Viral hepatitis. Etiology of hepatitis Classification of possible complications of hepatitis b c d

Hepatitis is an inflammation of the liver caused by factors of various etiologies. In the process of its development, it can be completely cured or have consequences in the form of fibrosis (scarring), cirrhosis or liver cancer.

General classification of hepatitis

This group of diseases is classified according to various parameters. Research into various types of liver inflammation is ongoing constantly in our time, their lists are being replenished, and new strains of viral hepatitis are being identified. Nevertheless, there are aspects by which today it is customary to distinguish between different types and stages of this disease.

Forms of hepatitis according to clinical course

There are acute and chronic hepatitis. Acute hepatitis most often occurs when infected by viruses, as well as as a result of exposure to potent substances, such as poisons. Lasts up to three months, after which a transition to a subacute (protracted) form is possible. After six months, the disease transforms into a chronic form. Chronic hepatitis often occurs as a continuation of acute hepatitis or can develop independently (for example, as a result of prolonged alcohol abuse).

The modern classification of chronic hepatitis is based on the following key evaluation criteria: etiology, pathogenesis, degree of activity (chronic aggressive and chronic persistent hepatitis), stage of chronicity.

There is also recurrent (returning) hepatitis, in which symptoms of the disease reappear several months after acute hepatitis.

According to severity

This criterion applies to the patient rather than to the disease itself. So, hepatitis can be mild, moderate or severe. Fulminant hepatitis refers specifically to the extremely severe course of the disease.

By etiology

Infectious hepatitis is caused, most often, by hepatitis viruses A, B, C, D, E, etc. Infectious hepatitis can also occur as a component of such infections: rubella virus, cytomegalovirus, herpes, syphilis, leptospirosis, HIV (AIDS) and some others. Non-viral hepatitis is formed as a result of exposure to any toxic substances that have a hepatotropic effect (for example, alcohol, certain medications). This type of hepatitis gets its name from the name of the damaging agent - alcohol, drugs, etc. Liver damage can also occur as a result of autoimmune processes in the body.

According to pathomorphological characteristics

The process can be localized exclusively in the liver parenchyma or also involve the stroma, be located in the form of a local focus or have a diffuse position. And finally, the nature of liver damage is assessed: necrosis, dystrophy, etc.

Viral hepatitis

Acute and chronic viral hepatitis seem to be a fairly relevant subject of global health attention in our time. Despite the obvious achievements of science in the diagnosis and treatment of hepatotropic viruses, the number of patients with them is steadily growing.

Key points in the classification of viral hepatitis are reflected in Table No. 1.

Table No. 1. Classification of viral hepatitis.

Etiology of viral hepatitis

Today, there are 8 known types of viruses that can cause viral hepatitis. They are designated by Latin letters.

This is the hepatitis A virus - Hepatitis A virus or Botkin's disease: HAV; B – HBV; C – HCV; D – HDV; E – HEV; F – HFV; G – HGV; TTV – HTTV and SAN – HSANV.

Hepatitis B and TTV viruses are DNA-containing viruses, while the others have RNA in their structure.

Also, in each type of virus, genotypes and sometimes subtypes are determined. For example, the hepatitis C virus currently has 11 known genotypes, which are designated by numbers, and many subtypes. Such a high mutation ability of the virus leads to difficulties in its diagnosis and treatment. The hepatitis B virus has 8 genotypes, which are designated by letters (A, B, C, D, E, etc.)

Determining the genotype of the virus - genotyping - is important for prescribing the correct treatment and the possibility of predicting the course of the disease. Different genotypes respond differently to therapy. Thus, HCV genotype 1b is more difficult to cure than others.

It is known that infection with HBV genotype C can cause a prolonged presence of HBeAg in the blood of patients.

Sometimes infection occurs simultaneously with several genotypes of the same virus.

Hepatitis virus genotypes have a specific geographic distribution. For example, HCV genotype 1b prevails in the CIS. In the Russian Federation, genotype D of HBV is detected more often. At the same time, genotypes A and C are much less common.

Epidemiology

The source of infection is a virus carrier or a sick person. Moreover, people with an asymptomatic form of infection, as well as with an anicteric or erased course, are especially dangerous. The patient is contagious already in the incubation period, when there are no obvious signs of the disease. Infectiousness persists in the prodromal period and the initial phase of the height of the disease.

Of all hepatotropic viruses, HBV is the most resistant to the adverse effects of the external environment. And hepatitis A (Botkin's disease) and E viruses are less tenacious in the external environment and die quickly.

Due to the urgency of the problem, it is necessary to mention the combination (co-infection) of hepatitis and HIV (AIDS) viruses. The majority of the risk group consists of drug addicts (up to 70%), who become infected with both HIV and hepatitis viruses, more often C. The presence of HIV (AIDS) and the hepatitis C virus correlates with a higher likelihood of severe liver damage. This also requires adjustment of HIV (AIDS) therapy.

What are the routes of infection?

The mechanisms of transmission of viral hepatitis are divided into 2 large groups:

1. Parenteral or hematogenous. Inherent in infection with hepatitis viruses B, C, D, G. Parenteral viral hepatitis often becomes chronic, and virus carriage can develop.
2. Enteral or fecal-oral. In this case, water, food and contact (through dirty hands) transmission routes are distinguished. Typical for infection with hepatitis viruses A, E, F. In the vast majority of cases, chronic virus carriage does not occur.

It is logical to assume that the most dangerous are hepatitis viruses transmitted through contact with blood (B, C, D, G).

The routes of transmission of parenteral hepatitis viruses are varied:

• Injecting drug use without maintaining personal hygiene and sterility. This route of transmission is relevant for all of the above pathogens, but the hepatitis C virus is currently most often transmitted this way.
• Transfusion of blood and its components.
• Poor quality sterilization or reuse of instruments when providing medical care, as well as during salon procedures (manicure, pedicure), tattooing, piercing, etc.
• Unprotected sexual intercourse. They play a significant role in the epidemiology of viral hepatitis. But the hepatitis C virus is transmitted in this way only in 3-5% of cases.
• From an infected mother to the fetus and newborn during pregnancy (vertical transmission) or during childbirth (intranatal).
• Sometimes the transmission route remains unverified (unknown).

Acute viral hepatitis

In a typical (icteric) course, it has 4 periods or stages: incubation, prodromal, icteric, convalescence.

1. Incubation period. The duration is determined by the etiological agent.
2. Prodromal period. The duration of this period directly depends on the severity of the disease. It manifests itself as an increase in body temperature, most often to subfebrile levels. However, sometimes the temperature remains at the normal level or, conversely, reaches 38–39 degrees and above. Along with an increase in temperature, the phenomena of dyspeptic and asthenovegetative syndromes are added. It can also manifest itself as a flu-like condition, pain in the joints and muscles, and skin rash, sometimes accompanied by itching, are common. After a few days, pain develops in the area of ​​the right hypochondrium and epigastrium. Towards the end of the period, signs of jaundice appear.
3. Jaundice period. Is the height of the disease. Lasts from several days to several weeks. It is characterized by icteric discoloration of the patient’s skin and mucous membranes, darkening of urine and lightening of feces. The severity of the yellow color does not always correlate with the severity of the patient's condition. Jaundice most often appears gradually, over one and a half to two weeks. Sometimes its appearance is sudden. Dyspeptic symptoms continue to progress. They usually bother the patient throughout the entire illness. The intensity of pain in the right hypochondrium may increase. Sometimes jaundice is accompanied by itchy skin, especially with hepatitis A (Botkin's disease). It is very important in such cases to distinguish viral liver damage from manifestations of obstructive jaundice due to cholelithiasis. Hemorrhagic complications in the form of bleeding occur. The central nervous system is often affected, which is manifested by headache, apathy, insomnia or, conversely, drowsiness, causeless euphoria. Extrahepatic manifestations of the pancreas (pancreatitis), the musculoskeletal system (arthralgia, myalgia), skin (various types of rashes) and others are also likely.
4. Convalescence or recovery. Lasts several months after the end of the icteric phase. Unexpressed manifestations of asthenovegetative syndrome persist. Laboratory parameters are gradually normalizing. Deviations in laboratory parameters that persist for more than 6–12 months suggest chronicity of the disease. In this case, further examination is necessary.

In addition to the typical course, there are anicteric and erased forms, which occur with minimal manifestations of liver damage. Their frequency, according to various sources, ranges from 2 to 80% of cases.

The latent course of the disease with the absence of obvious symptoms is distinguished.

The most dangerous form of acute viral hepatitis is fulminant hepatitis.

It is distinguished by a very severe course of the disease and a fairly rapid culmination in the form of acute liver failure. Fulminant hepatitis exists in early or late forms. The development of the early form occurs in the first two weeks of the jaundice period and has an aggressive course with a rapid transition to hepatic coma. The late form develops from the 15th day of jaundice and is also dangerous, although it progresses more slowly.

Complications

The most terrible complication of acute viral hepatitis is the formation of liver failure, which can lead to coma and death. With hepatitis A (Botkin's disease), this complication occurs much less frequently than with infection with viruses B, C, D, E, G.

Transformation into a chronic process with hepatitis B, C, D occurs much more often than with hepatitis A (Botkin's disease) and E.

More rare complications include biliary tract diseases and aplastic anemia.

Diagnostics

On examination, an enlarged liver is found, and sometimes the spleen is found. Hepatomegaly appears already in the prodromal period and persists for quite a long time.

Laboratory tests reveal changes in peripheral blood parameters, an increase (or decrease) in the number of leukocytes, lymphocytes, monocytes, and eosinophils. Anemia may occur later.

An increase in the activity of hepatic aminotransferases and aldolase is recorded, the maximum values ​​occur during the period of jaundice. An increase in bilirubin levels is also determined. At the height of the disease, the above is accompanied by signs of profound liver dysfunction: a decrease in the level of proteins, a-lipoproteins, and cholesterol. The functions of the blood coagulation system are disrupted towards hypocoagulation. Hypoglycemia (low blood sugar) often develops.

Specific diagnostics are shown in Table No. 2.

Table No. 2. Serological indicators (markers) of viral hepatitis.

Acute viral hepatitis is treated in an infectious diseases department.
General principles of treatment Instrumental examination methods are most often not required. In doubtful cases, ultrasound, MRI or CT, as well as liver puncture biopsy, are used.

• The protective regime is observed. A special diet is prescribed - table No. 5 or 5a (according to Pevzner), taking into account the severity of the disease.
• The basis of treatment for hepatitis A (Botkin's disease) and E is detoxification of the body, and for other types of viral hepatitis (B, C, D, G) it is one of the auxiliary therapies. For this purpose, enterosorbents, hemodilution, antioxidants and antihypoxants are used, and in some cases plasmapheresis is used. The volume of incoming fluid increases to 2–3 liters per day. Skin care and thermal comfort are required in order to improve microcirculation and activate the activity of the sweat and sebaceous glands.
• Therapy aimed at correcting protein synthesis by the liver and its recovery processes.

Protein food supplements, solutions of synthetic amino acids, infusion of protein preparations, multivitamins and microelements, especially potassium, are used.

• Treatment aimed at reducing the manifestations of liver necrosis and fibrosis.
• Correction of cholestasis symptoms.
• Correction of hemostasis parameters.
• Antiviral therapy. Unlike hepatitis A (Botkin's disease) and E, parenteral viral hepatitis (B, C, D, G and some others) are strict indications for etiological therapy.
• Specific immunoglobulins.
• Immunocorrective therapy.

Chronic viral hepatitis

Most often, the course of the disease is asymptomatic, sometimes there is an indication of acute hepatitis in the past: extremely rarely - A, E, more often - B, C, D. Sometimes the cause cannot be determined - unverified chronic hepatitis.

Clinical symptoms are very nonspecific: nausea, lack of appetite, weakness, discomfort in the right hypochondrium. There may be manifestations of jaundice, ascites, spider veins.

Examination almost always reveals hepatomegaly, and sometimes an enlarged spleen. Laboratory tests may reveal increased activity of serum liver transaminases, bilirubinemia, and identification of specific markers of chronic viral hepatitis. Moreover, laboratory test indicators often do not always reflect the true picture of the pathological process and the severity of liver damage.

Morphological examination of the liver is of great importance in diagnosis. This allows you to establish an accurate diagnosis, as well as determine the degree of activity and stage of development of the disease. Moreover, the hepatitis C virus can sometimes be detected only in liver tissue if blood tests are negative. The degree of activity of chronic hepatitis depends on the severity and severity of the processes of necrosis and inflammation in the liver.

The following morphological forms are known, characterizing the degree of activity of the pathological process: chronic persistent hepatitis (CPH) and chronic active hepatitis (CAH). It should be noted that persistent hepatitis does not always progress to active hepatitis, and CAH may not transform into liver cirrhosis. The formation of liver cirrhosis can also occur without previous CAH. Sometimes CPG and CAG can transform into each other. Obviously, this depends on the interaction of the virus and the state of the patient’s immune system.

Principles of treatment

What matters is the activity of the inflammation process, based on which the attending physician makes recommendations. However, there is a general approach to therapy that is prescribed to all patients.

• A gentle regimen is recommended. It is prohibited to work with physical and nervous overload. In case of exacerbation of the disease, bed rest is recommended. The use of drugs with potentially hepatotropic effects is excluded. Medicines that are slowly neutralized by the liver (analgesics, sedatives, some laxatives, etc.) are undesirable. Physiotherapy on the liver area is contraindicated. During the period of exacerbation, operations and vaccinations are carried out exclusively for health reasons.
• Diet No. 5, stopping drinking alcohol and smoking.
• Drug treatment. Antiviral therapy acts directly on the virus. The most commonly prescribed drugs are alpha-interferon, often in combination with ribavirin, and lamivudine. Research is underway to develop new, more effective drugs for the treatment of viral hepatitis. Antiviral therapy is selected separately for each patient, taking into account many factors. Outside of exacerbation, hepatoprotectors, drugs to improve metabolic processes, vitamins and minerals, and immunomodulators are used.
• Vaccination against HBV. It is recommended in some cases for patients with chronic hepatitis C to prevent HBV infection and the development of coinfection.

Viral hepatitis in children

Infection of children occurs both in utero - vertical transmission of the virus, and after birth.

Infectious hepatitis in children is caused by the same pathogens as in adults: hepatitis viruses A, B, C, D, E, F, G; rubella viruses, cytomegalovirus, herpes, HIV (AIDS), etc.

With intrauterine infection, fetal hepatitis forms in parallel with congenital malformations and damage to other organs in the newborn. Congenital hepatitis manifests itself immediately after birth, significantly worsening the adaptation processes of the newborn. The severity of clinical manifestations in newborns depends on the degree of damage by the infectious agent. As a rule, congenital hepatitis in a newborn child has an unfavorable prognosis. Such hepatitis is treated with etiotropic (acting on the pathogen) drugs.

Older children most often have hepatitis A or Botkin's disease and, less often, hepatitis B. Other types of hepatitis are quite rare in them.

