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 condition of portal hemodynamics.

The liver status is judged by the severity of cytolytic syndrome, hepatocyte insufficiency syndrome, mesenchymal inflammatory syndrome, cholestatic syndrome, liver shunting syndrome, the presence of indicators of regeneration and tumor growth.

The markers of viruses of hepatitis - antigens of viruses (Ag) and antibodies (Ab) are conducted 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 evaluation of the structure of the liver is performed with the help of puncture liver biopsy and histological examination of the biopsy, as well as evaluation with ultrasound or computed tomography, laparoscopy.

Differential diagnosis is carried out:

1. with congenital anomalies of development:
   • liver (congenital liver fibrosis, polycystic disease);
   • biliary ducts (arteriopecia dysplasia - Alagill's disease, Zellweger and Byler syndrome, Caroli's disease);
   • intrahepatic branching of the portal vein (venokoklyuzionnaya disease, septum and thrombosis of the hepatic veins);
2. with hereditary pigmentary hepatoses (diseases of Gilbert, Dabin-Jones, Rotor, Kriegler-Nayyar I and II types).

Gilbert's disease is the most common form of hereditary hyperbilirubinemia, the origin of which is associated with a lack of adsorption of bilirubin from the plasma and, possibly, a violation of its intracellular transport. Inherited by autosomal dominant type with high penetrance. Boys are sick 2 times more often than girls. Gilbert's disease manifests itself at any age, most often in the prepubertal and puberty periods.

The main manifestations are icteric sclera and a fickle light yellow color of the skin. In 20-40% of patients, asthenovegetative disorders are observed in the form of increased fatigue, psychoemotional lability, sweating. Dyspeptic phenomena 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. In all patients, low hyperbilirubinemia (18-68 μmol / L) is present, mainly represented by an unconjugated fraction. Other functions of the liver are not violated.

3. with metabolic diseases of the liver:

Hepatolenticular degeneration (Wilson-Konovalov's disease) is a hereditary disease transmitted through an autosomal recessive type (13ql4-q21), caused by a low or abnormal synthesis of ceruloplasmin-a protein transporting copper.

Due to a transport defect, copper deposits in the tissues, in particular around the iris (the green Kaiser-Fleischer ring) and in the central nervous system occur.

In typical cases, along with liver damage as chronic hepatitis or cirrhosis, there are hemolytic anemia, thrombocytopenia, leukopenia, nervous system damage (hyperkinesia, paralysis, paresis, athetosis, epileptic seizures, behavioral disorders, speech, letters, dysphagia, salivation, dysarthria). Renal tubular acidosis (glucosuria, aminoaciduria, phosphaturia, uraturia, proteinuria).

For the diagnosis of Wilson-Konovalov's disease use:

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

Hereditary disorders of carbohydrate metabolism (galactosemia, glycogenoses I, III, IV, VI types, fructoemia, mucopolysaccharidosis).

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

Hereditary disorders of lipid metabolism (Wolman's disease, cholesterosis, Gaucher's disease, Niemann-Pick type C), steatoroses (fatty liver disease).

Hemochromatosis, hepatic porphyria.

Cystic fibrosis, deficiency of a1-antitrypsin.

• with cirrhosis of the liver, characterized by disorganization of the lobular-vascular architectonics of the liver with the appearance of signs of portal hypertension, hepatic-cellular and mesenchymal-inflammatory disorders;
• with liver fibrosis - focal proliferation of connective tissue as a result of reactive and reparative processes with various liver diseases: abscesses, infiltrates, gums, granulomas, etc .;
• with parasitic liver diseases (echinococcosis, alveococcosis);
• with liver tumors (carcinoma, hepablastoma, hemangioma, metastasis);

With secondary (symptomatic) lesions of the liver:

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

[1], [2], [3], [4], [5], [6], [7], [8], [9],