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Hepatitis A(synonyms for the disease: Botkin's disease, infectious, or epidemic, hepatitis) - an acute infectious disease caused by the hepatitis A virus, predominantly with a fecal-oral mechanism of infection; characterized by the presence of an initial period with an increase in body temperature, dyspeptic, flu-like symptoms, predominant liver damage, symptoms of hepatitis, metabolic disorders, and often jaundice.

Historical data of hepatitis A

For a long time, the disease was mistakenly considered catarrhal jaundice, caused by blockage of the common bile duct with mucus and swelling of its mucous membrane (R. Virchow, 1849). For the first time, the position that so-called catarrhal jaundice is an infectious disease was scientifically substantiated was expressed by S. P. Botkin (1883). The causative agent of the disease, hepatitis A virus (HAV), was discovered in 1973. S. Feinstone.

Etiology of hepatitis A

The causative agent of hepatitis A belongs to the family Picornaviridae(Italian picollo - small, small; English RNA - ribonucleic acid), a genus of enteroviruses (type 72). Unlike other enteroviruses, HAV replication in the gut has not been definitively proven. HAV is a particle with a size of 27 - 32 nm, which does not contain lipids and carbohydrates. The virus can reproduce in some primary and continuous cell cultures of humans and monkeys. The virus is resistant to environmental factors, can survive at room temperature for several months, is sensitive to formalin, concentrated solutions of chloramine and bleach, is resistant to freezing, and remains viable for two years at a temperature of -20 ° C.
Sterilization with flowing steam at a temperature of 120 ° C for 20 minutes completely inactivates infectious material.

Epidemiology of hepatitis A

The only source of infection is a sick person. The release of the pathogen into the external environment with feces begins during the incubation period, 1-3 weeks before the onset of clinical symptoms of the disease. The greatest contagiousness is observed in the first 1-2 days of the disease and stops after the 10-14th day of the disease. The pathogen is found in urine, menstrual blood, and semen, which is of less epidemiological significance.
There is no pathogen in breast milk. Often the source of infection are patients with anicteric and inparant forms of viral hepatitis A, the number of which can significantly exceed the number of patients with the manifest form. Virus carriage is not observed.
The main mechanism of infection is fecal-oral, carried out by water, food and contact-household routes. There are a large number of cases of food and water outbreaks of infection. Often group outbreaks of viral hepatitis A occur in preschool institutions and schools. There is a possibility of parenteral infection with hepatitis A during medical procedures, however, the short duration of the period of viremia makes this route of infection secondary. Sexual transmission is possible.
The susceptibility of people to infection with hepatitis A is 100%. Due to the intensive spread of the disease, most people manage to recover from the icteric or anicteric form of the infection before the age of 14. In terms of age structure, the incidence of hepatitis A is close to childhood infectious diseases (measles, scarlet fever). Adults account for approximately 10-20% of all hepatitis A cases.
Seasonality is autumn-winter, observed only among children. The periodicity of the increase in incidence with an interval of 5-5 years is typical.
Hepatitis A is a very common infection; the incidence rate depends on the state of sanitary culture and public amenities. Immunity is strong and lifelong.

Pathogenesis and pathomorphology of hepatitis A

Pathogenesis has not been studied enough. This is largely due to the lack of an adequate model of the disease and the lack of data on the replication of the pathogen. According to the scheme developed by A.F. Bluger and I. GI. Novitsky (1988), there are seven main phases of pathogenesis.
I. Epidemiological phase, or penetration of the pathogen into the human body.
II. Enteral phase. The virus enters the intestines, but it cannot be detected in the cells of the intestinal mucosa. The hypothesis that the virus multiplies in the intestines is confirmed experimentally in tamarin monkeys. According to electron morphological studies, at the onset of the disease, signs of cytolysis of varying degrees are found in enterocytes, similar to those observed in various viral infections.
III. Regional lymphadenitis.
IV. The primary generalization of infection is the penetration of the pathogen through the blood into the parenchymal organs.
V. Hepatogenic phase, which begins with the penetration of the virus into the liver. There are two forms of liver damage. In one case, the changes cover the mesenchyme, hepatocytes are not damaged, and the process ends in the phase of parenchymal dissemination. In the second form, moderate damage to hepatocytes is observed. It was believed that cell damage was caused only by the cytopathic effect of the virus (CPE). However, the development of pathological changes in the liver coincides with the appearance of antibodies against the virus, and the most significant changes develop after the cessation of viral replication. It has been proven that the virus is capable of causing a strong and rapid immune response, antibodies appear even before the onset of clinical symptoms, and sensitization of immunocytes occurs early. All this gives reason to believe that the destruction of hepatocytes is largely associated with immunological processes.
VI. The phase of secondary viremia associated with the release of the virus from damaged liver cells.
VII. Convalescence phase.
Secondary viremia ends with strengthening of the immune system, liberation of the body from the virus, and the predominance of reparative processes.
Morphological changes in the case of hepatitis A are somewhat different from those observed in patients with viral hepatitis B. The characteristic morphological type of liver damage in hepatitis A is portal or periportal hepatitis. Inflammatory and alternative changes in the central zone of the hepatic lobule around the hepatic vein, as a rule, are not observed. Electron microscopic examination does not detect hepatitis A virus in liver tissue.

Hepatitis A Clinic

The following clinical forms of hepatitis A are distinguished: icteric (with cytolysis syndrome; with cholestasis syndrome), anicteric, subclinical.
The disease most often occurs in an acute cyclic form, although exacerbations, relapses, protracted course and transition to a chronic form are possible (0.3-0.5% of patients).
The following periods of illness are distinguished: incubation; initial, or pre-Zhovtyanichny; icteric; convalescence. The incubation period lasts 10-50 days, on average 15-30 days.

Jaundice form

Initial period. In most cases, the disease begins acutely. An increase in temperature (no more than 38.5 ° C) is observed within 2-3 days. Patients complain of general weakness, loss of appetite, nausea, sometimes vomiting, pain or a feeling of heaviness in the right hypochondrium and epigastric region. Upon examination, the liver and sometimes the spleen are moderately enlarged. This onset of the disease is observed in the dyspeptic variant. The flu-like variant of the initial period is characterized by short-term fever (2-3 days), short-term body aches, and sore throat.
At the end of the initial period, the urine becomes dark in color (strong tea or beer), which is due to the presence of bile pigments and precedes jaundice by 2-3 days.
The patient may complain of itchy skin. In the initial period of the disease, an important laboratory sign of viral hepatitis is an increase in the activity of serum enzymes, primarily alanine aminotransferase (ALT). The duration of the initial period is on average 3-7 days.