The main points of the epidemiology of HAV in childhood are:

• Botkin's disease most often affects children aged 3–7 years.
• There is a clear seasonality with a peak incidence in autumn and winter.
• Contact is often family, also in children's institutions and schools.
• The outcome of Botkin's disease is complete recovery without becoming chronic or fatal.
• The younger the child is, the more common the anicteric form is.

In the epidemiology of viral hepatitis B in children, the route of transmission is of great importance. Intrauterine or intrapartum infection significantly worsens the prognosis. The course of hepatitis is often anicteric, and in children under one year of age and newborns it can be asymptomatic, which significantly complicates diagnosis.

Prevention of viral hepatitis

Prevention measures depend on the mechanism of transmission of the virus.

Prevention of hepatitis A and E. First of all, careful adherence to the rules of personal and general hygiene. You should always keep your hands clean, especially after using the toilet. It is also necessary to monitor the purity of water and food.

Prevention of hepatitis B, C, D, G. Protection from contact with someone else's blood and biological fluids in any way. Practice only protected sex.

Acute hepatitis

According to statistics, 5–10% of the total population of the planet suffers from hepatitis, and these figures are increasing every year. In Russia, the vast majority of patients are drug addicts who inject drugs into the body intravenously.

It is not always possible to stop the pathological process, and extensive liver damage can result in death, cirrhosis and hepatic coma. Acute hepatitis C (AHCV) is especially dangerous, since an effective cure for this disease is still under development. But what is known about the acute phase of hepatitis, and why is it dangerous for human health? Doctors, oddly enough, came to a unanimous opinion on this issue.

Pathogenesis and etiology of the pathological process

Acute hepatitis C, also called “post-transfusion,” can progress at any age and affects males and females equally. The virus is transmitted from a patient to a healthy person by the parenteral route, that is, through contact with contaminated blood or through a blood transfusion. This is where people with drug addiction, patients after organ transplantation and dialysis, as well as cases of complex surgical interventions come to mind.
The non-parenteral route of infection prevails in medicine much less frequently, and the number of patients does not exceed 10%. And, nevertheless, the following are at risk:

• pregnant women;
• people with alcohol addiction;
• people with a genetic predisposition to the disease.

There are also clinical pictures in which it is very difficult to determine the main pathogenic factor.
The main causative agent is the HCV virus, the activity of which begins only after penetration into a healthy human liver. In recent years, scientists have been able to experimentally prove that its replication is also possible outside the “human filter,” for example, in numerous blood cells. A completely reasonable question arises: how does a pathogenic virus enter the body and infect it? This is where it is worth recalling the diagnoses that may precede this pathological process. This:

• Botkin's disease;
• Weil-Vasiliev disease;
• leptospirosis;
• amoebiasis;
• Infectious mononucleosis;
• malaria;
• syphilis;
• lobar pneumonia;
• yellow fever;
• flu;
• sepsis;
• toxic damage to the body.

Depending on the cause of the disease, the symptoms of the infectious process in the body have its own characteristic features.

Symptoms of the disease

Since acute hepatitis has several modifications, its symptoms are specific and it is important to consider each clinical case separately.
If this is an acute form of drug-induced hepatitis, then the patient’s body experiences a steady death of once healthy liver cells. As the pathology progresses, foci of necrosis become extensive, and important organs such as bone marrow, kidneys and heart can also be affected. The main symptoms of the diagnosis are persistent jaundice and itching of the skin, which becomes so unbearable that the patient experiences certain difficulties in the functioning of the nervous system.
Acute toxic hepatitis is accompanied not only by zonal necrosis, but also by morbid fatty liver. One of the complications of such a dangerous diagnosis is cataracts and death of the injured party.
Hepatitis, as a consequence of leptospirosis, worries the patient with attacks of fever, dizziness, nausea and vomiting, but extensive foci of an allergic rash cannot be ruled out, which significantly reduces the usual quality of life of the clinical patient.
When the disease worsens against the background of yellow fever, coagulative necrosis of hepatocytes, hemorrhage, signs of dyspepsia and hyperemia of the skin occur. Complications include toxic encephalitis and pathological enlargement of the affected organ. In 60% of all clinical pictures, the patient faces death, while the rest spend their lives on pills.
If we talk in general about a disease such as acute hepatitis, we should highlight the following changes in general well-being:

• disturbed temperature conditions;
• intestinal dysfunction;
• soreness in the right side;
• aversion to food and sudden weight loss;
• catarrhal phenomena;
• migraine attacks;
• discoloration of stool;
• jaundice of varying degrees of intensity;
• hyperemia of the skin.

It is these signs of the disease that should be the main reason for going to the doctor, and it is best not to delay this activity. The specialist, in turn, thanks to modern diagnostics, will determine which liver disease is progressing. This may be acute hepatitis B, C or A, and the treatment regimen for these diagnoses is somewhat different.

Diagnosis of the disease

The presence of a pathogenic virus in the blood cannot be determined immediately, and sometimes it takes 1 to 3 weeks to detect it. The main laboratory tests are enzyme immunoassay, which gives a 90% result only after 90 days, and recombinant immunoblotting analysis. These advanced techniques make it possible to determine the final diagnosis with maximum accuracy, as well as to identify a false-positive category of potential patients from the so-called “risk group”.
Instrumental methods of clinical examination only establish the fact of pathological problems in the liver, since already at the first ultrasound it is obvious that this vital organ is abnormally reduced in size. If acute hepatitis is diagnosed, immediate treatment should follow.

Effective treatment of acute hepatitis

If the patient hopes that acute viral hepatitis will cure itself, then this is definitely a bad start to intensive care. Of course, such clinical cases are well known in medical practice, but their number barely reaches 10–15% of the total number of patients with hepatitis.
There is an opinion that a stable positive effect of the disease is ensured by IFN therapy, which necessarily stipulates a three-month course of treatment. The effectiveness of such a prescription is indicated by negative HCV RNA results and normal ALT activity, but we can talk about final recovery only a year after the end of intensive therapy.

In general, the acute form of hepatitis is an extremely undesirable disease, which in any case does not leave the human body without a trace. Most often, chronic hepatitis C progresses against its background, which is not treated and significantly reduces the full life expectancy of an infected person. That is why it is necessary to take timely care of prevention and regularly donate blood to monitor its main indicators.

What is hepatitis C: causes and types

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Causes

The etiology of hepatitis C is based on the presence of the virus and a susceptible organism, subject to the conditions of the infection mechanism. It must be said that this is one of the most persistent infections; it persists for up to 4 days on instruments and surfaces with which infected blood has come into contact.

At what temperature does the hepatitis C virus die? Boiling destroys it within 2 minutes, and at 60 degrees Celsius it takes about half an hour.

Despite the fact that the virus was discovered more than thirty years ago, controversy surrounding it still does not subside. There are adherents of the theory that hepatitis C does not exist. However, the evidentiary basis is the isolation of virus RNA and antibodies to it during specific studies.

The classification of hepatitis C divides the disease into two forms: acute and chronic. In the acute form, there may be no symptoms or they may be similar to any other infectious hepatitis. The chronic course has such phases as latent (hidden) and clear clinical manifestations.

What is hepatitis C? In essence, this is an infection that deliberately selects the liver as a kind of “target”. The pathogen, which has six genotypes, feels great inside hepatocytes (liver cells), and the immune system is powerless to destroy it without at the same time destroying the liver parenchyma (tissue).

Type 1 hepatitis C is distributed throughout the globe. This is because subsequent variants are most likely the result of mutation - a means of adapting the virus to ways of fighting against it. Among drug addicts, type 3 hepatitis C predominates.

How dangerous is hepatitis C? First of all, the development of liver cirrhosis - a chronic irreversible process of replacement of functioning parenchyma with dense fibrous nodes.

The hepatitis C virus has several ways of entering the body. Among them:

1. Parenteral. Indicates infection through contact with blood. The amount of it in this case does not matter: just a tiny drop, not visible to the eye, can cause illness.
   Hepatitis C is transmitted during blood transfusions - this is a blood transfusion procedure, and hemodialysis - cleansing the body of metabolic products due to kidney diseases. Blood residues can be found on instruments for medical and non-medical procedures - surgical and endoscopic examinations, manicures, tattooing, ear piercing and other types of piercing.
   There is a risk even when using someone else's toothbrush or razor, kissing, if the infected person and his partner have wounds in the oral cavity. Of course, organ transplantation implies the same opportunities for the transmission of hepatitis C, while transplantation implies immunodeficiency, due to which the infectious process is more severe and faster.
   One of the most common mechanisms is the entry of the hepatitis C pathogen into the body with the same syringe needle in people who use injection drugs.
2. Sexual. Danger comes from discharge (secretion) of the glands of the genital organs, abrasions and microtrauma due to damage to the mucous membrane during unprotected sexual intercourse. The hepatitis C virus, as a rule, is secreted in significant quantities only during an active process in the body; During the latent period, hepatitis C is rarely transmitted sexually.
3. Vertical. This is an infection of a child in the womb transplacentally (through the vessels of the uteroplacental blood flow) or during the birth process, when the baby is forced to come into contact with the maternal mucosa and can receive minor damage, opening the “entrance gate” of the infection.
   Perhaps this mechanism provides a comprehensive answer to the question: is it possible to have children with hepatitis C? The disease does not affect reproductive function, i.e. the possibility of conception. The degree of viral load is important as a fundamental factor in the likelihood of pathogen transmission.

The source of infection can be not only the patient, but also a carrier of hepatitis C.

What it is? By carriage we mean a state when the virus is in the blood, but does not cause harm; there are no symptoms of liver damage. At the same time, it can be transmitted to another person, in whose body the disease is activated in full force.

Can hepatitis C be dangerous for family members who use the same household items as the patient? Contact and household transmission of this infection is not typical, however, in case of injuries to the oral mucosa, blood can remain on dishes, towels, and a toothbrush, therefore it is undesirable to transmit them to anyone.

What to do if you are diagnosed with hepatitis C? You must follow the instructions of your attending physician, who, if necessary, will prescribe additional diagnostic tests and select the optimal antiviral therapy regimen.

Symptoms

The incubation period for hepatitis C lasts from two weeks to six months; The virus RNA binds to cell surface receptors and penetrates the hepatocyte. Once under the reliable protection of a membrane impenetrable to immunity, the pathogen starts the process of replication (copying) and multiplies.

In the presence of immunodeficiency or concomitant liver diseases, it is reduced.

The hepatitis C clinic is characterized by the following symptoms:

• constant weakness, fatigue, apathy, depressed mood;
• decreased or lack of appetite, nausea, vomiting;
• abdominal pain mainly in the right hypochondrium;
• enlargement of the liver (hepatomegaly), less often – enlargement of the spleen (splenomegaly);
• darkening of urine, gray stool;
• yellowing of the skin, mucous membranes and sclera of the eyes;
• joint pain.

These signs are observed in the acute period. Depressive disorders are quite common with hepatitis C, but they are not a specific obligatory symptom.

Does your liver constantly hurt? The chronic form is accompanied by the formation of cirrhosis and portal hypertension, a syndrome that develops as a result of increased pressure in the portal vein.

Then, when examining the patient, you can notice dilated saphenous veins on the anterior abdominal wall, the liver is often enlarged and the person experiences discomfort, pain in the right hypochondrium during physical activity or dietary errors. Serous fluid accumulates in the abdomen - this phenomenon is called ascites.

During fibrogastroduodenoscopy (examination of the gastrointestinal tract with an optical tube), dilated venous vessels of the esophagus and stomach are detected. In later stages, disturbances in the coagulation system are characteristic, since one of the functions of the liver is the synthesis of vitamin K and blood clotting factors.

They manifest themselves as nasal and gastrointestinal bleeding of varying severity.

Such complications of hepatitis C indicate irreversible damage to the liver parenchyma.

Does hepatitis C cause disability and in what group? In fact, viral hepatitis with liver dysfunction is the basis for this. Clinical and laboratory indicators and the ability to self-care and work are taken into account.

Is it possible to work with hepatitis C? Since the virus is not transmitted through household contacts, there is no need to limit the patient’s activity in society, which also includes professional aspects.

Diagnostics

Today, medicine has ample opportunities to confirm hepatitis C.

Diagnostic methods are divided into nonspecific (reflect the general picture of damage to the liver and the body as a whole) and specific (aimed at detecting the virus or the immune response to its presence):

Sometimes this situation arises: there are antibodies to hepatitis C, but there is no virus. This is possible if self-healing has occurred - the immune system has managed to overcome the infection. Antibodies indicate that the immune system has responded to the pathogen.

A false positive result when diagnosing hepatitis C is a very rare but possible occurrence. The reasons may be a violation of the rules for preparing and studying the material, a banal mix-up with test tubes, or the patient intentionally donating blood that is not his own, which is possible with remote sampling (taking blood outside the walls of the laboratory).

Treatment

There is an opinion that hepatitis C is incurable. Is this so and how effective are the pharmaceutical drugs offered then? Unfortunately, once infected, the virus cannot be completely destroyed, but modern methods of therapy can suppress its replication so much that it will not be detected in the blood.

Positive hepatitis C must be treated, not with the goal of completely eliminating (removing) the virus from the body, but to prevent complications. Cirrhosis in the absence of proper medical care is a threat of liver failure, the consequences of which in hepatitis C are very serious.

How is hepatitis C treated? There are several main groups of medications used to fight the virus:

1. Interferons (viferon, alfaferon).
2. RNA polymerase inhibitors (ribavirin, sofosbuvir).
3. Protease inhibitors (simeprevir, boceprevir, telaprevir).

The duration of medication use ranges from 16 to 72 weeks, and these drugs are combined for a more effective effect on the virus.

To support the liver, hepatoprotectors are also prescribed - substances that stimulate regenerative abilities and help the organ resist the destructive effects of hepatitis C.

Alcohol and its substitutes are incompatible with treatment; the diet involves avoiding fatty and fried foods, spicy seasonings, and synthetic flavorings.

Patients complain of constant fatigue, so it is necessary to rationalize the work and rest regime, engage in strengthening physical exercises, but avoid excessive fatigue.

It is better to consult a doctor and replace or discontinue completely hepatotoxic medications - a weakened liver has a hard time coping with the increased load, and the risk of side effects increases tenfold.

There is also a risk for women after menopause.

The type of infection is important - genotype 1 recurs much more often, unlike other variants of the disease, this is due to its high resistance to treatment, which can lead to an insufficient effect on hepatitis C. This should be taken into account when planning the duration of the drug regimen.

Alcohol abuse seriously aggravates and accelerates the onset of the consequences of hepatitis C, since even in uninfected people it leads to the development of cirrhosis.

It is impossible to deny that hepatitis C is a serious disease, but nevertheless this is not a death sentence. The main obstacles to quality treatment are its high cost and late diagnosis, when the pathogen is detected already at the stage of liver cirrhosis. If detected early, the course of hepatitis C can be slowed down and even stopped.

Prevention

What to do to avoid becoming infected with hepatitis C? Strictly individual use of medical and cosmetology instruments or careful sterilization with proper quality control are required.

When performing procedures that involve the risk of the patient’s blood or other biological fluid coming into contact with the skin and mucous membranes, medical workers wear gloves, masks and goggles.

