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viral hepatitis B (clinic, diagnosis, treatment)

Etiology: hepatitis B virus (HBV, HBV) - DNA-based hepatadavirus. The viral envelope protein is represented by the surface antigen (HBsAg) - the “Australian” AG, the nucleocapsid contains the core antigen (HBcAg), infectious (HBeAg), HBxAg, DNA and enzymes (polymerase and protein kinase). Each of the HBV antigens causes a humoral immune response, manifested by the production of the corresponding antibodies (anti-HBs, anti-HBc, anti-HBe).

Epidemiology: source - patients with both manifest and asymptomatic forms of acute and chronic hepatitis B. The mechanism of infection: parenteral; transmission methods: natural (from mother to child - vertical and perinatal; through sexual contact with an infected person - sexual; during other contacts with an infected person - horizontal) and artificial (in violation of the integrity of the skin and mucous membranes).

Pathogenesis: the virus does not have a direct damaging effect on hepatocytes, their cytolysis is carried out immuno-indirectly due to a reaction from cellular immunity through cytotoxic T-lymphocytes.


a) the incubation period from 42 to 180 days, an average of 60-120 days.

b) the initial (preicteric) period - 7-14 days; the disease begins with signs of a mixed variant of the preicteric period without a significant increase in body temperature. Symptoms of intoxication and dyspeptic manifestations are moderate, in a third of patients an arthralgic variant of the initial period (increased pain in large joints at night and in the morning). The initial period of the disease lasts 7-14 days or more, however, with infections associated with blood transfusion, it can be shorter.

c) the icteric period - 3-4 weeks, more pronounced and prolonged pain, sometimes sharp pains in the right hypochondrium. Weakness persists, loss of appetite comes to anorexia. Nausea and even vomiting are frequent. Often itchy skin. The liver is always enlarged, on palpation it is smooth, with a slightly densified texture, an increase in the spleen is noted. Gallbladder symptoms may be positive. In peripheral blood, leukopenia with lympho- and monocytosis, sometimes with a plasma reaction. ESR is reduced to 2-4 mm / h, in the convalescence period it can accelerate to 18-24 mm / h with subsequent normalization in the absence of complications. Hyperbilirubinemia is more pronounced and persistent than with GA, especially in the 2-3rd week of the icteric period; there is an increase in the activity of aminotransferases in blood serum with a decrease in the sublimate test and prothrombin index. Serological blood tests show HBsAg, anti-HBc IgM.

In severe cases - signs of an increase in liver failure and progression of necrotic processes in the liver - increased general muscle weakness, dizziness, apathy, anorexia, nausea, increased vomiting, the appearance of unmotivated excitement, memory impairment; progressive increase in icteric color of the skin; a decrease in the size of the liver, increased soreness of its edge; the appearance of hemorrhagic syndrome (petechial rash on the skin, nosebleeds, hemorrhage at the injection site, “tarry” stool, vomiting with an admixture of blood); the appearance of edematous ascites syndrome (edema on the feet and lower third of the legs, ascites); the occurrence of fever, tachycardia, neutrophilic leukocytosis; an increase in the content of total bilirubin in blood serum with an increase in its indirect fraction; a decrease in cholesterol below 2.6 mmol / L.

d) the period of convalescence — normalization of the activity of aminotransferases by the 30-35th day of the disease with a mild form, with moderate form — by the 40-50th day, with severe form - by the 60-65th day.

Diagnosis: medical history (blood transfusion, surgery, etc.), clinic (gradual onset of the disease, prolonged icteric period, allergic skin rashes, lack of well-being or worsening with the appearance of jaundice, prolonged icteric period with a slow disappearance of the disease’s symptoms in the period of convalescence), serological reactions (early detection of HBsAg, HBeAg, anti-HBc IgM, and HBV DNA in the blood, with a favorable course - rapid disappearance of HBeAg first with the appearance of anti-HBe, HBV DNA, then HBsAg with the appearance Anti-HBs; replaced early anti-HBc IgM appear later anti-HBc IgG).

Long-term circulation (more than 3 months) in the blood of HBeAg, HBV DNA, as well as anti-HBc IgM and HBsAg in a stably high titer indicate a prolonged course of the infection process and a high probability of chronicity. The possible development of chronic hepatitis should also be considered when detecting HBsAg in a stable titer for 6 months. and more from the onset of the disease, even in the absence of markers of active viral replication (HBeAg, anti-HBc IgM, HBV DNA), clinical symptoms, and normal biochemical parameters.

For the diagnosis of chronic HBV - a puncture biopsy.

In this case, only the results of analyzes of puncture biopsy samples of the liver help to establish the correct diagnosis.


1. Therapy - as with HAV (see question 9.1.)

2. Antiviral - alpha-interferon (recombinant: intron A, roferon A, realdiron and native: wellferon, human leukocyte interferon) with a threat of chronicity or a gradient course, synthetic nucleosides - famciclovir (famvir), lamivudine (epivir, azidothymidine, thymoside), protease inhibitors - saquinavir (invirase), indinavir (crixivan), interferon inducers - neovir (cycloferon), amixin, immunomodulators - leukinferon, interleukin-1 (betaleukin), interleukin-2 (roncoleukin). It is indicated for severe hepatitis B (in the presence of markers of active viral replication) with the risk of developing acute liver failure, especially with signs of hepatic encephalopathy, as well as with the threat of chronicity.

3. For complications associated with encephalopathy: stopping the psychomotor agitation of sodium with oxybutyrate, sedux-sen; gastric lavage (via a nasogastric tube) and high or siphon enemas to reduce auto-toxicity; oral administration of poorly absorbed antibiotics (kanamycin 0.5 g 4 times a day), enterosorbents; fractional enteral nutrition in combination with parenteral; GCS (not less than 180-240 mg of prednisolone) parenterally; infusion therapy; with hemorrhagic manifestations - protease and fibrinolysis inhibitors (epsilon-aminocaproic acid, contracal, gordox).
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