Jaundice period

Subictericity of the sclera indicates the end of the initial period and the transition to icteric. Jaundice reaches its maximum development within 2-3 days, after which it lasts for an average of 5-7 days. First it appears on the sclera, mucous membrane of the soft palate, frenulum of the tongue, then on the skin of the face and torso. With the development of jaundice, a significant part of the clinical manifestations of the disease characteristic of the initial period disappear, the general condition of patients improves, in most of them appetite normalizes, nausea and signs of intoxication disappear.
In most cases, the disease has a mild course, only 3-5% of patients have a moderate course. Severe form of hepatitis A is rare (1-2%). When examining the patient (palpation), attention is drawn to a further enlargement of the liver, which can be dense, sensitive, and even painful. More often than in the initial period, an enlarged spleen is detected.
During the period of increasing jaundice, the main laboratory indicator is the level of bilirubin in the blood serum. The concentration of bilirubin in the blood of patients with hepatitis A can vary widely, reaching 300-500 µmol/l in severe forms of the disease, although such high levels are rarely found. Hyperbilirubinemia is characterized by the predominant accumulation of a bound (direct, soluble) fraction of pigment in the blood, which accounts for 70-80% of its total amount. The relatively low level of free bilirubin fraction (20-30%) indicates that the function of hepatocytes regarding the binding of bilirubin with glucuronic acid is the least vulnerable, excretory function is more impaired. Impaired excretion of bilirubin into the intestines leads to discoloration of stool. Thus, clinically, disorders of pigment metabolism are manifested by jaundice, darkening of urine and discoloration of feces. Urobilinuria stops at this time, since due to acholia, urobilinogen is not produced and does not enter the blood. Jaundice gradually decreases. The first sign of renewal of the excretory function of hepatocytes is the color of stool. From this time on, the level of bilirubin in the blood serum and the intensity of jaundice decrease.
During the height of the disease, increased activity of ALT remains. Among other laboratory indicators, an increase (sometimes significant) in the thymol test and an increase in the specific gravity of gamma globulins in the blood serum should be noted. In patients with severe forms of hepatitis, hemorrhagic manifestations may appear on the skin. In these cases, disorders of the blood coagulation system are detected (decreased prothrombin index, as well as plasma concentrations of coagulation factors V, II, VI, X).
When examining blood - leukopenia with relative lymphocytosis or a normal number of lymphocytes, ESR, as a rule, does not change.
Cholestasis syndrome is not typical for hepatitis A. It is characterized by the presence of cholestasis without pronounced signs of hepatocellular failure. The duration of the cholestatic form can be C-4 months. In addition to jaundice, acholic stool, clinical signs of cholestasis include skin itching. A blood test reveals moderate leukocytosis, an increase in ESR, an increase in the activity of alkaline phosphatase, cholesterol, and beta-lipoproteins.
The anicteric form of hepatitis A includes cases of the disease without jaundice syndrome, when the blood bilirubin level does not exceed 25-30 µmol/l. Other main clinical manifestations of icteric and anicteric forms of hepatitis A are the same, but with the latter they are weaker and the duration of the disease is shorter. Changes in the blood are insignificant, except for the level of ALT activity, which increases in all clinical forms of hepatitis A.
Chronic forms of the disease are possible (0.5-1% of cases).

Complications of hepatitis A

Exacerbation and relapses are observed in 2-5% of patients. They are often associated with violations of diet and regimen, irrational use of glycocorticosteroids, the addition of intercurrent diseases, and the like. In some patients, exacerbations are manifested by deterioration of laboratory parameters (biochemical exacerbations). In case of distant relapses, the possibility of infection with viral hepatitis B must be taken into account. In such cases, testing for markers of the hepatitis B virus (HBsAg, anti-HBc) is required.
The prognosis for patients with hepatitis A is favorable.

Diagnosis of hepatitis A

The main symptoms of the clinical diagnosis of hepatitis A in all variants of the initial (pre-zhovtyanichny) period are pain or a feeling of heaviness in the right hypochondrium, sometimes itching of the skin, enlargement and sensitivity of the liver, darkening of the urine. These signs indicate damage to the liver. It is important to increase the activity of ALT in the blood serum. In the icteric period, the above symptoms are accompanied by jaundice, acholia (white feces), the content of bilirubin in the blood serum increases with a predominance of the bound (direct) fraction, and the activity of ALT increases significantly. Epidemiological data, communication with patients and a certain duration of the incubation period are taken into account. Considering that hepatitis A affects mostly children.

Specific diagnosis of hepatitis A

Specific diagnosis is based primarily on the detection of antibodies to the hepatitis A virus, which belong to class M immunoglobulins - the so-called early antibodies (anti-HAV IgM). Detection of the virus in feces in the presence of clinical signs of the disease almost stops, so scatological examination is informative when examining persons who have had contact with patients in outbreaks, especially during outbreaks in children's institutions.

Differential diagnosis of hepatitis A

In the initial (pre-zhovtyanichny) period of the disease, hepatitis A most often needs to be differentiated from influenza and other respiratory diseases, acute gastritis, and food poisoning. Hepatomegaly, pain or a feeling of heaviness in the right hypochondrium, liver sensitivity on palpation, a feeling of bitterness in the mouth, sometimes itchy skin, dark urine, splenomegaly are not observed in these diseases. Sometimes rapid enlargement of the liver with stretching of its fibrous capsule and enlargement of the lymph nodes at the porta hepatis cause a pain syndrome that resembles the clinical picture of acute appendicitis. A carefully collected medical history in most cases allows us to establish that the patient had a loss of appetite, nausea, and dark urine several days before the onset of signs of an acute abdomen. A careful examination of the patient reveals an enlargement of the liver and sometimes the spleen.
Instead of the expected leukocytosis, a normal number of leukocytes or leukopenia with relative lymphocytosis is observed. Epidemiological history data are of great importance.
Determining the level of serum alanine aminotransferase activity helps to establish the diagnosis of hepatitis A in the initial period of the disease or in the case of anicteric form.
During the icteric period of viral hepatitis, it is necessary to find out the origin of the jaundice.
Prehepatic jaundice is caused by increased hemolysis of red blood cells (hemolytic jaundice) and the accumulation of unbound (indirect, insoluble) bilirubin fraction in the blood, which indicates against viral hepatitis. In such persons, unlike patients with viral hepatitis, the level of ALT does not increase, the color of urine does not change, and acholia does not occur - the feces are intensely colored.
Differentiating subhepatic (obstructive) jaundice from the cholestatic form of viral hepatitis can cause significant difficulties. In such cases, a thorough analysis of the characteristics of the pre-zhovtyanichny period helps to clarify the diagnosis; in case of hepatitis it has quite pronounced signs, but in the case of subhepatic (obstructive) jaundice there are none. Clinically, the possibility of subhepatic jaundice is indicated by an earthy-gray skin tone, intense itching, and sharp abdominal pain.
Often the development of jaundice is preceded by attacks of biliary colic or acute pancreatitis. Examination of the patient is of great importance - the presence of Courvoisier's symptom, local muscle tension, Ortner's symptom, etc. If jaundice is caused by cholelithiasis, fever, chills, leukocytosis, and an increase in ESR are often observed.
The differential diagnosis of viral hepatitis with cancer of the major duodenal papilla is quite difficult. In these cases, jaundice is often preceded by prolonged itching of the skin, while the mouth of the common bile duct and pancreatic duct is only partially blocked. In such patients, the manifestation of pancreatitis and cholangitis is possible, jaundice has an alternating character (an important sign of this pathology).
In all forms of obstructive jaundice, bilirubin testing has no differential diagnostic value. More attention is deserved by determining the activity of ALT in the blood serum, which in this form of jaundice is normal or slightly increased, while in viral hepatitis it is significantly increased. Of auxiliary importance is the ratio of transaminases - AST / ALT. In patients with viral hepatitis, the activity of ALT predominantly increases, so this coefficient is less than one, in case of obstructive jaundice it is more than one. The activity of alkaline phosphatase in viral hepatitis is normal or moderately increased, and in obstructive jaundice it increases significantly. However, with the cholestatic form of viral hepatitis, the activity of the enzyme in the blood serum increases markedly, and therefore its differential diagnostic value decreases. In difficult cases, special instrumental (including endoscopic), ultrasound, duodenography, and, if necessary, laparoscopy are used.
Viral hepatitis is differentiated from chronic hepatitis and liver cirrhosis on the basis of the clinical characteristics of the disease and laboratory parameters - duration of the course, signs of portal hypertension, profound disorders of protein metabolism, decreased albumin synthesis, an increase in the amount of gamma globulins of more than 30%, the presence of similar liver signs. In complex cases, a liver scan is of diagnostic value.
Jaundice can develop with infectious diseases such as infectious mononucleosis, leptospirosis, cytomegalovirus disease, toxoplasmosis, pseudotuberculosis, etc. Leptospirosis, for example, is characterized by an acute onset, fever, pain in the calf muscles, kidney damage, hemorrhagic syndrome, scleritis, leukocytosis and a significant increase in ESR; infectious mononucleosis is characterized by sore throat, polyadenitis, leukocytosis, and the presence of atypical mononuclear cells in the blood. Pseudotuberculosis is characterized by an acute onset, pain in the area of ​​the appendix, a clinical picture of mesadenitis, symptoms of socks, gloves, cuffs, various rashes, including scarlet fever.
Differential diagnosis of hepatitis A with other types of viral hepatitis (B, C, E) is carried out using specific research methods. Epidemiological data are taken into account.