It is recommended to use a condom during sexual intercourse. This also applies to a regular partner if he is a carrier or has a confirmed hepatitis C infection. Pregnant women and women planning to conceive undergo screening diagnostics for hepatitis C.

You can find out everything about the risk to the child by consulting an obstetrician-gynecologist.

(Los Angeles, 1994)

According to the international classification, hepatitis is classified:

According to etiology and pathogenesis:

Viral hepatitis with oral - HAV, HEV and parenteral - HBV, HCV, HDV infection. The role of other hepatotropic viruses - HGV, SEN, TTV in the development of CG is being studied

Medicinal (see above)

Autoimmune

Cryptogenic (unknown etiology)

According to the morphological picture: successive stages are distinguished

0 – no fibrosis

1 – mild periportal fibrosis

2 – moderate fibrosis with portoportal septa

3 - pronounced fibrosis with portocentral sets

4 – liver cirrhosis

According to the degree of activity of the inflammatory process:

Minimal (persistent hepatitis)

Mild

Moderately expressed

Severe (active hepatitis)

With the flow:

Acute and chronic

By phase (for viral hepatitis)

A. Replication

B. Integration

Example wording:

Chronic viral hepatitis B, pronounced activity, replication phase, with moderate fibrosis.

Morphology of CG

The basis of the morphological picture of chronic hepatitis is inflammatory infiltration of the parenchyma of varying severity.

With mild activity of the process (chronic persistent hepatitis), infiltration by mononuclear cells in the area of ​​the portal vein and portal tracts, protein degeneration of hepatocytes, and, less commonly, necrosis are observed.

High activity of hepatitis (chronic active hepatitis) is accompanied by severe inflammatory infiltration of the portal tracts and hepatic lobules, more pronounced degeneration and necrosis of hepatocytes, moderate sclerosis of the portal and periportal fields is possible, Kussmaul bodies are detected. Inflammatory infiltrates in the portal tracts and acini are represented by lymphocytes, plasma cells and antigen-containing cells.

At the morphological stage corresponding to chronic hepatitis, despite the presence of moderate fibrosis, the liver architecture is not disturbed.

Chronic hepatitis clinic

Clinical manifestations of hepatitis are determined by the severity of the activity of the inflammatory process; in the case of viral hepatitis, the phase of the disease (replication, integration). With minimal activity, the course may be latent; hepatitis can be detected during a random examination of the patient. On the contrary, with pronounced inflammatory activity, the clinical picture of the disease can be represented by a number of syndromes with greater or less specificity.

Nonspecific syndromes include:

Asthenovegetative – characterized by weakness, increased fatigue;

Mesenchymal-inflammatory - low-grade fever, lymphadenitis, inflammatory changes in general and biochemical blood tests (leukocytosis, acceleration of ESR; increase in CRP, seromucoids);

Painful – rare, may be caused by hepatomegaly;

Dyspeptic – usually associated with concomitant pathology of the stomach and biliary tract;

More specific is cholestatic syndrome associated with intrahepatic cholestasis. It is characterized by icterus of the skin and mucous membranes, hyperbilirubinemia, increased levels of alkaline phosphatase and GGTP in the blood.

The most important specific syndrome of hepatitis is cytolytic, characterized by weight loss, increased levels of ALT and AST enzymes in the blood (more than 2 times). The appearance of signs of hepatocyte cytolysis in a patient is a leading indicator of hepatitis activity, and in the case of viral etiology, a replication marker.

In most cases, hepatitis is asymptomatic or latent (70%).

Diagnosis of chronic hepatitis

The diagnosis of CG is quite complex, despite the availability of modern and fairly specific examination methods, and consists of several stages.

The first step is to analyze the above symptoms and syndromes and carefully collect anamnesis. It is necessary to collect information about previous acute hepatitis, medications taken, injections, surgical interventions, blood transfusions and blood substitutes, use of narcotic drugs, social status of the patient, etc.

During an objective examination, pay attention to the color of the skin and mucous membranes, the nature of nutrition, the presence of traces of intravenous injections, when palpating the liver, determine its size (hepatomegaly), the nature of the edge (smooth), with severe hepatitis, telangiectasias and palmar erythema may be detected (more typical for liver cirrhosis).

At the same stage of diagnosis, it is necessary to conduct a biochemical blood test to determine its protein composition, ALT, AST, bilirubin fractions, ALP, GGTP, etc. Ultrasound and other additional research methods - scanning, computed tomography, laparoscopy, FGDS can confirm the presence of inflammatory changes in the liver parenchyma and make a differential diagnosis.

The second and most important stage in verifying the diagnosis is examining the patient for markers of viral hepatitis. They are considered to be antigens, antibodies, and viral DNA (RNA) specific to each hepatotropic virus, found in the blood (or other biological fluids, hepatocytes during biopsy). For this purpose, modern immunological and molecular biological methods are used: ELISA, in the case of determining antigens and antibodies, PCR, when identifying fragments of DNA and RNA viruses.

For example, for hepatitis B, the markers are HBs Ag; anti-HBcor IgG, Ig M; HbeAg; anti HbeIgG, IgM; DNA, DNA-p HBV.

The third stage of diagnosis, if viral hepatitis is confirmed, is to determine its activity. Thus, markers of HBV activity are anti-HBcor Ig M; HbeAg; anti Hbe IgM; DNA; DNA-p HBV (in the replicative phase of hepatitis B).

In the absence of markers of viral hepatitis as a result of the immunological study, it is necessary to conduct studies confirming other types of hCG. For autoimmune hepatitis - detection of autoimmune anti-hepatic and other antibodies in serum.

Clinical features of various types of hCG

Viral hepatitis B.

Based on the pathogenesis (presence of replication, integration phases), it can occur with varying degrees of activity, characterized during the period of exacerbation by cytolytic, general inflammatory and other syndromes. It is often asymptomatic; most patients have anicteric forms of the disease.

With CHB, a clear epidemiological history is most often revealed - previous acute hepatitis, transfusion of blood and its substitutes, parenteral interventions, drug addiction, etc.

The main method for diagnosing CHB is laboratory (see CH markers).

Histologically, viral hepatitis B often reveals stepwise necrosis in the periportal zones, intralobular and portal lymphocytic infiltration.

This type of hepatitis often results in macronodular or mixed cirrhosis of the liver, especially with combined liver damage by a virus and alcohol.

Characteristic features of viral hepatitis C are:

Frequent incidence in risk groups (drug addicts, homosexuals, etc.).

The disease is known to be asymptomatic, often manifesting only asthenovegetative syndrome or the detection of CHC during a random examination. To confirm the diagnosis, it is necessary to identify serological markers, which are antibodies to HCV, fragments of HCV RNA (during the active period of hepatitis).

40-50% of patients may have extrahepatic manifestations - arthralgia, myalgia, autoimmune thyroiditis, etc.). This form of viral hepatitis is characterized by long periods of clinical and laboratory remissions, but with this relatively favorable course there is a frequent outcome in micronodular cirrhosis.

Chronic hepatitis D is characterized by the possibility of formation only with additional infection with HBV (co- or super-infection), a more severe course, and the presence of clear clinical manifestations of the disease. With HDV, there is often pronounced cytolytic syndrome, hepatomegaly, splenomegaly, and there may be hemorrhagic syndrome.

A laboratory blood test may show a combination of HDV and HBV markers, often with levels of the latter leveling out.

This viral hepatitis is characterized by a rapidly progressive course with the development of liver cirrhosis or hepatocellular carcinoma.

Autoimmune hepatitis (CAH).

This type of hepatitis is quite rare. Higher incidence has been reported in the Nordic countries. Young women are more likely to suffer from CAH.

The etiology is unknown, although the possible role of unknown viruses, preons, and hereditary immune disorders is discussed.

The leading mechanism of the pathogenesis of CAH is the formation of autoantibodies to modified hepatocytes.

Features of the clinical manifestations of this hepatitis include the presence of extrahepatic systemic manifestations: polyserositis, thyroiditis, autoimmune hemolytic anemia, glomerulonephritis, Raynaud's syndrome, myositis. In this case, a continuously progressive course of the disease is often observed.

Laboratory characteristics of CAH are significant hypergammaglobulinemia, hyperproteinemia (90-100 g/l), high transaminases (> 10 times). To verify the diagnosis, a preliminary examination for markers of viral hepatitis is necessary in order to exclude the latter.

A special immunological study allows us to detect smooth muscle (SMA) and antinuclear (ANA) antibodies in type I disease, hepatorenal microsomal antibodies in type II CAH, antibodies to soluble liver hypertension and hepatopancreatic antibodies (LP) in type III autoimmune hepatitis.

As for drug-induced hepatitis, it should be noted that there is no specific clinical picture of the disease. The diagnosis in this case is made on the basis of medical history (usually long-term use of hepatotoxic drugs) and is largely based on data from preliminary studies that exclude the above forms of hCG.

Thus, the diagnosis and differential diagnosis of chronic hepatitis requires the differentiation of various forms of the disease from each other, as well as from cirrhosis, metabolic liver diseases, and its alcoholic damage.

Treatment of hCG

The most important component of complex therapy for hepatitis is etiotropic treatment aimed at eliminating or containing the cause of the disease and predisposing factors - viruses, hepatotoxic drugs, alcohol, cholestasis, etc. The paths of drug etiotropic therapy are completely opposite in cases of viral and autoimmune nature of the disease.

In case of active viral hepatitis, antiviral therapy is indicated with drugs of the interferon group and (or) nucleosides, which have both a direct virus-inhibiting effect and immunostimulating activity (alpha-interferons).

On the contrary, with the autoimmune etiology of hCG, immunosuppressive drugs are prescribed - glucocorticosteroids and cytostatics.

Treatment with antiviral drugs is indicated in the replicative phase of the disease, confirmed by a laboratory increase in ALT levels by at least 2 times, and the presence of serological markers of hepatitis activity. The effect of antiviral therapy is most pronounced in young patients, often women who do not have bad habits. In other cases, the effectiveness of interferons is much lower; the side effects of interferon therapy cover the main ones. In addition, there is individual sensitivity to interferon drugs (due to the activity of special receptors).

For viral hepatitis B it is prescribed

 - interferon (reaferon, intron A, roferon A, velferon, etc.) 5-6 million IU intramuscularly 3 times a week for 6 months or 10 million IU 3 times a week for 3 months. ;

Lamivudine (Zeffix) – 100 mg once a day for 12 months. (monotherapy)

For chronic hepatitis C, interferon drugs are initially prescribed in smaller doses

 - interferon 3 million IU intramuscularly 3 times a week for 3 months, if there is an effect in the same or higher dose up to 12 months;

 - interferon in the same dose and ribaverine 100-1200 mg/day. within 6 months.

Induction high-dose therapy is possible; in recent years, pegylated interferons - Pegasys, etc. - have been used.

Chronic hepatitis D in the active phase also requires antiviral therapy, with higher doses of interferon (5-6, or 10 million IU) prescribed for a long period.

A feature of the treatment of autoimmune hepatitis, based on the pathogenesis of the disease, is the administration of glucocorticosteroids for immunosuppressive purposes - prednisolone in average therapeutic dosages (30 mg/day) with a gradual reduction in the dose to a maintenance dose (10-15 mg/day) for several years.

For the same purpose, the administration of cytostatic drugs, for example, azathioprine at an initial dose of 50 mg/day, up to a maintenance dose of 25 mg/day, is justified and effective.

The use of hepatoprotectors that increase the resistance of hepatocytes to the action of the virus and other pathogenic factors - Essentiale, Karsil, Heptral - is justified as a basic therapy; prescribing infusions of glucose, saline and others for metabolic and detoxification purposes.

To correct concomitant intestinal dysbiosis, the use of eubiotics, lactulose, and enzyme preparations is effective.

Considering the importance of cholestasis in the pathogenesis of chronic hepatitis, it is advisable to use ursodeoxycholic acid preparations (ursofalk, etc.) in complex therapy.

Prevention of chronic hepatitis

Anti-epidemic measures are of great importance for the prevention of hepatitis, including disinfection of surgical and dental equipment, a strict balanced approach to the issues of blood transfusion and its substitutes, household preventive measures and other sanitary and hygienic measures.

Vaccine prevention is highly effective, which was developed for two forms of hepatitis A and B.

In accordance with federal law, since 2002, vaccination must be carried out in the first 12 hours of a child’s life, immunization of children aged 13 years has been introduced, and immunization of medical workers is carried out.

Forecast

The prognosis of the disease is ambiguous and depends on the type of hepatitis, stage, activity of the process, histological signs, the presence of bad habits, etc.

The following options are possible:

Stable clinical remission - absence of symptoms, normalization of laboratory parameters for 1.5-2 years

Transition to liver cirrhosis in 30-50% of cases

Development of hepatocellular carcinoma

Chronic hepatitis in any case is the subject of long-term medical examination using modern special methods of serological immunological diagnostics and an objective assessment of the effectiveness of ongoing therapeutic and anti-epidemic measures .

Updated: February 21, 2015

Viral hepatitis (VH) is one of the most pressing problems of modern medicine. This is determined both by their widespread distribution and high incidence rates. According to WHO estimates, hundreds of millions of people around the world are infected with hepatotropic viruses.

It should be noted that among all infectious pathologies in Russia, VGs cause the greatest economic damage per 1 case of disease, and in terms of total economic damage they are second only to influenza and acute respiratory infections. The last decade, on the one hand, was characterized by the latest achievements in molecular biology, virology, and genetic engineering, which made it possible to discover new hepatotropic viruses, study pathogenesis in more detail, significantly improve the diagnostic system and develop new approaches to antiviral therapy and specific prevention of viral hepatitis. On the other hand, particularly in Russia, there was a change in the etiological structure of hepatitis due to the influence of several processes: the incidence rate of hepatitis A subject to sharp fluctuations, an increase in the incidence of hepatitis B, the introduction of diagnostic and registration methods, the emergence and progressive increase in the number of mixed hepatitis,
improving the diagnosis and registration of chronic hepatitis. For the first time on February 13, 2001, the State Duma of Russia held parliamentary readings “On state policy to prevent the spread of infectious hepatitis in the Russian Federation,” at which it was emphasized that the problem of viral hepatitis has grown from a medical one to a national one, infections have become catastrophic scale and pose a real threat to the health of the nation. In this regard, it is necessary to consolidate the efforts of the entire country to combat viral hepatitis.

Classification of viral hepatitis

Viral hepatitis (VH) is a group of infectious diseases characterized by predominant liver damage. Currently, viral hepatitis A (HA), viral hepatitis B (HB), C (HS), D (HD), E (HE) are distinguished, the pathogens of which differ according to taxonomic characteristics, and the diseases - according to epidemiological, pathogenetic characteristics and likelihood of transition to chronic forms. Recently, VH hepatitis G (rG) was discovered, as well as new viruses (TTV, SEN), the role of which in liver damage is still poorly understood.

Viral hepatitis A, like HEV E, is characterized by a fecal-oral transmission mechanism, realized by water, food and contact-household transmission routes. With sufficiently pronounced resistance of pathogens in the external environment, this ensures the widespread spread of diseases, often manifesting themselves in the form of outbreaks or epidemics covering entire regions.

