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viral hepatitis A (clinic, laboratory diagnostics, treatment)

Etiology: HAV (picornavirus family).

Epidemiology: the source of infection is a patient with all forms of acute infectious process (patients with anicteric and asymptomatic forms are of particular importance). Transmission mechanism: fecal-oral, infection occurs with the use of infected water and food, sometimes by contact and household. The greatest susceptibility to hepatitis A is characteristic of children.

Pathogenesis: HAV is introduced into the human body through the gastrointestinal mucosa, multiplies in the endothelium of the small intestine, mesenteric lymph nodes, then hematogenously enters the liver, where it penetrates into Kupffer's reticulohistiocytic cells, into the parenchymal cells of the liver (hepatocytes) and damages them. In the future, the pathogen enters the intestines with bile and excreted with feces from the patient's body.


a) the minimum incubation period is 7 days, the maximum is 50 days, most often from 15 to 30 days.

b) the initial (preicteric) period - 4-7 days, several options for the clinic:

1) flu-like - the disease begins acutely, body temperature rises rapidly to 38-39 ° C, often with chills, and lasts for 2-3 days. Patients are concerned about headache, aching muscles and joints, sometimes a slight runny nose, pain in the oropharynx. In smokers, the desire to smoke decreases or disappears. Asthenic and dyspeptic symptoms are mild.

2) dyspeptic - characterized by a decrease or disappearance of appetite, pain and heaviness in the epigastric region or right hypochondrium, nausea and vomiting, sometimes - frequent stool up to 2-5 times a day.

3) asthenovegetative - the disease begins gradually, body temperature remains normal. Weakness prevails, working capacity decreases, irritability, drowsiness, headache, dizziness appear.

4) mixed - signs of several syndromes.

On palpation of the abdominal organs, there is an increase, compaction and increased sensitivity of the liver, and often an increase in the spleen. 2-3 days before the appearance of yellowness of the sclera and integument, patients notice that their urine darkened (acquired a dark brown color), and the stool, on the contrary, became lighter (hypocholic).

c) the icteric period - is manifested by yellowness of the sclera, mucous membranes of the oropharynx, and then the skin. The intensity of jaundice increases rapidly and in the next week reaches its maximum. The color of urine becomes darker, and bowel movements become colorless. With the appearance of jaundice, a number of symptoms of the preicteric period subside and disappear in a significant portion of patients (the general weakness and loss of appetite persist for the longest, sometimes a feeling of heaviness in the right hypochondrium). The body temperature is normal.

An increase, compaction and increased sensitivity of the edge of the liver, a positive symptom of Ortner are revealed. The decrease in heart rate is characteristic. Blood pressure is normal or slightly reduced. The first heart tone at the top is weakened. The blood content of total bilirubin is increased, mainly due to direct (bound), the activity of aminotransferases, especially alanine aminotransferase (AlAT) sharply increases, thymol test values ​​are increased, prothrombin index is reduced. Hematological changes are characteristic: leukopenia, neutropenia, relative lympho- and monocytosis, normal or delayed ESR. Serological blood tests determine anti-HAV IgM.

d) the period of convalescence - the general condition improves, signs of a violation of pigment metabolism weaken, a “pigment crisis” sets in. The yellowness of the skin and mucous membranes decreases, urine brightens, bowel movements acquire the usual color, there is a clear tendency to normalize biochemical parameters (bilirubin and prothrombin).

Bilirubinemia with GA often does not exceed 100 μmol / L. A marked decrease in the level of blood bilirubin occurs most often at the 2nd week of jaundice, at the same time, the activity of aminotransferases decreases, and by the 20-25th day from the moment of jaundice, these indicators usually reach normal.

The severity of the condition is distinguished:

a) mild - mild symptoms of intoxication or their complete absence, low severity of jaundice. Bilirubinemia does not exceed 100 μmol / L, and the prothrombin index is more than 60%.

b) moderate - symptoms of intoxication (anorexia, weakness, sleep disturbance, nausea, vomiting, etc.), moderate liver enlargement. Bilirubinemia from 100 to 200 μmol / l, prothrombin index - from 50 to 60%.

c) severe - the symptoms of intoxication are pronounced (increasing general weakness, drowsiness, dizziness, anorexia, up to an aversion to food, repeated vomiting, bright jaundice of the skin, hemorrhagic syndrome, etc.).
Bilirubinemia exceeds 200 μmol / L, the prothrombin index is less than 50%.