Treatment of hepatitis A

Treatment of patients with mild and moderate forms of hepatitis A does not require the use of drugs. The basis of treatment is sufficient basic therapy, a gentle regimen in the acute period - bed rest and diet No. 5, which provides for the exclusion of fatty, smoked, pickled foods, fried foods, canned food, meat broths, sour cream, etc. from the patient’s diet. The consumption of foods is prohibited containing refractory fats (for example, lard), strong tea, coffee, cocoa and all types of alcohol. Low-fat cheese, vegetarian and dairy soups, oatmeal, semolina, buckwheat, rice porridge, kefir, yogurt, pasta, low-fat meat and fish are recommended. It is allowed to consume vegetable fats and butter within the limits of physiological need. To enrich the diet with vitamins, berries, fruits, vegetables (beets, carrots, cabbage) in grated form, as well as compotes, jelly, mousses and jellies from juices are recommended. Food should be prepared without salt (limited during meals), in grated form, meat (in the form of minced meat) is steamed. The amount of fluid should exceed the physiological need by 30-40%. Of the choleretic drugs in the acute period, it is advisable to prescribe only sorbitol and magnesium sulfate, which, without increasing the production of bile, promote its outflow due to osmotic action and the release of the hormone cholecystokinin. You need to make sure that you have bowel movements every day.
If necessary, detoxification and infusion therapy are used. In case of significant intoxication, a 5-10% glucose solution with the addition of ascorbic acid is administered.
Patients are discharged from the hospital according to clinical indications, after complete normalization of pigment metabolism.

Clinical examination

A month after discharge, the patient is examined in the infectious diseases hospital where he was treated. If the biochemical parameters are normal, the patient further requires observation by a CIZ doctor or gastroenterologist, or a local doctor at the place of residence with a re-examination after 3 and 6 months.
In case of residual effects of viral hepatitis, the patient is subject to monthly outpatient supervision by a doctor at an infectious diseases hospital, and, if indicated, hospitalization.

Prevention of hepatitis A

Patients are hospitalized and sometimes isolated at home under the supervision of an epidemiologist. Basic sanitary and epidemiological measures to prevent the fecal-oral spread of infection.
Surveillance of persons who were in contact with patients in outbreaks is carried out for 35 days. In children's institutions, quarantine is established for 35 days; within two months after the last case of hepatitis A, routine vaccinations are not carried out. Prevention of viral hepatitis A involves the administration of immunoglobulin according to epidemiological indications (intensity of incidence) in the most susceptible age groups of the population: children from 1 to 6 years old - 0.75 ml, 7-10 years old - 1.5 ml, over 10 years old and adults - 3 ml.

Among all viral hepatitis, hepatitis B and C are the most common. These diseases are transmitted parenterally (through blood) and sexually, are predominantly asymptomatic and lead to the development of severe complications.

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The danger of hepatitis B and C

According to WHO, about 240 million people in the world have chronic hepatitis B and about 780 thousand people die from this infection every year. Hepatitis C is less common - it affects about 150 million people, but the mortality rate from this infection is no lower - about 500 thousand patients die every year.

Hepatitis C is often called the “sweet killer” because it masquerades as completely different diseases or does not appear at all, but it constantly destroys the liver. Approximately 30% of patients with a chronic form of the disease develop cirrhosis if left untreated for 10-20 years.

In the Russian Federation in 2015, more than 12,000 cases of chronic hepatitis B and more than 40,000 patients with chronic hepatitis C were identified for the first time. Doctors diagnose acute forms of the disease much less frequently (an average of 2,000 cases per year). This is explained by the high frequency of the latent course of the disease or the immediate development of a chronic form of the disease.

The causative agent of hepatitis B

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The causative agent of hepatitisB is a virus of the hepadnavirus family (often abbreviated HBV or HBV). It is very resistant to various chemical and physical influences, so simple washing and boiling is not enough to disinfect objects that have been in contact with the patient’s blood. This explains the progressive spread of infection among the world's population.

Recently, mutated strains of the HBV virus have been increasingly discovered in patients. “Mutant” strains more often lead to the development of a chronic form of the disease, which is less treatable and is generally considered more unfavorable prognostically than the disease caused by the usual “wild” strain of HBV.

The causative agent of hepatitis C

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Hepatitis virusC(HCV or HCV) is a flavivirus that is represented by 11 genotypes. Each of them has its own geographic distribution, sensitivity to treatment with antiviral drugs, and the ability to cause certain characteristics of the disease. For Russia and the European region, viruses of genotypes 1, 2 and 3 are most relevant. The disease caused by HCV genotype 1 is less treatable and more often leads to the development of complications.

Routes of infection

The sources of parenteral hepatitis are both patients and carriers of the infection, and doctors only know approximate numbers about their number; in fact, there may be much more such people. Therefore, every person should know how hepatitis C and hepatitis B are transmitted.

You can become infected with these dangerous diseases in the following ways:

Viral hepatitis infection does not occur through hugs, kisses, or household contacts. However, relatives of sick people should take into account that the source of dangerous viruses are shaving utensils, toothbrushes, manicure and pedicure instruments of the patient, as well as other objects that receive blood.

Taking into account the routes of transmission of these infections, the following can be distinguished: Risk groups for infection with parenteral hepatitis:

• Injection drug addicts.
• People who have promiscuous sex.
• Sexual partners of patients with hepatitis.
• Relatives and cohabitants of patients with hepatitis.
• Medical workers.
• Homosexuals and people who prefer perverted forms of sex (with perverted sexual contacts there is a high probability of injury to the mucous membranes and, accordingly, infection).
• Children born to mothers with hepatitis.
• People suffering from illnesses that require blood transfusions or hemodialysis.
• Persons who often expose their body to tattooing and piercing.

Symptoms of parenteral hepatitis

Hepatitis B and hepatitis C have similar symptoms. From the moment the virus enters the body until signs of illness appear with hepatitis B, an average of 2-6 months passes, with C - 1.5-2 months. The onset of the disease can be acute or hidden.