Hepatitis B, C, D and G are spread by the parenteral route. This suggests a lower activity of infection transmission mechanisms carried out during transfusions of blood or its components, during invasive diagnostic and therapeutic procedures, during intravenous drug administration, etc. Sexual, ante-, peri- or postnatal, as well as hemopercutaneous routes are possible infection. The lower activity of the transmission mechanisms of pathogens of this group of diseases is compensated by prolonged viremia of the infected, insufficient manifestation of the disease (DS) and chronic pathology gical process, which ultimately leads to an increase in the population of “virus carriers”.

The hepatotropic nature of VH pathogens explains the similarity of clinical manifestations, the commonality of diagnostic methods and pathogenetic therapy, as well as systems of rehabilitation and dispensary observation of convalescents. All CH are characterized by common pathogenetic processes in the liver in the form of cytolytic, cholestasis and immunoinflammatory syndromes.

Cytolysis of hepatocytes of varying severity naturally develops with CH of different etiologies. It can be caused by direct cytopathic or immune-mediated (IM) effects of viruses. Cytolysis is based on disruption of intracellular metabolic processes, activation of pro-oxidant and inhibition of antioxidant systems of cells. As a result, free radicals accumulate on the membranes of hepatocytes, lipid peroxidation increases, which leads to an increase in their permeability and the release of intracellular enzymes (aminotransferases, etc.) and potassium ions from hepatocytes. The latter are replaced by sodium and calcium, which leads to fluid retention and cell swelling, changes in their pH, disruption of oxidative phosphorylation with a decrease in the bioenergetic potential of hepatocytes. As a result, their very diverse functions are disrupted, including detoxifying and synthetic functions; glucose utilization, cholesterol esterification, and the processes of transamination and deamination of amino acids are impaired.

The earliest manifestation of cytolytic syndrome is an increase in the activity in the blood serum of such intracellular enzymes as alanine aminotransferase (ALAT), aspartate aminotransferase (AST), cholinesterase, sorbitol dehydrogenase, arginase, etc. An increased level of serum iron is also considered as a marker of cytolysis in liver diseases.

A clinically significant reflection of a violation of pigment metabolism, detoxifying and secretory functions of the liver is hyperbilirubinemia, caused by a decrease in the processes of uptake of free bilirubin by hepatocytes, its glucuronidation and excretion into the biliary tract.

Inhibition of the synthetic function of liver cells leads to hypoalbuminemia, a decrease in almost all blood coagulation factors, especially prothrombin, coagulation and fibrinolysis inhibitors. With a critical drop in coagulation potential, hemorrhages appear, and in severe cases, massive bleeding (hemorrhagic syndrome).

In cases of severe cytolytic syndrome, the process of membrane disintegration extends to intracellular organelles. As a result of a violation of the integrity of lysosomal membranes, a massive release of proteolytic enzymes - hydrolases occurs, which leads to self-destruction of cells, which can acquire the character of a kind of chain reaction with the development of acute liver failure.

Cholestasis reflects a violation of the outflow of bile, usually as a result of a decrease in the secretory function of liver cells (hepatocellular cholestasis) and in combination with cytolysis. Not only various fractions of bilirubin accumulate in the blood, but also bile acids, cholesterol, excretory enzymes (alkaline phosphatase, gamma-glutamyl transpeptidase - GGTP, etc.) and some trace elements, in particular copper.

The syndrome of general infectious intoxication does not always correspond to the level of hyperbilirubinemia. In the initial (pre-jaundice) period, it can be a reflection of the viremia phase and manifest itself as fever, malaise and other general symptoms characteristic of it. During the height of the period, cytolytic syndrome with a violation of the detoxifying function of gelatocytes (anorexia, nausea, vomiting, weakness, lethargy, etc.) is essential. With its deepening and the development of acute liver failure, intoxication acquires the features of specific dysfunctions of the central nervous system, manifested in the so-called infectious-toxic or hepatic encephalopathy.

The commonality of pathophysiological processes allows us to classify CH (Table 1) according to its clinical form, severity and nature of the course. In recent years, mixed hepatitis (usually hepatitis B+C) has often been diagnosed, which is due to common mechanisms of infection. According to clinical manifestations, hepatitis can be manifest (icteric, anicteric) and latent, or asymptomatic (subclinical, inapparent).

Table 1

CLASSIFICATION OF VIRAL HEPATITIS

Nosological	Clinical		Character
Viral hepatitis A	Manifest.
	» icteric		cyclical
Viral hepatitis B	a) cytolytic (typical)		Acute protracted
		Extremely heavy	(progressive)
	b) cholestatic	(fuminant)	Chronic
Mixed hepatitis	(atypical)
unverified	"anicteric
	Latent
	(asymptomatic)
	subclinical inapparent

* Has not received approval from the International Committee on Taxonomy and Nomenclature of Viruses

Jaundice forms are among the most pronounced variants of the disease. They are characterized by jaundice (an increase in the level of bilirubin in the blood over 40 µmol/l) and positive enzyme tests; they can occur in a typical cytolytic form with pre-icteric (initial), icteric and recovery periods, often with severe cholestasis. Sometimes (atypical forms) the leading manifestation of the disease is cholestatic syndrome (jaundice with an increase in the blood level of bile pigments, cholesterol, beta-lipoproteins, excretory enzymes - alkaline phosphatase and gamma-glutamyl transpeptidase). This is characterized by bilirubin-transaminase dissociation (a significant increase in bilirubin content with relatively low activity of transaminases, in particular ALT).

Anicteric forms of viral hepatitis are characterized by a complete absence of clinical signs of jaundice with positive enzyme tests and mild general manifestations of the disease, including liver enlargement and subjective signs of dysfunction.

In subclinical forms, there are no clinical objective and subjective manifestations with minor hepatomegaly or even its absence. The diagnosis is established by the presence of specific markers of hepatitis viruses in combination with low activity in the blood serum of liver-specific and indicator enzymes (ALAT, etc.), as well as by pathomorphological changes in the liver.

The identification of only specific markers of pathogens in the complete absence of clinical and biochemical signs of hepatitis provides the basis for establishing an inapparent form of the disease.

In practical work, based only on clinical data and the results of laboratory tests of liver function, a time criterion is used to determine an acute cyclic course - up to 3 months, an acute protracted (progressive) course - up to 6 months, and a chronic course - over 6 months. However, the true criteria for assessing the nature of the course of CH are the duration of the replicative activity of the corresponding pathogens, as well as data from histological examination of liver biopsies.

Pathomorphological changes in the liver during VH are assessed based on the results of intravital liver puncture biopsy. It is informative in cases of protracted (progressive) and especially chronic course of the disease. In combination with clinical, laboratory and instrumental research methods, morphological control makes it possible to identify not only the nature and degree of inflammatory changes in the liver, but also to evaluate the effectiveness of complex and expensive treatment measures.

Acute CH may come to an end recovery, including recovery from post-hepatitis syndromes, or take a chronic course. Extremely severe (fulminant) forms with acute liver failure, mainly characteristic of hepatitis B and TD, often end fatal outcome, especially with untimely intensive care.

Complete clinical recovery occurs in almost all patients with HA and GE. The chronic course is characteristic only of viral hepatitis B, C and D, while chronicity develops much more often with HS.

Toward clinical recovery with so-called postges Patit syndromes include asthenovegetative syndrome, hepatomegaly, functional hyperbilirubinemia, as well as dyskinesia or inflammation of the biliary tract.

Posthepatitis asthenovegetative syndrome is manifested by increased fatigue, poor appetite, sleep disturbances, and sometimes a feeling of heaviness in the right hypochondrium. These phenomena are caused by functional disorders of the nervous, cardiovascular, and digestive systems. Despite the complaints, a morphological examination of liver biopsies reveals a normal structure, functional tests and enzymatic activity are within normal limits. The syndrome usually resolves within 1-3 months.

Posthepatitis hepatomegaly is characterized by an increase in the size of the liver (usually up to 2-3 cm along the right midclavicular line) in the absence of patient complaints and deviations in the biochemical parameters of its functions. These phenomena are purely benign in nature and do not develop into chronic hepatitis.

Posthepatitis (functional) hyperbilirubinemia is manifested by jaundice of the sclera and occasionally the skin, which can intensify after physical and mental stress. My health remains good. The content of bilirubin in the blood rarely exceeds 34 µmol/l, mainly due to its indirect fraction. Liver function tests and blood enzymatic activity were within normal limits. According to radiohepatography, there is a slight slowdown in the rate of uptake and excretion of radioactive Bengal pink colloid by the liver.

Biliary dyskinesia (usually of the hypertonic hyperkinetic type) is accompanied by heaviness or pain in the right hypochondrium associated with food intake, more often with dietary disorders. It should be borne in mind that these phenomena in some cases may be caused by diseases of the duodenum and pancreas. The nature of functional disorders of the biliary tract can be clarified by ultrasound examination with a choleretic breakfast, oral cholecystography and multi-stage duodenal intubation with oral administration of methylene blue.

Inflammation of the gallbladder and biliary tract is manifested by pain in the right hypochondrium with irradiation under the right shoulder blade and shoulder, usually appearing after errors in diet, as well as nausea, bitterness in the mouth, increased pain sensitivity in the gallbladder area, positive gall bladder symptoms. Low-grade fever, slight neutrophilic leukocytosis, and increased ESR may be observed. Detection of an increased number of leukocytes, mucus in the duodenal contents, seeding of microorganisms, and ultrasound results clarify the nature of the inflammatory changes.

Chronic hepatitis (CH) is an independent form diseases with a diffuse inflammatory process in the liver lasting more than 6 months. It is now known that CG has a predominantly viral etiology. In this case, the leading role in the formation of chronic infection, as a rule, belongs to mild icteric, anicteric, subclinical and inapparent forms of acute hepatitis B, C, D with a protracted progressive course. Alcoholism, drug addiction, abuse of certain medications, poor nutrition. In some cases, acute VH occurs as chronic from the very beginning.

Currently, 7 etiologically independent hepatitis have been identified, which are designated by the letters of the Latin alphabet: A, B, D, E, C, F, G. This does not exhaust the variety of viral liver lesions in humans. The antigenic heterogeneity of the viruses that cause hepatitis C and E has been proven, and it is possible to predict in the near future the identification of new etiologically independent forms of the disease.

HEPATITIS A

Hepatitis A (B 15) is an acute cyclical disease caused by an RNA virus; characterized by short-term symptoms of intoxication, quickly passing disturbances in liver function. The course is benign. According to ICD-10, there are acute hepatitis A (B 15), hepatitis A with hepatic coma (B 15.0) and hepatitis A without hepatic coma (B 15.9).

Etiology. Hepatitis A virus (HAV) was discovered by S. Feinstone and co-workers (1970). It is a spherical RNA-containing particle with a diameter of 27-30 nm. According to its physicochemical properties, HAV belongs to enteroviruses with serial number 72 and is localized in the cytoplasm of hepatocytes. The virus is insensitive to ether, but is quickly inactivated by a solution of formaldehyde, chloramine and ultraviolet rays; at a temperature of 85°C it is inactivated within 1 minute.

The possibility of virus reproduction in primary and continuous monolayer lines of human and monkey cell cultures has been demonstrated, which opens up a source of reagents for the production of diagnostics, as well as for the design of vaccine preparations.

Epidemiology. Hepatitis A is a common infectious disease in childhood. The incidence can be sporadic or in the form of epidemic outbreaks.

In the overall structure of hepatitis A incidence, children account for more than 60%. Children aged 3-7 years are most often affected. Children of the 1st year of life practically do not get sick due to transplacental immunity received from the mother.

Hepatitis A is a typical anthroponotic infection. Sources of infection are only people with obvious or erased forms of the disease, as well as virus carriers - healthy or convalescents. The main role in the active maintenance of the epidemic process is played by patients, especially with atypical forms. Often their disease remains unrecognized, they lead an active lifestyle, attend organized children's groups and become hidden and often powerful sources of infection.

In patients, the virus is contained in the blood, feces and urine. The virus appears in feces long before the first clinical symptoms, but its highest concentration occurs in the pre-icteric period. In the first days of the jaundice period, the virus can be detected in the blood and feces of no more than 10-15% of patients, and after the 4-5th day from the appearance of jaundice - only in isolated cases.

Hepatitis A is a typical intestinal infection. The virus is transmitted mainly through household contact, through hands contaminated with feces, as well as with food and drinking water. Airborne transmission has not been confirmed. The role of flies as a transmission factor has been exaggerated. Parenteral transmission of infection occurs only when the patient's blood containing the virus enters the recipient's bloodstream. This is theoretically possible, but in practice it is, apparently, extremely rare due to the instability of the virus in the blood. All researchers exclude transplacental transmission of the virus from mother to fetus.

Susceptibility to the virus is extremely high. Antibodies to the hepatitis A virus are found in 70-80% and even 100% of adults.

The incidence of hepatitis A has seasonal increases and periodicity. The highest incidence is recorded in the autumn-winter period (September - January), the lowest in the summer (July - August). Epidemic outbreaks are usually observed in child care institutions.

After hepatitis A, persistent lifelong immunity is formed.

Pathogenesis. In hepatitis A, a direct cytopathic effect of the virus on the liver parenchyma is allowed. Taking this into account, the pathogenesis of the disease can be presented as follows. The virus with saliva, food masses or water penetrates the stomach, and then into the small intestine, where, apparently, it is absorbed into the portal bloodstream and, through a related receptor, penetrates hepatocytes and interacts with biological macromolecules taking part in detoxification processes. The consequence of this interaction is the release of free radicals, which act as initiators of lipid peroxidation processes in cell membranes. Increased peroxidation processes lead to changes in the structural organization of lipid components of membranes due to the formation of hydroperoxide groups, which causes the appearance of “holes” in the hydrophobic barrier of biological membranes and, consequently, increases their permeability. The central link in the pathogenesis of hepatitis A appears - cytolysis syndrome. Biologically active substances move along a concentration gradient. In the blood serum, the activity of hepatocellular enzymes with cytoplasmic, mitochondrial, lysosomal and other localization increases, which indirectly indicates a decrease in their content in intracellular structures, and, consequently, a reduced bioenergetic regime of chemical transformations. All types of metabolism are disrupted (protein, fat, carbohydrate, pigment, etc.), resulting in a deficiency of energy-rich compounds and the bioenergetic potential of hepatocytes decreases. The ability to synthesize albumin, blood clotting factors, various vitamins is impaired, the use of glucose, amino acids for protein synthesis, complex protein complexes, and biologically active compounds is impaired; the processes of transamination and deamination of amino acids slow down, difficulties arise in the excretion of conjugated bilirubin, esterification of cholesterol and glucuronidation of many other compounds, which indicates a sharp disruption of the detoxifying function of the liver.

