Chronic hepatitis

Causes and classification

Chronic liver inflammation can be of both viral and non-viral origin.

1. Viral hepatitis The highest risk of chronicity is typical for hepatitis B, C, and D viruses. They are transmitted parenterally (via blood): through transfusions, the use of non-sterile surgical instruments, injections, or tattoos.

2. Non-viral hepatitis This group includes liver damage caused by other factors:

• Toxic: alcohol and hepatotoxic drugs (chlorpromazine, methyldopa, isoniazid, nitrofurans).
• Genetic and metabolic: Wilson's disease (copper metabolism disorder), hemochromatosis (iron overload), $\alpha_1$-antitrypsin deficiency.
• Autoimmune: accompanied by the production of specific antibodies (antinuclear, anti-liver-kidney microsomal, anti-DNA) and the appearance of LE cells.

Clinical presentation

The acute stage of viral hepatitis is often latent. Therefore, the diagnosis is frequently established retrospectively. A thorough history taking may reveal past episodes of unexplained fatigue (asthenia), nausea, and epigastric discomfort.

During an exacerbation or in severe disease, the following syndromes are observed:

• Dyspeptic: digestive disorders, diarrhea.
• Jaundice and cholestasis: icterus (yellowing) of the skin and sclera, pale stools (acholic stools), dark urine ("beer-colored urine").
• Extrahepatic manifestations: skin rashes (hemorrhagic vasculitis), joint and muscle pain (arthralgia, myalgia), fever, polyserositis.

Features of specific infections:

• Hepatitis C virus (HCV): characterized by a hidden and paucisymptomatic course that can last for decades, yet steadily leads to cirrhosis and hepatocellular carcinoma.
• Hepatitis D virus (HDV): cannot exist independently and superimposes on hepatitis B (coinfection or superinfection), drastically worsening the prognosis.

Laboratory and instrumental diagnostics

Confirmation of the diagnosis requires a comprehensive approach, including the assessment of liver function and the identification of the specific pathogen.

Biochemical and morphological methods:

• Blood biochemistry reveals cytolysis syndrome — increased transaminase activity (ALT, AST).
• Liver biopsy (histology) is necessary to assess the degree of inflammation, fibrosis, and sclerosis.

Specific markers of viral hepatitis:

• HBV (hepatitis B): the diagnosis is based on the detection of viral DNA and antigen systems. HBsAg indicates the presence of the virus (carrier state or chronic infection). HBcAg is located in liver tissue and enters the bloodstream only upon hepatocyte destruction. HBeAg is a marker of active viral replication and high infectivity of the patient. The antibody system is also evaluated (anti-HBs, anti-HBc, anti-HBe).
• HCV (hepatitis C): core antigens and viral RNA are detected (by PCR). Relying solely on antibodies (anti-HCV) is unreliable: in immunodeficiency or during the seronegative window period, antibodies may be absent despite the presence of the virus.

Complications: hepatocellular failure

In severe disease or decompensation of established cirrhosis (when sclerosis progresses to the formation of regenerative nodules and vascular shunts), hepatocellular failure syndrome develops.

Its key manifestations:

1. Hemorrhagic syndrome (increased bleeding tendency).
2. Progressive jaundice.
3. Ascites (accumulation of fluid in the abdominal cavity).
4. Hepatic encephalopathy (brain damage caused by toxins).
5. "Minor liver signs": palmar erythema (redness of the palms), telangiectasias (spider angiomas).

Principles of treatment

With the advent of specific antiviral therapy, management approaches have changed radically. Treatment is prescribed in the presence of laboratory signs of virus replication (DNA or RNA in serum) and inflammatory activity (based on biochemistry and biopsy).

• For hepatitis B and C, a combination of $\alpha$-interferon and nucleoside analogues is used.
• For hepatitis D, monotherapy with $\alpha$-interferon is used.

Briefly: answers to topical questions

What else to study on this topic

• Pathomorphology of cirrhosis: how sclerosis leads to the formation of regeneration nodules and vascular shunts.
• Autoimmune liver diseases: diagnostic significance of ANA, LKM, and LE cells.
• Genetic causes of chronic hepatitis: mechanisms of Wilson's disease and hemochromatosis.
• Extrahepatic manifestations of exacerbations: the link between hepatitis and hemorrhagic vasculitis and Sjögren's syndrome.
• Current antiviral therapy regimens: indications and specific features of using interferons and nucleosides.

Other topics in the section "Liver, Biliary Tract, and Spleen"

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