With an acute onset the following appear: signs of hepatitis:

• yellowness of the skin and whites of the eyes;
• darkening of urine;
• lightening of the stool;
• high body temperature;
• weakness, poor health;
• nausea.

The outcome of acute hepatitis is either complete recovery, or the transition of the disease to a chronic form, which is largely determined by the patient’s immunity. If hepatitis infection occurs in childhood, the risk of chronic infection is much higher. For example, in children in the first year of life, chronic hepatitis develops in 80-90% of cases. This explains the need for it to be carried out immediately after birth.

Quite often, due to the asymptomatic onset of the disease, the patient learns about his condition when a chronic inflammatory process in the liver leads to an enlargement of the organ and disruption of its function. In this case, unpleasant painful sensations appear in the right hypochondrium (due to stretching of the liver membrane), nausea, and digestive disorders. The biochemical blood test of such patients will also have corresponding deviations. Therefore, if you are concerned about the described symptoms or during the examination changes in biochemical blood parameters that reflect the condition of the liver are revealed (even if there are no complaints), it is necessary to be examined for viral hepatitis.

Complications

Complications of viral hepatitis pose a potential danger to the patient's life. Such complications include:

• Liver cirrhosis, with all its consequences - ascites, portal hypertension, bleeding.
• Liver failure.
• Liver cancer.

To prevent the development of these conditions, people at risk should regularly have their blood tested for hepatitis.

Parenteral hepatitis and pregnancy

Due to the fact that a child can become infected with viral hepatitis from his mother, all pregnant women are checked for the presence of HBV antigens in their blood, and women from risk groups are additionally examined for hepatitis C. Infection of the fetus from a sick mother is possible in utero with placental abruption and procedures that violate integrity of the membranes (for example, amniocentesis). In most cases, infection occurs during childbirth, so doctors recommend that such patients undergo a cesarean section, which is considered safer in such situations. The final choice depends on the woman’s condition and the activity of the infectious process.

Immediately after birth, children of mothers with hepatitis B are given immunoglobulin and vaccinated according to a special scheme. With hepatitis C, this is not possible, so children are regularly examined in order to detect the onset of the disease in time.

Breastfeeding if the mother has viral hepatitis B or C is not contraindicated.

Diagnosis of hepatitis B

To confirm that the patient has hepatitis B , and also to determine its form (acute or chronic), a special blood test is carried out for markers of hepatitis. There are quite a lot of these markers and they are not all searched for at once. The very first diagnostic test is the determination of HBsAg, the surface antigen of HBV, which is present in the blood of both patients and carriers.

If HBsAg is detected, the patient is prescribed other tests - (search for viral DNA), HBeAg, antibodies, etc. Based on the results of these tests, it is determined whether there is a disease and in what phase the infectious process is.

Markers are assessed as follows:

Diagnosis of hepatitis C

At the first stage of diagnosis, antibodies to HCV are detected. If they are present, HCV PCR is performed (viral RNA detection is qualitative). A positive result of this test confirms the presence of infection in the body. At the next stage, the viral load is determined (HCV quantitative PCR) and hepatitis C genotype . In addition, the patient’s liver must be examined using a biopsy or elastometry (a non-invasive method that allows one to determine the degree of liver fibrosis). All this data is necessary to choose treatment tactics.

Hepatitis B treatment

In the acute form of the disease, specific antiviral treatment is not carried out. Patients are recommended diet, rest, and detoxification therapy. If chronic hepatitis is detected, antiviral therapy can prevent the development of cirrhosis and improve the patient’s condition, but does not guarantee complete recovery. Treatment regimen for patients with chronic hepatitisB includes:

Features of hepatitis C treatment

With hepatitis C, diet and avoidance of alcohol are also important. Standard treatment regimens for the disease include the administration of pegylated interferons and ribavirin. These drugs are not always well tolerated by patients, especially when taken for a long time.

New drugs for hepatitis C (Ledipasvir, Sofosbuvir, etc.) have become a real breakthrough in medical science, but research in this direction is still ongoing.

Prevention of viral hepatitis

For hepatitisBThe most effective preventive measure is vaccination. It is carried out according to the following scheme: the child receives three doses of the drug - in the first days of life, per month and six months. Immunity develops in almost all vaccinated people and lasts for 10 years or more. Revaccination every 10 years is carried out if indicated (for example, if a person is at risk). Adults should also be vaccinated.

Other measures to prevent hepatitis B are the same as for hepatitis C, for which there is no vaccination: protected sexual contact, use of disposable syringes, minimizing visits to manicure, piercing, and tattoo salons if possible, compliance with safety measures at home (for relatives of a person with hepatitis), responsible attitude of medical personnel to their duties (disinfection of instruments), etc.

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Viral hepatitis A

What is Viral Hepatitis A -

Viral hepatitis A- benign acute cyclic viral infection from the group of fecal-oral hepatitis, accompanied by necrosis of hepatocytes. Clinically manifested by intoxication syndrome, hepatosplenomegaly and often jaundice. Synonyms - Botkin's disease, viral hepatitis type A.

For the first time, the idea of ​​​​the infectious nature of “catarrhal jaundice” was expressed by SP. Botkin (1888); from this time on, this disease was called “Botkin’s disease” for a long time. In 1947, F. McCollum proposed the term “hepatitis A”; the causative agent of the disease was discovered much later (S. Finestone, 1973).

What provokes / Causes of Viral hepatitis A:

The causative agent of viral hepatitis A- RNA genomic virus of the Hepatovirus genus of the Picornaviridae family. Virions are small, simply structured, and lack a supercapsid. The genome is formed by single-stranded RNA. Currently, only one serovar of the virus is known. In the external environment, it is more stable than typical enteroviruses. It can be stored in the external environment for several months at 4 °C, for several years at -20 °C, for several weeks at room temperature. The virus is inactivated by boiling after 5 minutes. When exposed to ultraviolet irradiation, the pathogen dies within 60 s. In the presence of chlorine at a concentration of 0.5-1 ml/l, at a pH of 7.0, it survives for 30 minutes or more, which determines its ability to persist for a certain time in chlorinated tap water.

Reservoir and source of infection- a person with any manifestations of the disease (icteric, anicteric, asymptomatic inapparent forms). A significant portion of those infected experience the disease in an asymptomatic and therefore undetectable form. In children this value reaches 90-95%, in adults - 25-50%. A sick person is dangerous to others starting from the 2nd week of the incubation period of the disease; Peak virus shedding occurs in the first week of illness. The contagiousness of the patient with the appearance of jaundice decreases significantly: in the first week of the jaundice period, the frequency of positive findings is 30-50%, in the second - 15-25%, later, virus isolation is observed only in a few patients. Chronic carriage of the virus has not been established. Cases of human infection from chimpanzees and some other species of monkeys have been described.

Transmission mechanism- fecal-oral. The virus is shed in fecal matter. 1 ml of feces can contain up to 108 infectious virions. People become infected by consuming water and food contaminated with the virus, sometimes through household contact. The possibility of sexual transmission of infection is being discussed, especially among homosexuals. In a number of countries (USA, European countries), cases of diseases associated with infection through parenteral administration of psychotropic substances, transfusion of blood and its preparations have been described. The role of each transmission route varies in different settings. The waterway typically leads to outbreaks of disease among persons who have used contaminated water or swam in contaminated pools and lakes. Since the hepatitis A virus can survive in water from 12 weeks to 10 months, infection can occur through consumption of various raw shellfish and mussels collected from areas contaminated with sewage.