In the convalescence phase, protective factors and reparative processes are strengthened with complete fixation of the virus and complete restoration of the functional state of the liver. Most children recover within 1.5 to 3 months from the onset of the disease. For only some (3-5%) the initial protective factors may be insufficient; Relatively long-term (from 3 to 6-8 months or more) replicative activity of the virus in hepatocytes is maintained with disruption of their structure and function. In such cases, the course of the disease becomes protracted with a complex mechanism of structural and functional changes. However, even in these children, the defense mechanisms ultimately prevail - viral activity is blocked and recovery occurs. A chronic process does not develop as a result of hepatitis A.

Pathomorphology. The morphology of hepatitis A was studied based on data from intravital liver puncture biopsies. Changes are noted in all its tissue components: parenchyma, connective stroma, reticuloedothelium, biliary tract. The degree of organ damage can vary from mildly expressed dystrophic and necrotic changes in the epithelial tissue of the lobule in mild forms to more widespread focal necrosis of the liver parenchyma in moderate and severe forms. There is no widespread necrosis of the liver parenchyma, and especially massive necrosis of the liver with hepatitis A.

Clinical manifestations. In the typical course of the disease, a cyclicity is clearly expressed with a successive change of 5 periods: incubation, initial or prodromal (pre-icteric), peak (icteric), post-icteric and the period of convalescence.

Incubation period with hepatitis A it lasts from 10 to 45 days, usually 15-30 days. During this period, there are no clinical manifestations of the disease, but viral antigen and high activity of liver cell enzymes (AlAT, AST, F-1-FA, etc.) can already be detected in the blood.

Initial (prodromal) period. The disease in most children begins acutely, with a rise in body temperature to 38-39°C and the appearance of symptoms of intoxication: malaise, weakness, headaches, loss of appetite, nausea and vomiting. Pain occurs in the right hypochondrium, in the epigastrium, or without a specific localization.

Children become capricious, irritable, lose interest in games and studies, and have trouble sleeping. Transient dyspeptic disorders often occur: flatulence, constipation, and less commonly, diarrhea.

After 1-2, less often after 3 days from the onset of the disease, the body temperature normalizes and the symptoms of intoxication weaken somewhat, but general weakness, anorexia, and nausea remain.

The most important objective symptoms in this period of the disease are enlargement of the liver, its sensitivity and pain on palpation.

In isolated cases, the spleen is palpable. By the end of the pre-icteric period, partial discoloration of feces (clay color) is observed.

In some children, the clinical manifestations of the initial period are mild or absent altogether; the disease begins immediately with a change in the color of urine and feces (see Fig. 73, 74 on the color insert). This onset of hepatitis usually occurs in mild and mild forms of the disease.

The duration of the prodromal (pre-icteric) period for hepatitis A is 3-8 days, on average 6±2 days, rarely it extends to 9-12 days or shortens to 1-2 days.

The height of the period (icteric period). The transition to the 3rd period usually occurs with a clear improvement in the general condition and a decrease in complaints. With the appearance of jaundice, the general condition in half of the patients can be regarded as satisfactory, in the other half - as moderate for another 2-3 days of the icteric period. First, yellowness of the sclera appears, and then of the skin of the face, torso, hard and soft palate, and later of the extremities. Jaundice grows quickly, within 1-2 days; often the patient turns yellow as if “overnight.”

Jaundice in hepatitis A can be mild, moderate or intense and lasts 7-14, usually 9-13 days; the icteric staining of the skin folds, ears and especially the sclera in the form of marginal icterus lasts the longest.

At the height of jaundice, the liver is maximally enlarged, its edge is compacted, rounded, and painful on palpation. The edge of the spleen is often palpated.

Changes in other organs with hepatitis A are mild. One can note only moderate bradycardia, a slight decrease in blood pressure, weakening of heart sounds, unclearness of the first tone or a slight systolic murmur at the apex, a slight accent of the second tone on the pulmonary artery; There are short-term extrasystoles.

After reaching the maximum level (usually on the 7-10th day from the onset of the disease), jaundice begins to decrease. This is accompanied by the complete disappearance of intoxication symptoms, improved appetite, and a significant increase in diuresis (polyuria). Bile pigments disappear in the urine and urobilin bodies appear, and the feces become colored. With a cyclical course of the disease, the decline in clinical manifestations takes 7-10 days. After this the 4th begins, post-icteric period with a relatively slow decline in the liver. Children feel quite healthy, but in addition to an enlarged liver and, in rare cases, the spleen, their liver function tests remain pathologically altered.

5th, recovery period, or period of convalescence, in most children it is accompanied by normalization of liver size, restoration of its functions and a completely satisfactory condition. In some cases, children complain of rapid fatigue during physical activity and abdominal pain; sometimes there remains a slight enlargement of the liver, symptoms of dysproteinemia, episodic or constant slight increase in the activity of hepatic cellular enzymes. These symptoms are observed in isolation or in various combinations. The convalescence period takes about 2-3 months.

Classification. Hepatitis A is classified by type, severity and course.

Typical include all cases with the appearance of icteric staining of the skin and visible mucous membranes. Based on severity, they are classified into mild, moderate and severe forms. Atypical cases (anicteric, erased, subclinical hepatitis) are not divided by severity, since they are always regarded as mild hepatitis.

The severity of the clinical form of the disease is determined in the initial period, but not before the maximum of clinical symptoms of viral hepatitis; At the same time, manifestations of the initial (pre-icteric) period are also taken into account.

When assessing severity, the severity of general intoxication, jaundice, as well as the results of biochemical studies are taken into account.

Light form. It occurs in half of the patients and is manifested by a short-term moderate increase in body temperature or low-grade fever, mild signs of intoxication, minor subjective complaints during the height of the disease, and moderate enlargement of the liver.

In the blood serum, the content of total bilirubin does not exceed 85 µmol/l (with a norm of up to 17 µmol/l), and free bilirubin - 25 µmol/l (with a norm of 15 µmol/l), the value of the prothrombin index is at the normal limit, the thymol test is moderately increased, the activity of hepatocellular enzymes exceeds the norm by 5-10 times. The course of the disease is cyclical and benign. The duration of the icteric period is about 7-10 days. The size of the liver returns to normal on the 25-35th day. In 5% of children the disease takes a protracted course.

Moderate form. It occurs in 30% of patients and manifests itself with moderately severe symptoms of intoxication. The severity of jaundice ranges from moderate to significant. The liver is painful, its edge is dense, protrudes from under the costal arch by 2-5 cm. The spleen is often enlarged. The amount of urine is noticeably reduced. In the blood serum, the level of total bilirubin ranges from 85 to 200 µmol/l, including unconjugated (indirect) - up to 50 µmol/l. The prothrombin index is consistently reduced (up to 60-70%). The activity of hepatocellular enzymes exceeds the norm by 10-15 times.

The course of the disease is smooth. Symptoms of intoxication persist until the 10-14th day of illness, jaundice - 2-3 weeks, on average 14±5 days. Liver function is completely restored on the 40-60th day of illness. A protracted course is observed in only 3% of children.

Severe form hepatitis A is rare, occurring in no more than 1-3% of patients. In this form, the phenomena of general intoxication and jaundice are clearly expressed. The symptoms of the initial (prodromal) period differ little from those in the moderate form of the disease (vomiting, lethargy, anorexia). However, with the appearance of jaundice, the symptoms of intoxication not only do not weaken, but may even intensify. Apathy, lethargy, anorexia, dizziness, repeated vomiting, bradycardia, nosebleeds, hemorrhagic rashes, and a significant decrease in diuresis are noted. The liver is sharply enlarged, its palpation is painful, the spleen is enlarged. The bilirubin content in the blood serum is more than 170-200 µmol/l, while unconjugated (indirect) bilirubin is more than 50 µmol/l, the prothrombin index is reduced to 50-60%, the activity of hepatocellular enzymes is increased 15-30 times.

Anicteric form. Throughout the entire disease, icterus of the skin and sclera is not observed during systematic monitoring of the patient. The remaining symptoms in the anicteric form correspond to those in the icteric form. A short-term increase in body temperature, loss of appetite, lethargy, weakness, nausea and even vomiting are possible, lasting no more than 3-5 days. The leading symptom of the anicteric form is acute enlargement of the liver with its hardening and pain on palpation. There may be an enlarged spleen, dark urine and somewhat discolored feces. Increased activity of ALT, AST, F-1-FA and other liver enzymes is always detected in the blood serum; the thymol test and the content of β-lipoproteins were increased. There is often a short-term increase in conjugated (direct) bilirubin by 1.5-2 times the norm.

The anicteric form occurs in approximately 20% of patients with verified hepatitis A.

At subclinical (inapparent) form There are completely no clinical manifestations. The diagnosis is established only by biochemical examination of children who are in contact with patients with viral hepatitis. The most significant for the diagnosis of such forms is an increase in enzyme activity (AlAT, AST, F-1-FA, etc.), less often - a positive thymol test. The diagnosis is reliably confirmed by the detection of IgM antibodies to HAV in the blood serum. There is reason to believe that in the focus of hepatitis A infection, most children carry inapparent forms, which, while remaining undetected, support the epidemic process.

At cholestatic form Symptoms of obstructive jaundice come to the fore in the clinical picture. There is reason to believe that this form of the disease does not have clinical independence. Its development is based on bile retention at the level of the intrahepatic bile ducts. According to statistics, cholestasis syndrome with hepatitis A occurs rarely - in no more than 2% of patients and, as a rule, in girls in the prepubertal and pubertal periods.

The leading clinical symptom of hepatitis A with cholestatic syndrome is severe and prolonged (30-40 days or more) congestive jaundice and itching of the skin. Often the jaundice has a greenish or saffron tint, but sometimes it may be completely absent, then itching of the skin predominates. Symptoms of intoxication are not expressed, the liver is slightly enlarged, the urine is dark, the feces are discolored. In blood serum, the bilirubin content is usually high, exclusively due to the direct fraction. The activity of hepatocellular enzymes is within normal limits or slightly increased. There is an increased level of total cholesterol, β-lipoproteins, and alkaline phosphatase. The course of hepatitis A with cholestatic syndrome, although long-term, is always favorable. Chronic hepatitis does not develop.

Flow. Hepatitis A can be acute and protracted, smooth without exacerbation, with exacerbations, as well as with complications from the biliary tract and the addition of intercurrent diseases.

Acute course observed in 95% of children with verified hepatitis A. In the acute course, there are cases with particularly rapid disappearance of clinical symptoms, when by the end of the 2-3rd week of the disease a complete clinical recovery occurs and the functional state of the liver is normalized. In children, the total duration of the disease, although it fits within the time frame of acute hepatitis (2-3 months), but within 6-8 weeks after the disappearance of jaundice, certain complaints may remain (appetite disturbance, discomfort in the liver, rarely - enlarged spleen , incomplete normalization of liver function, etc.). These cases can be considered as prolonged convalescence. The further course of the disease in these children is also benign. The formation of chronic hepatitis is not observed.

Protracted current accompanied by clinical, biochemical and morphological signs of active hepatitis lasting from 3 to 6 months or more. The initial manifestations of the disease in a prolonged course are practically no different from those in acute hepatitis. Violation of cyclicity is detected only in the post-icteric period. At the same time, the liver and sometimes the spleen remain enlarged for a long time. In the blood serum, the activity of hepatocellular enzymes does not show any tendency towards normalization. However, prolonged hepatitis A always ends in recovery.

The course is aggravated. Exacerbation is understood as an increase in clinical signs of hepatitis and deterioration in liver function tests against the background of a persistent pathological process in the liver. Exacerbation should be distinguished from relapses - re-occurrence (after a period of absence of visible manifestations of the disease) of the main symptom complex in the form of an enlarged liver, spleen, the appearance of jaundice, a possible increase in body temperature, etc. Relapses can also occur in the form of an anicteric variant. Both exacerbations and relapses are always preceded by an increase in the activity of hepatocellular enzymes.

In all children with a “relapse” of hepatitis A, the addition of another hepatitis - B, C, etc. is usually determined. The main reason for the exacerbation is the activation of the virus in a child with a functional deficiency of the T-immune system of the hyposuppressor type, which results in incomplete elimination of infected hepatocytes and repeated breakthrough of the virus into free circulation with subsequent damage to new hepatocytes.

Course with damage to the bile ducts. With hepatitis A, damage to the biliary tract is usually manifested by dyskinetic phenomena of the hypertensive type. They occur in any form of hepatitis A, but are more pronounced in the moderate form, especially in patients with cholestatic syndrome. Clinically, damage to the biliary tract can manifest itself with all the symptoms characteristic of the cholestatic form of the disease, but often occurs without clear symptoms and is diagnosed based on the results of a laboratory test. In most children, dyskinetic disorders of the biliary tract resolve without any treatment, as the symptoms of hepatitis A disappear. The total duration of the disease in most cases falls within the framework of acute hepatitis.

Course with the addition of intercurrent infections. Intercurrent diseases usually do not have a significant impact on the severity of clinical manifestations, functional disorders, as well as the course, short-term and long-term outcomes of hepatitis A. In some patients, when an intercurrent infection occurs, a slight enlargement of the liver, an increase in the activity of hepatic-cellular enzymes, and the thymol test are observed.

Exodus. As a result of hepatitis A, recovery with complete restoration of the liver structure is possible; recovery from anatomical defects (residual fibrosis) or the formation of various complications from the biliary tract and gastroduodenal zone.

Recovery with complete restoration of liver structure and function - the most common outcome of hepatitis A.

Residual fibrosis or recovery with anatomical defect (post-hepatitis hepatomegaly)- long-term or lifelong enlargement of the liver in the complete absence of clinical symptoms and changes in laboratory test results. The morphological basis of hepatomegaly is residual liver fibrosis in the complete absence of degenerative changes in hepatocytes.

Biliary tract damage it is more correct to interpret it not as an outcome, but as a complication of hepatitis A as a result of activation of microbial flora.

Clinically, damage to the biliary tract is manifested by various complaints: pain in the right hypochondrium, nausea, vomiting. As a rule, complaints in children appear 2-3 months after hepatitis A. In most patients, combined gastroduodenal and hepatobiliary pathology is determined, often with an abnormal development of the gallbladder.

Diagnostics hepatitis A is based on clinical, epidemiological and laboratory data. Clinical signs can be considered reference, epidemiological - suggestive, but the results of laboratory methods are crucial at all stages of the disease.

Laboratory indicators are divided into specific and nonspecific. Specific are based on the detection of HAV RNA in the blood by PCR and specific anti-HAV IgM antibodies by ELISA. Determination of IgG class antibodies has diagnostic value only when the titer increases in the dynamics of the disease. In addition, testing for anti-HAV IgG may be important for assessing the immunostructure of the population, i.e. for broad epidemiological generalizations.

Non-specific methods play a decisive role in establishing the fact of liver damage, assessing the severity, course and prognosis of the disease. Among the numerous laboratory biochemical tests, the most effective are the determination of the activity of hepatic cellular enzymes (AlAT, AST, F-1 - FA, etc.), indicators of pigment metabolism and protein-synthesizing function of the liver.