According to the severity of the course, there are forms of the HAV

a) mild - a general satisfactory condition in the midst of the disease, the rapid disappearance of jaundice of the skin (after 2-3 weeks), the rapid normalization of AlAT activity (within 1 month).

b) moderate - the average severity of the patient during the height of the disease, the duration of jaundice of the skin up to 3-4 weeks, increased AlAT activity up to 1.5 months.

c) severe - at the height of the disease, the patient is in a serious condition, the duration of jaundice exceeds 4 weeks, the increase in ALAT activity is more than 1.5 months.

d) fulminant (fulminant) - rapid, within hours - days, the development of acute hepatic encephalopathy. In most patients, hemorrhage at the injection site, nosebleeds, vomiting with "coffee grounds" type contents. High activity of aminotransferases, while AcAT prevails over AlAT. The development of coma is fatal.

The cyclic course is observed in 90-95% of cases, in 5% or more the infectious process acquires a wavy character in the form of one or two exacerbations (usually within 1-3 months from the onset of the disease, sometimes later). Exacerbations are manifested by increased signs characteristic of the height of hepatitis. Moreover, the general condition after improvement worsens again, appetite disappears, unpleasant sensations in the liver area intensify, urine darkens, feces become discolored, the intensity of yellowness of the skin increases, and the activity of aminotransferases increases. In GA, even with a prolonged phase of convalescence, the disease usually ends in complete recovery.

Diagnosis: epidemiological history (stay in the HA focus 15–40 days before the disease), acute onset of the disease, a short initial period (usually of the flu-like type), dyspeptic manifestations (anorexia, nausea, vomiting, discomfort in the abdomen) with 3-5- day of the disease, rapid development of jaundice, OAK (characterized by lymphocytosis, ESR slowdown), LHC (early and long-term increase in transaminase activity even in the incubation period), positive qualitative urine reaction to urobilin and bile pigments, ELISA (detection of anti-HAV in blood serum IgM during ne O 2-3 weeks the disease and / or four-fold and a more pronounced increase in titer of anti-HAV IgG, taken in icteric period diseases and convalescence period).


1) for mild and moderate forms - semi-bed mode, for severe - bed; strict observance of general hygiene rules, including oral and skin hygiene; with itching of the skin - rubbing it with a solution of food vinegar (1: 2), 1% solution of menthol alcohol, hot shower at night.

2) control of the daily fluid balance, regular bowel movements - for constipation, laxatives of plant origin, magnesium sulfate.

3) therapeutic diet No. 5, warm food, fractional nutrition, without extractive substances.

4) with GA, a benign course of antiviral is not shown.

5) in the absence of a pigment crisis within a week from the beginning of the peak period, enterosorbents (polyphepan, bilignin, granular carbon sorbents of the type SKN-P, KAU, SUGS, etc.).

6) enzyme preparations to enhance the digestive function of the stomach and pancreas (pancreatin, creon, lycrease, mezim forte, pancytrate, festal, enzystal, panzinorm, unienzym, zymoplex, pancreoflat, abomin, etc.)

7) infusion-detoxification therapy (5% glucose solution, hemodes).

8) if the patient's condition worsens against the background of the ongoing pathogenetic therapy, GCS is administered orally and parenterally, and if they are ineffective for 2-3 days, extracorporeal detoxification (hemosorption, plasmapheresis with partial plasma exchange, plasma absorption, ultrafiltration).

9) with edematous ascites syndrome: concentrated (10-20%) solutions of albumin, plasma; restriction of sodium chloride to 5 g / day; potassium-containing solutions; aldosterone antagonists (veroshpiron), triampur, in the absence of effect - furosemide 40 mg / day 2-4 times a week

10) hepatoprotectors for 1-3 months: silymarin derivatives (legal, karsil, leprotek, silegon, silymar, siromin), preparations from plant extracts (hepatil, hepatofalk, hepabene), essentiale, riboxin, potassium orotate.

11) immunocorrective therapy: thymus preparations (thymalin, thymogen, tactivin, leukinferon), interleukin-2 (roncoleukin).

12) phenobarbital (in the presence of prolonged posthepatitis hyperbilirubinemia)
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