Food outbreaks are most often associated with the contamination of products at food enterprises by personnel with a mild form of the disease and failure to comply with personal hygiene rules. It is also possible that vegetables and berries (especially strawberries, lettuce) can become infected when they are fertilized with human feces. Contact-household transmission usually occurs in preschool settings, children's homes and other similar institutions, especially in conditions of their unsatisfactory sanitary condition.

Natural human sensitivity high. After an infection, a strong, strong immunity is developed. Children aged 2 to 14 years are most susceptible. Asymptomatic forms of the disease form a less strained immune system.

Main epidemiological features. Viral hepatitis A is characterized by widespread distribution, uneven intensity in certain areas, cyclicality in long-term dynamics, pronounced autumn-winter seasonality, predominant infection of preschool children, adolescents and young adults.

Viral hepatitis A is one of the most widespread intestinal infections in the world. Of all the fairly numerous forms of viral hepatitis, it is the most common. WHO reports approximately 1.4 million cases of viral hepatitis A occurring annually. On average, direct and indirect costs associated with infection can reach US$2,459 per case for an adult and US$1,492 for a child. The costs associated with viral hepatitis are estimated to be between US$1.5 and US$3 billion annually worldwide.

Although this disease is characteristic mainly of third world countries with poor hygiene and sanitation, isolated cases or outbreaks of viral hepatitis A can be observed even in the most developed countries. In the United States, it is estimated that about 33% of the population has serological markers indicating previous infection. There are 143 thousand cases of viral hepatitis A infection per year.

The incidence of viral hepatitis A in children is constantly higher than in the adult population. The level of childhood morbidity is determined by the age group of 3-6 years; the rate among them in 1998 was 82.7 per 100,000 population, in 1999 - 77.0. The incidence among the urban and rural populations has almost equalized, the rates are 30.0 and 32.6 per 100,000 population, respectively.

In 1999, 14,152 studies of environmental objects were carried out for viral hepatitis A virus antigens, of which 474 (3.4%) were positive; the largest number of positive results were obtained when studying water from decentralized water supply sources (9.6%) and fecal wastewater (6.4%). This indicates widespread circulation of the pathogen in the external environment with the development of outbreaks mainly of water origin in regions with unsatisfactory sanitary and communal conditions.

Long-term dynamics are characterized by periodic (every 4-6 years) increases in incidence. The most recent years have been characterized by another rise in incidence. A feature of the latest rise was the emergence of epidemic outbreaks with foodborne transmission.

A summer-autumn seasonality of incidence is noted, which reflects a pronounced increase in the introduction (importation) of infection from disadvantaged territories with migration flows of the population and the supply of various low-quality food products sold in small-scale wholesale and unauthorized (street) trade. Among adults, workers of all public catering establishments, as well as catering units of medical, children's, sanatorium and other institutions, are primarily at risk of contracting viral hepatitis A. The high-risk group additionally includes military personnel and persons traveling or living in areas with poor sanitary and communal services, using water from open reservoirs for household purposes, as well as medical personnel. In recent years, people with chronic diseases of the liver and biliary tract, homosexuals and drug addicts have been considered risk groups, since group cases of viral hepatitis A diseases have been described among them.

Pathogenesis (what happens?) during Viral hepatitis A:

The usual portals of entry for hepatitis A virus are the mucous membranes of the oropharynx and small intestine. At the site of penetration, an inflammatory process develops, causing the formation of catarrhal syndrome, dyspeptic symptoms and temperature reaction. Penetration of the pathogen into the blood leads to viremia, thanks to which it reaches the liver. It is currently assumed that damage to hepatocytes is caused by cellular cytotoxic immune reactions. At the same time, a direct cytopathic effect of the virus on hepatocytes cannot be ruled out. In patients with viral hepatitis A, liver biopsy revealed significant damage to the portal zone with intense cellular infiltration and destruction of the border plate, pronounced signs of cholestasis.

Even with slight damage to hepatocytes, hepatolienal syndrome is formed and biliary dyskinesia develops; with more severe liver damage, jaundice occurs. Subsequently, it takes several weeks to restore hepatocytes, and several months to restore the complete cytoarchitecture of the liver.

Antigens of the hepatitis A virus exhibit high immunogenicity: activation of the immune system and specific sensitization of lymphocytes begin from the moment of introduction of the pathogen.

Viral antigens (envelope proteins) are expressed on hepatocyte membranes in complex with major histocompatibility complex (HLA) type I antigens, and infected cells are killed by cytotoxic T lymphocytes and killer T cells.

The similarity of virus antigens and hepatocyte antigens determines the development of general autoimmune processes, the intensity of which largely determines the outcome of the disease. Individuals with a genetic predisposition due to viral hepatitis A may develop chronic autoimmune hepatitis type I. Nephrotic syndrome with the development of mesangioproliferative glomerulonephritis, arthritis, vasculitis, cryoglobulinemia have been described; in this case, viral hepatitis A acted as a provoking factor. In very rare cases (0.1%), fulminant forms of viral hepatitis A may develop.

Already during the incubation period, specific IgM is detected; The duration of incubation is explained by the individual characteristics of the immune response. With a rapid increase in antibody titers, jaundice does not develop.

As a result of immune reactions, in most cases, recovery occurs quite quickly, within 2-3 weeks, with the body completely freed from the virus. Viral carriage and chronic forms of viral hepatitis A are not observed.

Symptoms of Viral Hepatitis A:

Incubation period lasts 3-4 weeks. Viral hepatitis A occurs as an acute cyclic disease and is characterized by a sequential change of several periods - prodromal (pre-icteric), peak (icteric) and the period of convalescence.

Pre-icteric period. It is characterized by a fairly wide variety of symptoms, conditionally grouped into several variants of its course.
1. Flu-like (febrile, catarrhal) The variant with viral hepatitis A is most common. Typically, the disease begins quite acutely with an increase in body temperature (from low-grade to high levels), weakness, malaise, muscle pain, and the development of mild catarrhal symptoms (nasal congestion, pain or sore throat, coughing). However, flu-like symptoms in most patients are accompanied by dyspeptic disorders of varying severity.
2. Dyspeptic option. There are no catarrhal symptoms, and symptoms of gastrointestinal involvement come to the fore. Patients are concerned about discomfort in the epigastric region, loss of appetite to the point of complete anorexia, nausea, and sometimes vomiting, which occurs more often after eating. Possible dull pain in the right hypochondrium, bitterness in the mouth, belching, constipation or loose stool.
3. Asthenovegetative option. It is characterized by a number of nonspecific symptoms: the development of general weakness, loss of performance, irritability or indifference, persistent insomnia or, conversely, drowsiness.

Viral hepatitis A can clinically manifest itself immediately with the development of jaundice; in this case, there are no prodromal signs (latent variant of the initial period).

It should be emphasized that clinical symptoms attributed to various variants of the pre-icteric period can be combined in various combinations. In these cases they talk about a mixed version.

Complications of viral hepatitis A
They develop relatively rarely. These include exacerbation of inflammatory processes in the bile ducts (cholecystitis, cholangitis, dyskinesia), as well as the development of secondary infections (pneumonia, etc.). Acute hepatic encephalopathy with viral hepatitis A develops extremely rarely.

Diagnosis of Viral hepatitis A:

Diagnosis of viral hepatitis A in its initial period it is extremely difficult. It is necessary to rely on epidemiological history data (contact with icteric patients). When examining patients, already at this time one can detect an enlarged liver and an increase in aminotransferase levels.