Treatment Patients with hepatitis A are best treated at home. Restrictions in motor activity should depend on the severity of symptoms of intoxication, the patient’s well-being and the severity of the disease. With erased, anicteric and in most cases with mild forms, the regime can be semi-bed from the first days of the icteric period. For moderate and especially severe forms, bed rest is prescribed during the entire period of intoxication - usually the first 3-5 days of the icteric period. As intoxication disappears, children are transferred to semi-bed rest. The criteria for expanding the regimen are improvement of well-being and appetite, reduction of jaundice.

Children are exempt from physical education for 3-6 months, and sports for 6-12 months. An increase in physical activity should be individualized and fully consistent with the course of the pathological process, functional recovery of the liver, taking into account residual effects, age and premorbid background of the child.

Patients need a complete, high-calorie and, if possible, physiological diet with a ratio of proteins, fats and carbohydrates of 1:1:4-5.

Proteins are introduced into the diet in the form of cottage cheese, milk, kefir, lean meats (beef, veal, chicken), lean fish (cod, pike perch, navaga, pike), omelettes, and low-fat cheeses. Fats are given in the form of butter and vegetable oil (corn, olive, sunflower). Carbohydrates are found in rice, semolina, oatmeal, buckwheat porridge, bread, pasta, sugar, and potatoes.

A child’s daily diet must include a sufficient amount of raw and boiled vegetables (carrots, cabbage, cucumbers, tomatoes, zucchini), herbs, fruits, and juices.

Exclude from the diet are extractives, refractory fats (lard, margarine, shortening), fatty sausages, pork, ham, canned meat, fatty poultry, fatty fish, spicy sauces, marinades, legumes, sharp cheeses, garlic, radishes, radishes, chocolate. , cakes, pastries, sweets, hot seasonings (mustard, pepper, mayonnaise), smoked meats, mushrooms, nuts, horseradish, etc.

Honey, jam, marshmallows, savory cookies, dried apricots, prunes, raisins, mousses, jellies, jelly, salads, vinaigrettes, soaked herring, jellied fish are allowed.

Patients with hepatitis A usually do not need medications, but it is still advisable to prescribe drugs with a choleretic effect. In the acute period of the disease, it is better to use drugs with predominantly cholelytic action (magnesium sulfate, flamin, berberine, etc.), and in the period of convalescence - cholesecreting agents (allochol, cholenzyme, etc.). In case of hepatitis A, it is pathogenetically justified to prescribe a complex of B vitamins (B 1, B 3, B 6), as well as vitamins C and PP orally in the standard dose. During the period of convalescence and especially with prolonged hepatitis A, you can prescribe phosphogliv 1 capsule 3 times a day with meals for 2-4 weeks, Liv52 K (children from 2 years old) 10-20 drops 2 times a day 30 minutes before food, Liv52 in tablets (children from 6 years old) 1-2 tablets 2-3 times a day 30 minutes before meals for 2-4 weeks, or take a course of treatment with Legalon 1/2 -1 tablet ( 1/2 -1 spoon) 3 times a day for 2-3 weeks. Pathogenetically justified is the administration of a complex of vitamins A (B1, B3, B6), as well as vitamins C and PP orally in the standard dose.

In the cholestatic form, relief of cholestasis is achieved by prescribing the drug ursodeoxycholic acid (ursosan) at a dose of 10-15 mg/(kg day) for the entire period of clinical and laboratory manifestations plus 2-3 weeks to eliminate subclinical cholestasis.

In the period of early and late convalescence, especially with a protracted course of hepatitis A and significant severity of residual effects, taking into account the possibility of the formation of pathology of the biliary tract and gastroduodenal zone, as a drug that can effectively influence these adverse effects and complications, the prescription of ursosan for a longer course is pathogenetically justified ( 3-6 months). For the same purpose, during the period of convalescence, you can prescribe phosphogliv or essentiale, 1 capsule 3 times a day with meals for 2-4 weeks, or carry out a course of treatment with legalon. Infusion therapy is prescribed for severe forms and for individual patients with moderate forms of the disease. A 1.5% solution of reamberin is injected intravenously at a rate of 10 ml/kg body weight reopolyglucin, hemodez, 10% glucose solution.

After the end of the acute period, all children are subject to mandatory dispensary observation. It is better to carry out clinical examination in a special room organized at the hospital. If it is impossible to organize such an office, medical examination should be carried out by a local pediatrician in a children's clinic.

The first examination and examination of the child is carried out on the 45-60th day from the onset of the disease, repeated - after 3 months. In the absence of residual effects, convalescents are removed from the register. If there are clinical or biochemical signs of incompleteness of the process, clinical observation is carried out until complete recovery.

Regardless of the form and severity of the disease, enterosorption therapy (enterosgel, enterodesis) must be prescribed for the entire duration of treatment. Enterosorbents bind toxic substances and metabolites in the gastrointestinal tract and interrupt their recycling processes. All this, of course, leads to a reduction in the metabolic and toxic load on liver cells and accelerates the repair processes of liver tissue.

Clinical examination of convalescents living in rural areas is carried out at the infectious diseases departments of central regional children's hospitals and in children's clinics.

Prevention. Measures to prevent the spread of hepatitis A infection involve influencing the source of infection, the routes of its transmission and the susceptibility of the body.

Neutralization of the source of infection is ensured by early diagnosis of all cases of the disease and timely isolation of patients.

In all contact children, the skin and sclera are examined daily, and attention is paid to the size of the liver, the color of urine and feces.

In the focus of hepatitis A, to identify atypical forms, it is recommended to conduct a laboratory examination: determine the activity of ALT and anti-HAV IgM in the blood serum (blood is taken from a finger). These studies should be repeated every 10-15 days until the outbreak ends. This makes it possible to identify almost all infected people and quickly localize the source of infection.

To suppress the transmission of infection, strict control over public catering, the quality of drinking water, and public and personal hygiene is crucial.

When a patient with hepatitis A is identified, current and final disinfection is carried out at the source of infection.

To increase the immunity of the population to hepatitis A, the introduction of normal immunoglobulin is of particular importance. Timely use of immunoglobulin in the focus of hepatitis A helps stop the outbreak. To achieve a preventive effect, it is necessary to use immunoglobulin with a high content of antibodies to the hepatitis A virus - 1:10,000 or higher.

There is planned or pre-season immunoprophylaxis for hepatitis A and immunoprophylaxis for epidemic indications. Planned pre-season (August-September) prevention is carried out in regions with a high incidence of hepatitis A - more than 12 per 1000 children.

In areas with low incidence, immunoprophylaxis is carried out only for epidemic indications.

Titrated immunoglobulin is administered to children from 1 to 14 years of age, as well as to pregnant women who have had contact with hepatitis A patients in the family or child care facility within 7-10 days after the first case of the disease. Children aged 1 to 10 years are administered 1 ml of 10% immunoglobulin, over 10 years and adults - 1.5 ml.

In children's institutions, with incomplete separation of groups, immunoglobulin is administered to all children who have not had hepatitis A. In case of complete separation (school classes), the issue of administering immunoglobulin to children of the entire institution should be decided individually.

Effective prevention of hepatitis A is possible only through universal vaccination. The following vaccines are registered and approved for use in Russia:

Vaccine against hepatitis A, purified concentrated adsorbed inactivated liquid GEP-A-in-VAK, Russia;

Vaccine against hepatitis A with polyoxidonium GEP-A-in-VAK-POL, Russia;

Havrix 1440 from Glaxo Smith Klein, England;

Havrix 720 from Glaxo Smith Klein, England;

Avaxim from Sanofi Pasteur, France;

Waqta 25 units (and 50 units). Merck Sharp and Dome, USA;

Twinrix is ​​a vaccine against hepatitis A and B from Glaxo Smith Klein, England.

It is recommended to start vaccination against hepatitis A at 12 months of age. The vaccine is administered intramuscularly twice according to the schedule: 0 and 6 months - 12 months. The hepatitis A vaccine can be administered simultaneously with the hepatitis B vaccine if the timing of vaccinations in different parts of the body coincides. A protective level of immunity is formed in 95% of vaccinated people.

Reactions to hepatitis A vaccine are relatively rare. Some children may experience pain, hyperemia and swelling at the injection site; general reactions rarely occur: fever, chills, allergic rash. In hypersensitized children, anaphylactic reactions are theoretically possible, which can be easily eliminated with generally accepted desensitizing drugs.

HEPATITIS E

Hepatitis E (B 17.2) is a widespread disease in many developing countries with hot climates.

Etiology. The causative agent of the disease is a virus-like spherical particle with a diameter of 27 nm. It has no antigenic similarity to HAV and is not considered a variant or subtype. The virus is found in the feces of individuals with a clinical picture of acute hepatitis, classified as “neither A, nor B” hepatitis, as well as in monkeys experimentally infected with this type of virus. Viral particles react with the sera of the same sick and experimental animals in the convalescent stage.

Epidemiology. The source of infection is a sick person who suffers a typical or atypical (anicteric, erased) form of the disease. Chronic carriage of the virus has not been described. The infection is transmitted through the fecal-oral route, mainly through contaminated water; transmission through food and household contact is possible. Seasonality coincides with the period of increased incidence of hepatitis A.

In the CIS countries, the largest number of diseases is recorded in Central Asia, mainly in the autumn-winter period.

The majority of cases are between 15 and 30 years of age, and only about 30% are children. It is possible that the relatively low incidence in children is explained by the predominance of erased and subclinical forms that are not diagnosed. Susceptibility to hepatitis E has not been precisely established; there is reason to consider it high. The lack of widespread spread of hepatitis E in our country is probably due to the predominance of the water mechanism of infection and the high infectious dose. There is an opinion that hepatitis E is a natural focal disease.

Pathogenesis. The mechanisms leading to liver damage in hepatitis E are not precisely known. One can only assume that they do not differ from those with hepatitis A. In an experiment on monkeys, it was shown that by the end of the month from the moment of their infection with a suspension of fecal extract from patients with hepatitis E, a picture of acute hepatitis was found in the liver of animals, accompanied by an increase in the level of transaminases; at the same time, virus-like particles appear in the feces, and after that, on the 8-15th day, antibodies to the virus are detected in the blood serum.

The morphological picture of the liver with hepatitis E is generally the same as with hepatitis A.

Clinical manifestations. The incubation period ranges from 10 to 50 days. The disease begins with the appearance of lethargy, weakness, loss of appetite; Possible nausea and repeated vomiting, abdominal pain. An increase in body temperature, unlike that with hepatitis A, is uncommon. The pre-icteric period lasts from 1 to 10 days. Usually the urine darkens on the 3-4th day from the onset of the disease. Jaundice appears and gradually increases over 2-3 days. With the appearance of jaundice, the symptoms of intoxication do not disappear (with hepatitis A they disappear). Patients still complain of weakness, poor appetite, pain in the epigastric region and right hypochondrium. Sometimes there is itching of the skin and low-grade body temperature. The liver is enlarged in all patients, the edge of the spleen is palpable only in isolated cases.

At the height of the disease in the blood serum, the content of total bilirubin is increased by 2-10 times, mainly due to the direct fraction, the activity of hepatocellular enzymes is increased by 5-10 times, the thymol test, unlike that in hepatitis A, remains within normal limits or increased by no more than 1.5-2 times, i.e., as with hepatitis B. A decrease in the mercuric acid test seems unusual, since it, as a rule, does not decrease in mild and moderate forms of hepatitis A and B.

The icteric period lasts 2-3 weeks. The size of the liver, the activity of enzymes and the protein-synthesizing function of the liver are gradually normalized.

Flow. The disease is usually acute. After 2-3 months from the onset of the disease, most children experience complete restoration of the structure and function of the liver. The protracted course is clinically no different from that of hepatitis A. In adults, especially often in pregnant women, malignant forms with a fatal outcome have been described. In children, such forms apparently do not occur. The formation of chronic hepatitis has not been described.

Diagnostics. The diagnosis of hepatitis E is currently established based on the detection in the blood serum of antibodies to the hepatitis E virus of the IgM class in ELISA and viral RNA in PCR.

Treatment. Hepatitis E is treated in the same way as other viral hepatitis.

Prevention. When a case of hepatitis E appears, an emergency notification is sent to the SES. Patients are isolated for up to 30 days from the onset of the disease. In children's institutions, after isolating the patient, final disinfection is carried out, and the group is quarantined for 45 days. Contact children are subject to regular medical observation until the end of quarantine; those who have not had hepatitis E can be given immunoglobulin. However, the effectiveness of this measure requires further study. Obviously, it is effective only if commercial batches of immunoglobulin contain antibodies to the hepatitis E virus.

HEPATITIS B

Hepatitis B (B 16) is an acute or chronic liver disease caused by a DNA virus. Transmission of infection occurs parenterally. Hepatitis B occurs in various clinical and morphological variants: from “healthy” carriage to malignant forms, chronic hepatitis, liver cirrhosis and hepatocellular carcinoma.

According to ICD-10 there are:

B16.0 - acute hepatitis B with delta agent (co-infection) and hepatic coma;

B16.1 - acute hepatitis B with delta agent (co-infection) without hepatic coma;

B16.2 - acute hepatitis B without delta agent with hepatic coma;

B16.9 - acute hepatitis B without delta agent and without hepatic coma.

Etiology. The causative agent of the disease is a DNA-containing virus from the hepadnavirus family (from the Greek hepar - liver and English DNA - DNA).

Hepatitis B viruses (HBV), or Dane particles, are spherical formations with a diameter of 42 nm, consisting of an electron-dense core (nucleocapsid) with a diameter of 27 nm and an outer shell 7-8 nm thick. In the center of the nucleocapsid is the viral genome, represented by double-stranded DNA.

The virus contains 3 antigens that are of utmost importance for the laboratory diagnosis of the disease: HBcAg - a nuclear, core antigen of a protein nature; HBeAg - transformed HBcAg (infectiousness antigen); HBsAg is a surface (Australian) antigen that forms the outer shell of the Dane particle.

VGV is very resistant to high and low temperatures. At a temperature of 100° C, the virus dies in 2-10 minutes; at room temperature it lasts 3-6 months, in the refrigerator - 6-12 months, frozen - up to 20 years; in dried plasma - 25 years. The virus is extremely resistant to chemical factors: a 1-2% chloramine solution kills the virus after 2 hours, a 1.5% formalin solution kills it after 7 days. The virus is resistant to lyophilization, exposure to ether, ultraviolet rays, acids, etc. When autoclaving (120°C), the activity of the virus is completely suppressed only after 5 minutes, and when exposed to dry heat (160°C) - after 2 hours.

Epidemiology. Hepatitis B is an anthroponotic infection: the only source of infection is humans.

The main reservoir of the virus is “healthy” virus carriers; Patients with acute and chronic forms of the disease are less contagious.

Currently, according to incomplete data, there are about 300 million virus carriers in the world, including more than 5 million living in our country.

The prevalence of “healthy” carriage varies in different territories. There are territories with low (less than 1%) carriage of the virus in the population: the USA, Canada, Australia, Central and Northern Europe; medium (6-8%): Japan, Mediterranean countries, South-West Africa; high (20-50%): Tropical Africa, the islands of Oceania, Southeast Asia, Taiwan.

