role in liver tissue necrosis is played by the macroorganism's immune system.
The outcome of the infection strictly depends on immune reactivity:
- Adequate response (replicative phase): controlled cytolysis leads to virus elimination and complete recovery.
- Weak response (integrative phase): cytolysis is mild, viral DNA integrates into the hepatocyte genome, and full clearance does not occur. Persistence and carrier state are established.
- Hyperergic reaction: the immune system destroys both infected and intact cells. Massive parenchymal necrosis develops, which underlies severe fulminant (malignant) forms.
Clinical periods of typical course
The disease proceeds cyclically and is divided into four stages:
- Incubation period: lasts from 2 to 6 months. There are no clinical symptoms, but by the end of the period, transaminases are already rising and serological markers appear.
- Pre-jaundice (prodromal) period: lasts from several hours to 2–3 weeks. Asthenic and arthralgic/myalgic syndromes are characteristic. Temperature is normal or low-grade (subfebrile), and catarrhal symptoms are absent. Urine darkens early, stool becomes acholic, and the liver enlarges.
- Icteric (jaundice) period: lasts from 7–10 days to 1.5–2 months. Important differential sign: unlike hepatitis A, intoxication does not subside with the appearance of jaundice, but rather progresses. Maximum cytolysis is registered, prothrombin index (PTI) and albumin levels drop, while the thymol turbidity test remains normal or only slightly elevated.
- Convalescence: extends up to 4–5 months. Seroconversion occurs: HBsAg and HBeAg disappear, and protective anti-HBs appear.
Principles of therapy and follow-up (dispensary care)
Patients are subject to strict hospitalization. Basic therapy includes a strict bed rest/regimen, medical nutrition, enterosorbents, choleretics, and vitamins.
For moderate forms, infusion detoxification with dextrose solutions is indicated. For severe courses, blood products (fresh frozen plasma, albumin) are added, and a short course of glucocorticosteroids (prednisolone 2–3 mg/kg/day) is prescribed.
Treatment of malignant forms:
- Megadoses of GCS (up to 10–15 mg/kg/day fractionally).
- Protease inhibitors (aprotinin) and heparin to correct hemostasis.
- Extracorporeal methods (plasmapheresis, hyperbaric oxygenation).
- Sanation of the gastrointestinal tract (lavage, lactulose, cephalosporins) to suppress toxin absorption.
After discharge, dispensary follow-up continues for 1 year. Sports training is prohibited for 12 months.
Antigen markers: HBsAg — virus on the Surface, HBcAg — in the Core, HBeAg — marker of infectivity/Envelop. Anti-HBs antibodies mean protection (recovery/vaccination).
Class and exam questions
Why can massive hepatic necrosis develop in hepatitis B?
Due to the hyperergic response of the immune system, when not only infected but also healthy (intact) hepatocytes are destroyed.
How to differentiate hepatitis B from hepatitis A by the course of the icteric period?
In hepatitis A, the onset of jaundice is accompanied by an improvement in the patient's well-being, whereas in hepatitis B, the intoxication syndrome continues to progress.
What biochemical parameters are characteristic of hepatitis B?
A sharp increase in transaminases (5–10 fold) and the direct bilirubin fraction, a decrease in PTI and total protein. Meanwhile, the thymol turbidity test usually remains within the normal range.
What else to study on this topic
- Pathogenesis of hepatic encephalopathy and stages of the fulminant form
- Specific serological profiles (atypical seroconversion)
- Differences between hepatitis B and delta infection (hepatitis D) in co- and superinfection
- Differential diagnosis with obstructive (mechanical) and hemolytic jaundice
- Indications for extracorporeal detoxification methods
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