The initial period of the disease lasts from 2 to 7-10 days and gradually turns into icteric. By this point, the temperature reaction is normalized, catarrhal symptoms disappear, but dyspeptic symptoms persist or may even increase in intensity.

The beginning of the icteric period must be considered from the moment dark urine appears. Following this, icterus appears on the frenulum of the tongue, soft palate, sclera, and then on the skin. Its intensity progresses rapidly, usually reaching a maximum after 3-4 days; in this case, jaundice often takes on a saffron hue. It is generally accepted that the intensity of jaundice is directly proportional to the severity of the disease, but it is necessary to focus more on the severity of the intoxication syndrome: repeated vomiting, dyspeptic disorders, the degree of loss of appetite. With a more severe course of the disease, bruising may appear on the skin, especially at the injection sites. Some patients experience nosebleeds.

The tongue is usually coated. Palpation determines the enlarged liver, sensitive to palpation; the degree of its increase may vary. In 30-40% of cases, splenomegaly is detected by this time. In some patients, at the height of jaundice, discolored stool appears. From the cardiovascular system, bradycardia and a tendency to decrease blood pressure are quite characteristic. Against the background of jaundice, in addition to dyspeptic symptoms, patients note weakness, dizziness, and sometimes sleep disorders.

The duration of the icteric period with viral hepatitis A does not exceed 30 days. More often it lasts about 2 weeks and goes into a period of convalescence. By this time, the intensity of the icteric syndrome gradually decreases, the liver decreases in size, and signs of intoxication disappear. The period of convalescence is much longer than the period of jaundice and can last up to 3-6 months.

In 5-10% of patients with viral hepatitis A, it can acquire a longer course, characterized by minor manifestations or absence of intoxication, small amounts of bilirubinemia and hyperfermentemia, and a persistent increase in the size of the liver. Most often, this explains the development of cholestasis. Despite the increased duration, the disease ends favorably.

Viral hepatitis A usually occurs in mild or moderate forms, but severe variants and exacerbations are not excluded.

Diagnosis of viral hepatitis A is mainly carried out with severe icteric syndrome, but a large number of reports have accumulated that viral hepatitis A can often occur in an anicteric form, which in most cases is not diagnosed. According to a number of researchers, the ratio of icteric and anicteric forms can reach 3:7.

In the pre-icteric period, viral hepatitis A must be differentially diagnosed with acute respiratory and intestinal infections. Epidemiological history data can provide some assistance in differential diagnosis: contact with icteric patients, the patient’s stay in areas unfavorable for hepatitis A. In some cases, already in the pre-icteric period, an enlarged liver can be detected, as well as an increase in aminotransferase activity.

During the icteric period, the disease is differentiated from obstructive and hemolytic jaundice, mononucleosis, yersiniosis, and leptospirosis. The clinical picture, which is in many ways similar to the listed diseases, requires determination of hepatitis markers using ELISA and PCR, determination of bilirubin and its fractions in the blood.

Laboratory diagnostics
Laboratory tests are of particular importance to establish the etiology of hepatitis and assess its severity. When analyzing blood, it is necessary to take into account the presence of leukopenia, relative lymphocytosis and slow ESR.

The intensity of jaundice is determined based on determining the level of bilirubin in the blood (especially its bound fraction). The activity of aminotransferases [alanine aminotransferase (ALT) and aspartate aminotransferase (ACT)] increases several times, and the degree of its increase indicates the intensity of hepatocyte cytolysis. Disturbances in the protein synthetic function of the liver reflect changes in the parameters of colloid tests (decrease in sublimate and increase in thymol samples), a decrease in the level of albumin and prealbumin in the blood, as well as a decrease in the prothrombin index.

It is possible to isolate the hepatitis A virus from feces, but virological studies are not used in widespread medical practice. To verify the diagnosis, serological reactions are used - ELISA, RIA, which reveal an increase in specific IgM during the icteric period and an increase in IgG titers by the period of convalescence. The most reliable diagnostic method is detection of virus RNA in the blood using PCR.

Treatment of Viral Hepatitis A:

Once the diagnosis of viral hepatitis A has been established, the patient can be treated on an outpatient basis. Patients with a severe course of the disease, protracted forms, in the presence of severe concomitant diseases, as well as persons of decreed groups are hospitalized.

Patients are prescribed bed rest for the period of severe intoxication syndrome and proper nutrition. The diet excludes refractory fats, hard-to-digest meats (lamb, pork, waterfowl), fried foods, canned food, marinades, onions, garlic and spices. Drinking alcohol is strictly prohibited. Dairy-vegetable foods are recommended. Additionally, vitamins C and B are added to food products.

Due to the lack of etiotropic therapy, pathogenetic treatment is carried out. To relieve intoxication, depending on its degree, use plenty of fluids or infusion solutions. For daily cleansing of the intestines and suppression of anaerobic flora, it is recommended to prescribe lactulose derivatives, the doses of which are selected individually. To relieve the cholestatic component, antispasmodics (no-spa, aminophylline) and ursodeoxycholic acid derivatives are used.

After completion of the disease, the patient is subject to clinical observation for 3-6 months.

Prevention of Viral Hepatitis A:

Basic measures to prevent infection with viral hepatitis A- providing the population with good-quality water and creating conditions that guarantee compliance with sanitary rules for the procurement, storage, preparation and sale of food products. Ensuring an appropriate anti-epidemic regime in organized children's and adult groups is of great importance. In the fall (a time of high risk), they should take on an anti-epidemic character: in particular, kindergartens and school institutions, even in the absence of diseases, should be considered as potential foci of viral hepatitis A. Activities should be aimed at actively searching for sources of infection, including identifying IgM in ELISA, strengthening disinfection regime, substantive sanitary education of children and adults in relation to the real danger of infection with viral hepatitis A. During the pre-season increase in incidence, immunoglobulin prophylaxis is effective, providing protection for 3-4 months. Vaccination coverage of 50-60% of preschool children and 70-80% of schoolchildren ensures a 2-3-fold reduction in morbidity in these groups. Preschool children are administered immunoglobulin at 0.75 ml, primary schoolchildren - 1.5 ml, older children and adults, depending on weight - up to 3 ml. Administration of immunoglobulin is allowed no more than 4 times during life with an interval of at least 1 year.

Currently, a vaccine against viral hepatitis A has been proposed as a means of specific prevention, since the administration of immunoglobulin provides rapid but short-term protection. Vaccinal prevention forms active immunity, accompanied by prolonged circulation of one’s own antibodies. They produce effective and harmless vaccines against viral hepatitis A for children and adults, ensuring the preservation of immunity for up to 10 years. However, widespread vaccination against viral hepatitis A is hampered by its relatively high cost. However, it is known that the damage caused by viral hepatitis A significantly exceeds the cost of vaccination. Considering the high incidence of children and the fact that they are the main source of infection for adults, a promising direction is vaccine prevention of viral hepatitis A in young children and schoolchildren, which has long been widely carried out in the USA and a number of countries (Israel, Spain, Italy).