In the CIS countries, the number of virus carriers also varies widely. A large number of them are registered in Central Asia, Kazakhstan, Eastern Siberia, Moldova - about 10-15%; in Moscow, the Baltic states, Nizhny Novgorod - 1-2%.

In all people infected with HBV, regardless of the nature of the process (“healthy” carriers, patients with acute, chronic hepatitis), HBsAg - the main marker of infection - is found in almost all biological environments of the body: in blood, semen, saliva, urine, bile, tear fluid , breast milk, vaginal secretions, cerebrospinal fluid, synovial fluid. However, only blood, semen and saliva, where the concentration of the virus is significantly higher than the threshold, pose a real epidemic danger. The most dangerous is the blood of the patient and the virus carrier.

HBV is transmitted exclusively by the parenteral route: through the transfusion of infected blood or its preparations (plasma, red blood cells, albumin, protein, cryoprecipitate, antithrombin, etc.), the use of poorly sterilized syringes, needles, cutting instruments, as well as during scarification, tattoos, and surgical interventions. , dental treatment, endoscopic examination, duodenal intubation and other manipulations during which the integrity of the skin and mucous membranes is disrupted.

Natural transmission routes of HBV include transmission of the virus through sexual contact and vertical transmission from mother to child. Sexual tract transmission should be considered parenteral, since infection occurs through inoculation of the virus through microtraumas of the skin and mucous membranes of the genitals.

Vertical transmission HBV is carried out mainly in regions with a high prevalence of virus carriage. A mother can infect her baby if she is a carrier of the virus or has hepatitis B, especially in the last trimester of pregnancy. Infection of the fetus can occur transplacentally, during childbirth or immediately after birth. Transplacental transmission occurs relatively rarely - no more than 10% of cases. The risk of infection increases sharply when HBeAg is detected in the mother's blood, especially in high concentrations (up to 95%).

Infection of children from mothers who are carriers of HBV occurs mainly during childbirth as a result of contamination from blood-containing amniotic fluid through macerated skin and mucous membranes of the child. In rare cases, a child becomes infected immediately after birth through close contact with an infected mother. Transmission of infection in these cases occurs through microtrauma, i.e., parenterally, and possibly during breastfeeding. Infection of the child most likely occurs not through milk, but as a result of the contact of the mother’s blood (from cracked nipples) on the macerated mucous membranes of the child’s oral cavity.

When using all routes of transmission of infection, the risk of perinatal infection of a child from a mother with hepatitis B or a virus carrier can reach 40%. Most often, infection through close household contact occurs in the family, as well as in orphanages, boarding schools and other closed institutions. The spread of infection is facilitated by overcrowding, low sanitary and hygienic living standards, and poor communication culture. In close relatives (father, mother, brothers, sisters) of children with chronic hepatitis B, during the first study, markers of hepatitis B are detected in 40% of cases, and after 3-5 years - in 80%.

The population's susceptibility to the hepatitis B virus appears to be universal, but the outcome of a person's encounter with the virus usually results in asymptomatic infection. The frequency of atypical forms cannot be accurately counted, but judging by the identification of seropositive individuals, then for each case of manifest hepatitis B there are tens and even hundreds of subclinical forms.

As a result of hepatitis B, persistent lifelong immunity is formed. Recurrence of the disease is unlikely.

Pathogenesis. In the mechanism of development of the pathological process in hepatitis B, several leading links can be distinguished:

Introduction of a pathogen - infection;

Fixation on the hepatocyte and penetration into the cell;

Reproduction and release of the virus onto the surface of the hepatocyte, as well as into the blood;

Inclusion of immune reactions aimed at eliminating the pathogen;

Damage to extrahepatic organs and systems;

Formation of immunity, release from the pathogen, recovery.

Since HBV infection always occurs through the parenteral route, the moment of infection is almost equivalent to the penetration of the virus into the blood.

The tropism of HBV to liver tissue is predetermined by the presence in HBsAg of a special receptor - a polypeptide with a molecular weight of 31,000 D (P31), which has albumin-binding activity. A similar zone of polyalbumin is also found on the membrane of human and chimpanzee liver hepatocytes, which essentially determines the tropism of HBV to the liver.

When a hepatocyte is infected, the process can develop along a replicative and integrative path. In the 1st case, there is a picture of acute or chronic hepatitis, and in the 2nd case - virus carriage.

The reasons that determine the interaction of viral DNA and hepatocytes have not been precisely established. Most likely, the type of response is genetically determined.

The final result of the replicative interaction is the assembly of cow antigen structures (in the nucleus) and the assembly of the complete virus (in the cytoplasm), followed by the presentation of the complete virus or its antigens on the membrane or in the membrane structure of hepatocytes.

In the future, the liver is necessarily included in the immunopathological process. The damage to hepatocytes is due to the fact that as a result of the expression of viral antigens in the membrane of hepatocytes and the release of viral antigens into free circulation, a chain of successive cellular and humoral immune reactions is activated, aimed at removing the virus from the body. This process is carried out in full accordance with the general patterns of the immune response during viral infections. To eliminate the pathogen, cellular cytotoxic reactions are activated, mediated by various classes of effector cells: K cells, T cells, natural killer cells, macrophages. During these reactions, the destruction of infected hepatocytes occurs, which is accompanied by the release of viral antigens (HBcAg, HBeAg, HBsAg), which trigger the antibody genesis system, as a result of which specific antibodies accumulate in the blood, primarily to the cow - anti-HBc and e-antigen - anti- NWe. Consequently, the process of liberating the liver cell from the virus occurs through its death as a result of cellular cytolysis reactions.

At the same time, specific antibodies accumulating in the blood bind virus antigens, forming immune complexes that are phagocytosed by macrophages and excreted by the kidneys. In this case, various immune complex lesions may occur in the form of glomerulonephritis, arteritis, arthralgia, skin rashes, etc. During these processes, the body of most patients is cleared of the pathogen and complete recovery occurs.

In accordance with the concept of the pathogenesis of hepatitis B, the entire variety of clinical variants of the course of the disease is explained by the peculiarities of the interaction of the pathogen virus and the cooperation of immunocompetent cells, in other words, by the strength of the immune response to the presence of viral antigens.

In conditions of an adequate immune response to virus antigens, acute hepatitis develops with a cyclical course and complete recovery. With a decrease in the immune response, immune-mediated cytolysis is insignificantly expressed, so effective elimination of infected liver cells does not occur. This leads to mild clinical manifestations with long-term persistence of the virus and, possibly, to the development of chronic hepatitis. On the contrary, in the case of a genetically determined strong immune response and massive infection (blood transfusion), extensive areas of liver cell damage occur, which clinically correspond to severe and malignant forms of the disease.

Pathomorphology. Based on the characteristics of morphological changes, there are 3 variants of acute hepatitis B: cyclic, massive liver necrosis, cholestatic pericholangiolytic hepatitis.

At cyclic form of hepatitis B dystrophic, inflammatory and proliferative changes are more pronounced in the center of the lobules, and with hepatitis A they are localized along the periphery of the lobules, spreading to the center. These differences are explained by different routes of virus penetration into the liver parenchyma. The hepatitis A virus enters the liver through the portal vein and spreads to the center of the lobules, while HBV enters through the hepatic artery and the branching capillaries that uniformly supply all lobules down to their center.

The greatest morphological changes in the parenchyma are observed at the height of clinical manifestations, which usually coincides with the 1st decade of the disease. During the 2nd and especially the 3rd decade, regeneration processes intensify. By this period, necrobiotic changes have almost completely disappeared and processes of cellular infiltration begin to predominate, with a slow subsequent restoration of the structure of the hepatocellular plates. However, complete restoration of the structure and function of the liver parenchyma occurs only after 3-6 months from the onset of the disease and not in all children.

At massive liver necrosis morphological changes are maximally expressed. Depending on the severity and prevalence, liver necrosis can be massive or submassive. With massive necrosis, almost the entire epithelium dies or a small border of cells remains along the periphery of the lobules. With submassive necrosis, the majority of hepatocytes are destroyed, mainly in the center of the lobules. Massive necrosis represents the peak of the changes that are characteristic of viral hepatitis B.

Cholestatic (pericholangiolytic) hepatitis - a special form of the disease in which the greatest morphological changes are found in the intrahepatic bile ducts; a picture of cholangiolitis and pericholangiolitis is observed. This is a relatively rare form in children and occurs almost exclusively in hepatitis B. In the cholestatic form, there is cholestasis with dilation of the bile capillaries with stasis of bile in them, with proliferation of cholangioles and cellular infiltrates around them. Liver cells are slightly affected in this form of hepatitis.

Clinical manifestations. In typical cases of the disease, 4 periods are distinguished: incubation, initial (pre-icteric), peak period (icteric) and convalescence.

Incubation period lasts 60-180 days, more often 2-4 months, in rare cases it is shortened to 30-45 days or extended to 225 days. The duration of the incubation period depends on the infecting dose and the age of the children. With massive infection (blood or plasma transfusions), the incubation period is 1.5-2 months, and with parenteral manipulations (subcutaneous and intramuscular injections) and especially with domestic infection, the incubation period is 4-6 months. In children of the first months of life, the incubation period is usually shorter (92.8±1.6 days) than in children of older age groups (117.8±2.6 days; p<0,05).

Clinical manifestations of the disease in this period are completely absent, but, as with hepatitis A, at the end of incubation, high activity of hepatocellular enzymes is constantly detected in the blood and markers of an active infection are detected: HBsAg, HBeAg, anti-HBc IgM.

Initial (pre-icteric) period. The disease often begins gradually (65%). An increase in body temperature is not always observed (40%) and usually not on the 1st day of illness. The patient experiences lethargy, weakness, increased fatigue, and decreased appetite. Often these symptoms are so mild that they are not noticed, and the disease begins with darkening of the urine and the appearance of discolored feces. In rare cases, the initial symptoms are pronounced: nausea, repeated vomiting, dizziness, drowsiness. Dyspeptic disorders often occur: loss of appetite up to anorexia, aversion to food, nausea, vomiting, flatulence, constipation, and less often diarrhea. Older children complain of dull pain in the abdomen. When examined during this period, general asthenia, anorexia, enlargement, hardening and tenderness of the liver, as well as darkening of urine and often discoloration of feces can be detected.

Muscular and joint pain, often found in adult patients, is very rare in children in the pre-icteric period.

Rarely in the pre-icteric period, skin rashes, flatulence, and stool disorders are observed.

Catarrhal phenomena are not at all characteristic of hepatitis B.

The most objective symptoms in the initial period are enlargement, hardening and tenderness of the liver.

Changes in peripheral blood in the initial period of hepatitis B are not typical. Only slight leukocytosis and a tendency to lymphocytosis can be noted; ESR is always within normal limits.

In all patients, already in the pre-icteric period, high activity of ALT, AST and other hepatocellular enzymes is detected in the blood serum; at the end of this period, the content of conjugated bilirubin in the blood increases, but the indicators of sediment samples, as a rule, do not change, and there is no dysproteinemia. HBsAg, HBeAg, and anti-HBc IgM circulate in the blood in high concentrations, and viral DNA is often detected.

The duration of the initial (pre-icteric) period can range from several hours to 2-3 weeks; on average 5 days.

Jaundice period (the height of the disease). 1-2 days before the onset of jaundice, all patients experience darkening of urine and most patients experience discoloration of stool. Unlike hepatitis A, hepatitis B, passing into the third, icteric period, in most cases is not accompanied by an improvement in general condition. On the contrary, in many children the symptoms of intoxication intensify.

Jaundice increases gradually, usually over 5-7 days, sometimes 2 weeks or longer. Yellowness can vary from faint canary or lemon yellow to greenish yellow or ocher yellow, saffron. The severity and shade of jaundice are associated with the severity of the disease and the development of cholestasis syndrome.

Having reached its peak severity, jaundice with hepatitis B usually stabilizes within 5-10 days, and only after that does it begin to decrease.

A rare symptom of hepatitis B in children is a skin rash. The rash is located symmetrically on the limbs, buttocks and torso, and is maculopapular, red, and up to 2 mm in diameter. When squeezed, the rash takes on an ocher color; after a few days, slight peeling appears in the center of the papules. These rashes should be interpreted as Gianotti-Crosti syndrome, described by Italian authors for hepatitis B.

In severe forms, at the height of the disease, manifestations of hemorrhagic syndrome may be observed: pinpoint or more significant hemorrhages in the skin.

In parallel with the increase in jaundice in hepatitis B, the liver enlarges, its edge thickens, and pain on palpation is noted.

An enlarged spleen is observed less frequently than an enlarged liver. The spleen is often enlarged in more severe cases and with a long course of the disease. Enlargement of the spleen is observed throughout the acute period with slow reverse dynamics. Often the spleen is palpated after the disappearance of other symptoms (with the exception of liver enlargement), which, as a rule, indicates a protracted or chronic course of the disease.

In the peripheral blood at the height of jaundice, the number of red blood cells tends to decrease. In severe forms, anemia develops. In rare cases, more severe changes in the bone marrow are possible, up to the development of panmyelophthisis.

During the icteric period, the number of leukocytes is normal or reduced. In the blood count, at the height of toxicosis, a tendency towards neutrophilia is revealed, and during the recovery period - towards lymphocytosis. ESR is usually within normal limits. Low ESR (1-2 mm/h) with severe intoxication in a patient with severe hepatitis B is an unfavorable sign.

Convalescent, recovery period. The total duration of the icteric period with hepatitis B ranges from 7-10 days to 1.5-2 months. With the disappearance of jaundice, children no longer complain, they are active, their appetite is restored, but in half of the patients hepatomegaly remains, and in 2/3 there is slight hyperfermentemia. Sometimes the thymol test is elevated and dysproteinemia, etc., are observed.

In the convalescent period, HBsAg and especially HBeAg are usually no longer detected in the blood serum, but anti-HBe, anti-HBc IgG and often anti-HBs are always detected.

Classification. Hepatitis B, like hepatitis A, is classified by type, severity and course.

The criteria for determining the type and distinguishing clinical forms are the same as for hepatitis A. However, along with mild, moderate and severe forms, there is also a malignant form, which occurs almost exclusively in hepatitis B and hepatitis delta, and the course, in addition to acute and protracted, can be chronic.

Clinical and laboratory criteria for anicteric, erased, subclinical, as well as mild, moderate and severe forms of hepatitis B are not fundamentally different from those for hepatitis A.

Malignant form occurs almost exclusively in children 1 year of age.

Clinical manifestations of malignant forms depend on the prevalence of liver necrosis, the rate of their development, and the stage of the pathological process. There is an initial period of the disease or a period of precursors, a period of development of massive liver necrosis, which usually corresponds to a state of precoma and rapidly progressive decompensation of liver functions, clinically manifested by coma of I and II degrees.

The disease often begins acutely: body temperature rises to 38-39°C, lethargy, adynamia, and sometimes drowsiness appear, followed by attacks of anxiety or motor agitation. Dyspeptic disorders are expressed: nausea, regurgitation, vomiting (often repeated), sometimes diarrhea.

