Diagnosis of chronic hepatitis in children

Diagnosis of chronic hepatitis is based on a comprehensive examination of the patient:

Diseases of the digestive system

1. clinical and biochemical;
2. virological;
3. immunological;
4. morphological;
5. assessment of the state of portal hemodynamics.

The condition of the liver is assessed by the severity of cytolytic syndrome, hepatocyte failure syndrome, mesenchymal-inflammatory syndrome, cholestatic syndrome, liver shunt syndrome, and the presence of indicators of regeneration and tumor growth.

Determination of markers of hepatitis viruses is carried out - viral antigens (Ag) and antibodies (Ab) to them.

Serological markers of hepatitis viruses

Virus	Serological markers
HAV	HAV Ab IgG, HAV Ab IgM, HAV RNA
HBV	HBsAg, HBsAb. HBeAg, HBeAb, HBc Ab IgM, HBc Ab IgG, HBV DNA
HCV	HCV Ab IgG, HCV Ab IgM, HCV RNA
HDV	HDV Ab IgG, HDV Ab IgM, HDV RNA
HEV	HEV Ab IgG, HEV Ab IgM, HEV RNA

Morphological assessment of the liver structure is carried out using a liver puncture biopsy and histological examination of the biopsy, as well as assessment using ultrasound or computed tomography, laparoscopy.

Differential diagnosis is carried out:

1. with congenital developmental anomalies:
   • liver (congenital liver fibrosis, polycystic disease);
   • bile ducts (arteriohepatic dysplasia - Alagille disease, Zellweger and Byler syndromes, Caroli disease);
   • intrahepatic branches of the portal vein (veno-occlusive disease, septa and thrombosis of the hepatic veins);
2. with hereditary pigment hepatoses (Gilbert's disease, Dubin-Jones, Rotor's disease, Crigler-Najjar disease type I and II).

Gilbert's disease is the most common form of hereditary hyperbilirubinemia, the origin of which is associated with insufficient adsorption of bilirubin from plasma and, possibly, a violation of its intracellular transport. It is inherited in an autosomal dominant manner with high penetrance. Boys are ill twice as often as girls. Gilbert's disease manifests itself at any age, most often in the prepubertal and pubertal periods.

The main manifestations are icteric sclera and variable light yellow skin color. Asthenovegetative disorders in the form of increased fatigue, psychoemotional lability, and sweating are observed in 20-40% of patients. Dyspeptic symptoms are less common. In 10-20% of patients, the liver protrudes from the hypochondrium by 1.5-3 cm, the spleen is not palpable. Anemia is not typical. All patients have low hyperbilirubinemia (18-68 μmol/l), represented mainly by the unconjugated fraction. Other liver functions are not impaired.

3. with metabolic liver diseases:

Hepatolenticular degeneration (Wilson-Konovalov disease) is a hereditary disease transmitted in an autosomal recessive manner (13ql4-q21), caused by low or abnormal synthesis of ceruloplasmin, a protein that transports copper.

As a result of the transport defect, copper is deposited in tissues, particularly around the iris (green Kayser-Fleischer ring) and in the central nervous system.

In typical cases, along with liver damage such as chronic hepatitis or cirrhosis, there is hemolytic anemia, thrombocytopenia, leukopenia, damage to the nervous system (hyperkinesis, paralysis, paresis, athetosis, epileptic seizures, behavioral, speech, writing disorders, dysphagia, salivation, dysarthria), renal tubular acidosis (glucosuria, aminoaciduria, phosphaturia, uraturia, proteinuria).

To diagnose Wilson-Konovalov disease, the following are used:

• slit lamp eye examination (reveals Kayser-Fleischer ring);
• determination of the level of ceruloplasmin in the blood serum (typically a decrease of less than 1 μmol/l);
• detection of a decrease in copper in the blood serum (in the late stages of the disease, less than 9.4 μmol/l) and an increase in copper in daily urine (above 1.6 μmol/day or 50 μg/day).

Hereditary disorders of carbohydrate metabolism (galactosemia, glycogenosis types I, III, IV, VI, fructosemia, mucopolysaccharidoses).

Hereditary defects of urea metabolism; tyrosinemia types I and II, cystinosis.

Hereditary disorders of lipid metabolism (Wolman disease, cholesterolosis, Gaucher disease, Niemann-Pick type C), steatorosis (fatty liver disease).

Hemochromatosis, hepatic porphyria.

Cystic fibrosis, a1-antitrypsin deficiency.

• with liver cirrhosis, characterized by disorganization of the lobular-vascular architecture of the liver with the appearance of signs of portal hypertension, hepatocellular and mesenchymal-inflammatory disorders;
• with liver fibrosis - focal proliferation of connective tissue as a result of reactive and reparative processes in various liver diseases: abscesses, infiltrates, gummas, granulomas, etc.;
• with parasitic liver diseases (echinococcosis, alveolar echinococcosis);
• with liver tumors (carcinoma, hepatoblastoma, hemangioma, metastases);

With secondary (symptomatic) liver damage:

• in case of extrahepatic blockade of portal circulation;
• for diseases of the cardiovascular system (Epstein's anomaly, adhesive pericarditis, heart failure);
• for diseases of the blood system (leukemia, lymphogranulomatosis, reticulohistiocytosis, porphyria, sickle cell anemia, lymphomas, myeloproliferative diseases, hemochromatosis);
• in immunopathological diseases (systemic lupus erythematosus, amyloidosis, sarcoidosis, primary immunodeficiency diseases - Shwachman syndrome, etc.).

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