The vaccines are formaldehyde-inactivated hepatitis A virions adsorbed on aluminum hydroxide. They are administered intramuscularly. The vaccine is used in children from 3 years of age and in adults. For adults, the vaccine is administered in a dose of 0.5 ml into the deltoid muscle. Course - 3 vaccinations according to the scheme 0, 1 and 6 months. Children are injected with 0.25 ml into the deltoid muscle twice with an interval of 1 month. The Avaxim vaccine (France) is administered to children from 2 years of age and adults once intramuscularly, revaccination is carried out once after 6-18 months, subsequent revaccinations are carried out every 10 years. The Vakta vaccine (USA) is administered starting from 2 years of age as a single primary dose (children 25 antigenic units - 0.5 ml, adults 50 antigenic units - 1 ml) with a repeat dose after 6-18 months. The Havrix vaccine (Belgium) is used both in children from 1 year of age and in adults. Available in ampoules of 0.5 ml (720 units) for children and 1 ml (1440 units) for adults.

Vaccination stimulates the development of immunity after 21-28 days. Antibody titers, although lower than after the disease, provide reliable protection against infection.

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Hepatitis A (Botkin's disease) is an acute infectious viral liver disease with a benign course, belonging to the group of intestinal infections. The disease is widespread in developing countries. This is due to the large overcrowding of the population and poor sanitary and hygienic living conditions. In developed countries, the incidence rate of hepatitis A decreases annually due to the hygienic skills developed among the population, as well as vaccination.

Jaundice stage of hepatitis A

Causes and risk factors

The causative agent of hepatitis A belongs to the RNA-containing viruses of the Hepatovirus genus. It is stable in the external environment, remains active at room temperature for several weeks, and dies under the influence of ultraviolet radiation and high temperatures.

The source of infection is a sick person who releases the virus into the environment with feces from the last days of the prodromal period until the 15-20th day of the icteric period. Patients with anicteric (erased) forms of hepatitis A, as well as virus carriers, play a great role in the spread of infection.

The main routes of transmission of the virus are food and water. Contact-household transmission (through personal hygiene items, utensils) is also possible, but is observed much less frequently. The risk of infection is mainly associated with poor sanitation practices and the use of untreated water.

Hepatitis A is widespread in developing countries, which are characterized by overcrowded populations and poor sanitary and hygienic living conditions.

Adults and children of all ages, including infants, are susceptible to hepatitis A.

Forms of the disease

Depending on the clinical picture, there are two forms of hepatitis A:

• typical (icteric);
• atypical (anicteric, erased).

Symptoms of the icteric form of hepatitis A

Stages of the disease

In the clinical picture of viral hepatitis A there are several successive stages:

1. Incubation period. It lasts from the moment of infection until the first signs of the disease appear, from 20 to 40 days (on average 14–28).
2. Prodromal period. Symptoms of general malaise appear (weakness, fever, dyspepsia). Duration – 7–10 days.
3. Jaundice period. Dyspepsia intensifies, icteric discoloration of the sclera and skin appears. In the atypical course of the disease, the jaundice of the skin is minimally expressed and is often not noticed either by the patient himself or by the people around him. Duration – 5–30 days (average – 15).
4. The period of convalescence. Symptoms of the disease gradually disappear, the condition of patients improves. The duration is individual - from several weeks to several months.

Hepatitis A in most cases results in complete recovery within 3–6 months.

Symptoms

Viral hepatitis A usually begins acutely. The prodromal period can occur in different clinical variants: dyspeptic, febrile or asthenovegetative.

The febrile (flu-like) form of the prodromal period is characterized by:

• increased body temperature;
• general weakness;
• headache and muscle pain;
• sore throat, dry cough;
• rhinitis.

In the dyspeptic variant of the pre-icteric period, the manifestations of intoxication are mild. Typically, patients complain of various digestive disorders (belching, bitterness in the mouth, bloating), pain in the epigastrium or right hypochondrium, defecation disorders (constipation, diarrhea or their alternation).

The asthenovegetative form of the prodromal period in viral hepatitis A is not specific. Manifested by weakness, lethargy, adynamism and sleep disorders.

The transition of the disease to the icteric stage is characterized by an improvement in general condition, normalization of body temperature against the background of the gradual development of jaundice. However, the severity of dyspeptic manifestations in the icteric period not only does not weaken, but, on the contrary, intensifies.

In severe cases of viral hepatitis A, patients may develop hemorrhagic syndrome (spontaneous nosebleeds, hemorrhages on the skin and mucous membranes, petechial rash).

Palpation reveals a moderately painful liver protruding from the hypochondrium. In approximately 30% of cases, there is an enlarged spleen.

As jaundice increases, stool becomes lighter and urine becomes darker. After some time, the urine acquires a rich dark color, and the feces become light gray in color (acholic stool).

The icteric period gives way to the stage of convalescence. There is a gradual normalization of laboratory parameters and an improvement in the general condition of patients. The recovery period can last up to six months.

Diagnostics

Diagnosis of hepatitis A is carried out based on the characteristic clinical symptoms of the disease, physical examination of the patient and laboratory tests. A biochemical blood test reveals:

• bilirubinemia (increased bilirubin concentration mainly due to the bound form);
• significant increase in the activity of liver enzymes (AST, ALT);
• decrease in prothrombin index;
• decrease in albumin content;
• decrease in thymol and increase in sublimate samples.

Changes in the general blood test are also noted: increased ESR, lymphocytosis, leukopenia.

Specific diagnosis is carried out based on the detection of antibodies using RIA and ELISA. The most accurate method of serodiagnosis is the detection of viral RNA in the blood using polymerase chain reaction (PCR).

Virological research with the isolation of the virus itself is not carried out in clinical practice due to the high complexity of this method.

Treatment

Most cases of hepatitis A are treated on an outpatient basis; Hospitalization is indicated only for epidemiological reasons or in case of severe disease.

Viral hepatitis A usually begins acutely. The prodromal period can occur in different clinical variants: dyspeptic, febrile or asthenovegetative.

• eating 5-6 times a day in small portions;
• exclusion from the diet of fatty and spicy foods, as well as foods that stimulate bile synthesis;
• inclusion of a sufficient amount of plant and dairy products in the diet.

Causative therapy for the disease has not been developed, so treatment measures are aimed at eliminating symptoms. In case of severe intoxication, patients are prescribed plenty of fluids (rosehip decoction, still mineral water), intravenous drip administration of crystalloid solutions, and vitamin therapy. To improve the functions of the digestive system, the use of lactulose is indicated. To prevent cholestasis, antispasmodic drugs are used.

Possible complications and consequences

Viral hepatitis A usually occurs in a mild or moderate form, and they are not characterized by any complications. In rare cases, the virus can provoke an inflammatory process in the biliary system, which may result in:

• cholecystitis;
• cholangitis;
• biliary dyskinesia.

Acute hepatic encephalopathy with hepatitis A develops extremely rarely.

Forecast

The prognosis for viral hepatitis A is favorable. The disease in most cases ends with complete recovery within 3–6 months. Virus carriage and chronicity of the pathological process in the liver are not typical for this type of hepatitis.

In developed countries, the incidence rate of hepatitis A decreases annually due to the hygienic skills developed among the population, as well as vaccination.

Prevention

General preventive measures aimed at preventing the spread of the hepatitis A virus include:

• providing the population with quality drinking water;
• careful control over wastewater discharge;
• control over compliance with sanitary and hygienic requirements by employees of public catering establishments, catering units of medical and children's institutions.

In the event of a hepatitis outbreak, quarantine measures are carried out in an organized team. The sick are isolated for 15 days, since from the 14-15th day from the beginning of the icteric period, their release of the virus stops. Contact persons are subject to medical observation for 35 days. Disinfection is carried out at the source of infection. Persons who have had hepatitis A are allowed to study or work only after complete clinical recovery.

It is possible to carry out specific prevention of hepatitis A through vaccination. The vaccine is recommended for children over one year of age and adults living in regions with high rates of hepatitis A, as well as those traveling to these regions.

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The hepatitis A virus belongs to the picornavirus family, a genus of enteroviruses.

The hepatitis A virus is morphologically similar to other representatives of the enterovirus genus. forms a single-stranded +RNA molecule; it contains three main proteins. Does not have a supercapsid shell.
Antigenic structure: has one virus-specific protein nature.
The virus has a reduced ability to reproduce
in cell cultures. Reproduction of the virus is not accompanied by a cytopathic effect.

The virus is resistant to physical and chemical factors.
The main hepatitis A virus is . The patient excretes the pathogen within 2-3 weeks before the onset of the icteric stage and 8-10 days after its end. The virus is pathogenic only for humans.

The hepatitis A virus enters the human body with water or food and reproduces in the epithelium of the mucous membrane of the small intestine and regional lymphoid tissues. The pathogen then enters the bloodstream with the development of short-term viremia.
Maximum virus titers in the blood are detected at the end of the incubation and pre-icteric periods. At this time, the pathogen is excreted in the feces. The main target for cytopathogenic action is hepatocytes. Reproduction of the virus in their cytoplasm
leads to disruption of intracellular metabolic processes and cell death. The cytopathic effect is enhanced by immune mechanisms, in particular NK cells, the synthesis of which is induced by the virus.
Damage to hepatocytes is accompanied by the development of jaundice
and increasing the level transaminases. Next, the pathogen enters the intestinal lumen with bile and is excreted in feces, which contain a high concentration of the virus.
The hepatitis A virus causes the development of an acute, highly contagious disease, which can be subclinical or produce typical clinical forms.
After suffering a clinically pronounced or asymptomatic infection, a lifelong humoral system is formed.

Laboratory diagnostics:

1) determination of the content of bile pigments and aminotransferases in serum;
2) cultivation on leukocyte or organ cultures;
3) ELISA and solid-phase RIA method - to detect anti-
bodies (IgM), which appear in the blood serum at the end and persist for 2-3 months after recovery. From the middle of the icteric period
IgG is produced, which lasts for life;
4) molecular genetic methods - detection of RNA virus in.

Treatment:

There are no specific antiviral therapies; treatment is symptomatic.

Specific prevention:

killed vaccine based on CR 326 strain.

Hepatitis B virus

Belongs to the family Hepadnaviridae. These are icosahedral,
enveloped DNA-containing viruses that cause in various animals and humans. forms an incomplete (with a break in one strand) circular double-stranded DNA molecule.
The nucleocapsid contains a primer protein and a DNA polymerase associated with DNA.

For efficient replication, the synthesis of virus-induced reverse transcriptase is necessary, since viral DNA is formed on a matrix; In the dynamics of the process, viral DNA integrates into the DNA of the cell.
DNA synthesis and virus assembly occur in the cytoplasm of the infected cell. Mature populations are released by budding from the cell membrane.

Antigenic structure

1) HBsAg (includes two polypeptide fragments):
a) the preS1 polypeptide has pronounced immunogenic properties; genetically engineered
the polypeptide can be used for the preparation of vaccine preparations;
b) preS2 polypeptide (a polyglobulin receptor that causes adsorption on hepatocytes; is able to interact with serum albumin, as a result of which the latter is converted into polyalbumin);
2) HBcorAg (is a nucleoprotein, represented by a single antigenic type; it is found only in the core of the virus);
3) HBeAg (splits off from HBcorAg due to the passage
it through the hepatocyte membrane).
Infection occurs through injection of infected blood
or blood products; through contaminated medical instruments, sexually and intranatally, intrauterine infection is possible.

The site of primary viral replication is unknown; reproduction
in hepatocytes is observed only 2 weeks after infection. In this case, the replicative cycle is not accompanied by death
hepatocytes. In the second half the virus
isolated from blood, semen, urine, feces and nasopharyngeal secretions.
The pathological process begins after recognition of the virus-induced immunocompetition on the membranes of hepatocytes.
tent cells, i.e. it is caused by immune mechanisms.
Clinical manifestations range from asymptomatic
and anicteric forms to severe liver degeneration. Flow
hepatitis B is more severe, with a gradual onset, prolonged
infectious cycle, higher mortality rate than with hepatitis A. The process may become chronic.

Laboratory diagnostics

1) detection of viral immunofluorescence
method; material - feces, blood and liver biopsy material;
2) serological studies include determination
antigens and using reagents - HBsAg, HBeAg;
antigens to HBsAg, HBcorAg, HBeAg and IgM to HBcorAg;
3) determination of DNA polymerase.

Treatment

There are no specific drug therapies; treatment is mainly symptomatic.

Specific prevention

1) passive immunization - specific immunotherapy is introduced

globulin (HBIg);
2) active immunization (recombinant vaccines, semi-
genetically engineered).
Immunization is indicated for all risk groups, including newborns.

Other pathogens of viral hepatitis

Hepatitis C virus- RNA virus. Its taxonomic position is currently not precisely determined; it is close to the flavivirus family.
It is a spherical particle consisting of
a nucleocapsid surrounded by a protein-lipid shell. Size - 80 nm. has zones encoding the synthesis of structural and non-structural proteins of the virus. The synthesis of structural proteins is encoded by the C and E zones, and the synthesis of non-structural proteins
viruses encode NS-1, NS-2, NS-3, NS-4 and NS-5 RNA zones.
The hepatitis C virus is characterized by antigenic variability; there are seven main variants of the virus.
The source of infection is patients with acute and chronic hepatitis C and virus carriers. The virus is transmitted parenterally, sexually and from mother to fetus (during peri- and postnatal infection).
Characterized by the predominance of anicteric forms and frequent re-
progression into a chronic form of the disease. The virus is one of
factors in the development of primary hepatocellular carcinoma.

Laboratory diagnostics

1) identification of RNA virus using;
2) determination of the virus in ELISA.

Hepatitis D virus does not belong to any of the known
families of animal viruses. It is a spherical particle with an average diameter of 36 nm. It is represented by a single-stranded, cyclic RNA molecule that forms a rod-shaped, unbranched structure. The virus-specific virus is encoded in RNA
polypeptide - HDAg (nucleocapsid self antigen). On the-
The outer shell forms a surface antigen.

Replication of the hepatitis D RNA virus occurs in the nucleus of the infected hepatocyte.
Sources of infection- a sick person and a virus carrier.
parenteral. The hepatitis D virus cannot participate
contribute to the development of hepatitis infection without simultaneous rep-
lication of the hepatitis B virus. This fact determines two possible
forms of their interaction:
1) simultaneous infection with viral hepatitis B and D
(conversion);
2) infection of a carrier of the hepatitis D virus with the hepa-
tita B (superinfection).

With superinfection, rapid damage to the parenchyma occurs
we have liver with massive necrosis.
Diagnostics: detection of the virus in ELISA.

The hepatitis E virus belongs to the Calicinovirus family.
This is a spherical RNA virus, 20-30 nm in size.
- water, food, contact possible.
Source of infection- a patient with acute or chronic form.
The clinical picture is close to hepatitis A.
Diagnostics: detection of antibodies in ELISA.