With the appearance of jaundice, the most constant symptoms are: psychomotor agitation, repeated vomiting with blood, tachycardia, rapid toxic breathing, bloating, severe hemorrhagic syndrome, increased body temperature and decreased diuresis. Vomiting "coffee grounds", sleep inversion, convulsive syndrome, hyperthermia, tachycardia, rapid toxic breathing, hepatic breath, liver shrinkage are observed only in malignant forms of the disease. Following these symptoms or simultaneously with them, a blackout occurs with the clinical symptoms of hepatic coma (see Fig. 75, 76 on the color plate).

Among the biochemical indicators, the most informative are the so-called bilirubin-protein dissociation (with a high content of bilirubin in the blood serum, the level of protein complexes decreases sharply) and bilirubin-enzyme dissociation (with a high content of bilirubin, there is a drop in the activity of hepatocellular enzymes, as well as a drop in the level of blood clotting factors ).

Flow. According to the classification, the course of hepatitis B can be acute, protracted and chronic.

An acute course is observed in 90% of children. The acute phase of the disease ends by the 25-30th day from the onset of the disease, and in 30% of children a complete recovery can already be stated. The rest have a slight enlargement of the liver (no more than 2 cm below the edge of the costal arch) in combination with hyperfermentemia, exceeding normal values ​​by no more than 2-4 times.

A protracted course is observed in approximately 10% of children. In these cases, hepatomegaly and hyperfermentemia persist for 4-6 months. Chronic course (chronic hepatitis B) as a result of manifest (icteric) forms does not occur in children. Chronic hepatitis almost always develops as a primary chronic process.

The most common outcome of acute manifest hepatitis B is recovery with complete restoration of liver function. As with hepatitis A, it is also possible to recover with an anatomical defect (liver fibrosis) or with the formation of various complications from the biliary tract and gastrointestinal tract. These outcomes of hepatitis B are almost no different from those of hepatitis A.

In practical work, in all cases of chronic hepatitis B, which appears to form as a result of an acute infection, it is necessary to exclude hepatitis A and hepatitis delta against the background of latent HBV infection.

Diagnostics. In hepatitis B, the supporting diagnostic signs include pronounced hepatolienal syndrome and gradually progressive jaundice. Only with hepatitis B is there an increase in jaundice of the skin and visible mucous membranes for 7 days or more. Following this, you can usually observe the so-called plateau of jaundice, when it remains intense for another 1-2 weeks. The size of the liver undergoes similar dynamics, and less commonly, the size of the spleen.

From epidemiological data, indications of previous operations, blood transfusions, injections and other manipulations associated with violation of the integrity of the skin or mucous membranes 3-6 months before the disease, as well as close contact with a patient with chronic hepatitis B or a virus carrier, are important.

Among biochemical tests, only low levels of the thymol test are typical for hepatitis B.

Specific laboratory research methods based on the determination of hepatitis B virus antigens (HBsAg, HBeAg) and antibodies to them (antiHBc, IgM and IgG, anti-HBe) in blood serum are of decisive importance in diagnosis.

Differential diagnosis. Acute hepatitis B must be differentiated primarily from other viral hepatitis: A, C, E, etc. The main differential diagnostic signs of these hepatitis are given in Table. 6.

Presented in table. 6 data should be considered indicative, since on their basis it is possible to carry out differential diagnosis only with group analysis, but a final etiological diagnosis is possible only by determining specific markers in the blood serum.

Objective difficulties may also arise in the differential diagnosis of hepatitis B with other diseases, the list of which is determined by the age of the children, the form, severity and phase of the pathological process.

Treatment. The general principles of treatment for patients with acute hepatitis B are the same as for hepatitis A. However, it must be taken into account that hepatitis B, unlike hepatitis A, often occurs in severe and malignant forms. In addition, the disease can result in the formation of chronic hepatitis and even cirrhosis, so specific recommendations for the treatment of patients with hepatitis B should be more detailed than for the treatment of patients with hepatitis A.

There is currently no fundamental objection to children with mild to moderate forms of hepatitis B being treated at home. The results of such treatment are no worse, and in some respects even better, than with hospital treatment.

Specific recommendations regarding physical activity, therapeutic nutrition and criteria for their expansion are in principle the same as for hepatitis A; one should only take into account that the terms of all restrictions for hepatitis B are usually somewhat extended in full accordance with the course of the disease.

In general, we can say that if the infection progresses smoothly, all restrictions on movement and nutrition should be lifted after 6 months from the onset of the disease, and sports can be allowed after 12 months.

Table 6. Differential diagnostic signs of viral hepatitis in children

Drug therapy is carried out according to the same principles as for hepatitis A. In addition to this basic therapy, for moderate and severe forms of hepatitis B, interferon can be used intramuscularly at a dose of 1 million units 1-2 times a day for 15 days. If necessary, treatment can be continued at 1 million units 2 times a week until recovery. The use of cycloferon is indicated both parenterally and in tablet form at a rate of 10-15 mg/kg body weight.

In severe forms of the disease, for the purpose of detoxification, hemodez, rheopolyglucin, 10% glucose solution up to 500-800 ml/day are administered intravenously, and corticosteroid hormones are prescribed at the rate of 2-3 mg/(kg. day) for prednisolone during the first 3- 4 days (until clinical improvement) followed by rapid dose reduction (course no more than 7-10 days). In children of the 1st year of life, moderate forms of the disease are also indications for prescribing corticosteroid hormones.

If a malignant form is suspected or there is a threat of its development, the following is prescribed:

Glucocorticosteroid hormones up to 10-15 mg/(kg day) for prednisolone intravenously in equal doses every 3-4 hours without an overnight break;

Plasma, albumin, hemodez, rheopolyglucin, 10% glucose solution at the rate of 100-200 ml/(kg day) depending on age and diuresis;

Proteolysis inhibitors: trasylol, gordox, contrical in an age-related dose;

Lasix 2-3 mg/kg and mannitol 0.5-1 g/kg intravenously in a slow stream to enhance diuresis;

According to indications (disseminated intravascular coagulation syndrome), heparin 100-300 units/kg intravenously.

To prevent the absorption of endotoxin from gram-negative bacteria and toxic metabolites from the intestine resulting from the vital activity of microbial flora, enterosorption therapy (enterosgel, enterodesis, etc.) is prescribed. Enterosorption prevents the reabsorption of toxic substances in the lumen and interrupts their circulation in the body. It should be taken into account that the level of toxic substances passing through the intestinal barrier depends on the condition of the mucous membrane, therefore, the result of enterosorption also depends on the effect of the enterosorbent on the mucous membrane, therefore it is preferable to use enterosorbent Enterosgel, which has exceptional hydrophobic and selective properties and clearly promotes the regeneration of the mucosa intestinal lining. Gastric lavage, high cleansing enemas, and broad-spectrum antibiotics (gentamicin, polymyxin, ceporin) are also prescribed.

If the complex of therapeutic measures is ineffective, repeated sessions of plasmapheresis should be performed. Repeated hemosorption sessions and replacement blood transfusions are less effective.

It is advisable to include hyperbaric oxygenation in the complex of pathogenetic agents (1-2 sessions per day: compression 1.6-1.8 atm, exposure 30-45 minutes).

The success of treatment of malignant forms mainly depends on the timeliness of the above therapy. If deep hepatic coma develops, therapy is ineffective.

Just as with hepatitis A, with cholestatic forms of hepatitis B and in the period of convalescence with a prolonged course and pronounced residual effects, ursodeoxycholic acid (ursosan) is indicated. The drug is prescribed in usual doses (10-15 mg/kg/day). The duration of treatment is determined in accordance with the clinical and laboratory manifestations of the disease.

Discharge from hospital and follow-up. Typically, children are discharged on the 30-40th day from the onset of the disease, and moderate hepatomegaly and hyperfermentemia are allowed. Upon discharge from the hospital, the patient is given a leaflet outlining the recommended regimen and diet. If the child continues to have HBsAg at the time of discharge, information about this is entered into the outpatient observation card and reported to the SES at the place of residence.

Subsequent monitoring of convalescence is best carried out in a consultation and dispensary office, organized at an infectious diseases hospital. If it is impossible to organize such an office, dispensary observation of survivors of hepatitis B should be carried out by the attending physician. The first clinical examination is carried out no later than a month after discharge from the hospital, subsequent ones - after 3; 4; 6 months In the absence of subjective complaints and objective deviations from the norm, convalescents are removed from the dispensary register, otherwise they continue to be examined once a month until complete recovery.

Children with significant or increasing clinical and laboratory changes, as well as with exacerbation of the disease or suspected development of chronic hepatitis, are readmitted to the hospital to clarify the diagnosis and continue treatment. Children without signs of chronic hepatitis, but with persistent HBs antigenemia, are also subject to repeated hospitalization. Subsequently, such children undergo clinical and laboratory examination as indicated.

Patients are removed from the dispensary register when, during 2 regular examinations, normalization of clinical and biochemical data is established, and HBsAg is not detected in the blood.

Clinical observation is indicated for children who have received transfusions of blood products (plasma, fibrinogen, leukocyte mass, red blood cell mass, etc.). This is especially true for children 1 year of age. The follow-up period is 6 months after the last blood transfusion. During this period, the child is examined monthly and, if hepatitis is suspected, is hospitalized in an infectious diseases hospital. In doubtful cases, blood serum is examined for the activity of hepatocellular enzymes and HBsAg.

Prevention consists primarily of a thorough examination of all categories of donors with a mandatory blood test for HBsAg at each blood donation using highly sensitive methods for its identification (ELISA, radioimmunoassay - RIA), as well as determination of ALT activity.

Persons who have had viral hepatitis in the past, patients with chronic liver diseases, as well as persons who have received transfusions of blood and its components within the last 6 months are not allowed to donate. It is prohibited to use blood and its components from donors who have not been tested for HBsAg for transfusion.

To improve the safety of blood products, it is recommended that donors be tested not only for HBsAg, but also for anti-HBc. Removal from donation of persons with anti-HBc, considered as hidden carriers of HBsAg, practically eliminates the possibility of post-transfusion hepatitis B.

To prevent infection of newborns, all pregnant women are tested twice for HBsAg using highly sensitive methods: when registering a pregnant woman (8 weeks of pregnancy) and when registering for maternity leave (32 weeks). If HBsAg is detected, the question of pregnancy should be decided strictly individually. It is important to consider that the risk of intrauterine infection of the fetus is especially high if a woman has HBeAg and is negligible if it is absent, even if HBsAg is detected in high concentrations. The risk of infection of the child during delivery by cesarean section is also significantly reduced.

Interruption of infection transmission routes is achieved by the use of disposable syringes, needles, scarifiers, probes, catheters, blood transfusion systems, other medical instruments and equipment used during manipulations associated with violation of the integrity of the skin and mucous membranes.

All medical instruments and reusable equipment must undergo thorough pre-sterilization cleaning and sterilization after each use.

For the prevention of post-transfusion hepatitis, strict adherence to the indications for hemotherapy is of great importance. Transfusion of canned blood and its components (erythrocyte mass, plasma, antithrombin, etc.) is done only for health reasons and noted in the medical history. It is necessary to switch, if possible, to transfusion of blood substitutes or, as a last resort, transfusion of its components (albumin, specially washed red blood cells, protein, plasma). This is due to the fact that pasteurization of plasma (60°C, 10 hours), although it does not guarantee complete inactivation of HBV, still reduces the risk of infection; The risk of infection during transfusion of albumin and protein is even lower, and the risk of infection during transfusion of immunoglobulins is negligible.

In departments at high risk of hepatitis B infection (hemodialysis centers, resuscitation units, intensive care wards, burn centers, oncology hospitals, hematology departments, etc.), hepatitis B prevention is ensured through strict adherence to anti-epidemic measures (use of one disposable instrumentation, assignment of each device to a fixed group of patients, thorough cleaning of blood from complex medical devices, maximum separation of patients, limitation of parenteral interventions, etc.). In all these cases, HBsAg identification is carried out using highly sensitive methods and at least once a month.

To prevent occupational infections, all employees must work with blood wearing rubber gloves and strictly observe personal hygiene rules.

To prevent the spread of infection in families of patients with hepatitis and HBV carriers, routine disinfection is carried out, personal hygiene items (toothbrushes, towels, bed linen, washcloths, combs, shaving accessories, etc.) are strictly individualized. All family members are explained under what conditions infection can occur. Family members of patients with chronic hepatitis B and carriers of HBsAg are subject to medical supervision.

Specific prevention of hepatitis B is achieved through passive and active immunization of children at high risk of infection.

For passive immunization, immunoglobulin with a high content of antibodies to HBsAg is used (titer in the passive hemagglutination reaction is 1:100,000 - 1:200,000). This immunoglobulin is obtained from the plasma of donors in whose blood anti-HBs is detected in high titer.

Born from mothers who are carriers of HBsAg or who have developed acute hepatitis B in the last months of pregnancy (immunoglobulin is administered immediately after birth, and then again after 1, 3 and 6 months);

After virus-containing material enters the body (blood or its components are transfused from a patient or a carrier of HBV, accidental cuts, injections with suspected contamination with virus-containing material); in these cases, immunoglobulin is administered in the first hours after the suspected infection and after 1 month;

If there is a long-term threat of infection - for children admitted to hemodialysis centers, patients with hemoblastosis, etc. (re-administered at various intervals - after 1-3 months or every 4-6 months); the effectiveness of passive immunization depends primarily on the timing of immunoglobulin administration; when administered immediately after infection, the preventive effect reaches 90%, within up to 2 days - 50-70%, and when administered after 5 days, immunoglobulin prophylaxis is practically ineffective.

With intramuscular injection of immunoglobulin, the peak concentration of anti-HBs in the blood is reached after 2-5 days. To obtain a faster protective effect, immunoglobulin can be administered intravenously.

The elimination period of immunoglobulin ranges from 2 to 6 months, but a reliable protective effect is ensured only in the 1st month after administration, therefore, to obtain a prolonged effect, repeated administration of immunoglobulin is necessary. In addition, the use of immunoglobulin is effective only at a low infectious dose of HBV. In case of massive infection (blood transfusion, plasma, etc.), immunoglobulin prophylaxis is ineffective.

Despite the shortcomings, the introduction of specific immunoglobulin should take its rightful place in the prevention of hepatitis B. According to the literature, timely specific immunoglobulin prophylaxis can prevent hepatitis B infection in 70-90% of vaccinated people.

For active prevention of hepatitis B, genetically engineered vaccines are used.

Several recombinant vaccines against hepatitis B have been created in our country (JSC NPK Combiotech Regevak B and other vaccines). In addition, several foreign drugs have been registered and approved for use (Engerix B; NV-VAX II, Euvax; Shanvak-B; Eberbiovak).

The following are subject to active immunization against hepatitis B:

Newborns from mothers with hepatitis or carriers of HBsAg, especially if they have HBeAg;

Newborns in areas where hepatitis B is endemic with HBsAg carriage rates greater than 5%;

Patients who often undergo various parenteral procedures (chronic renal failure, diabetes mellitus, blood diseases, proposed surgery using a heart-lung machine, etc.);

Persons in close contact with HBsAg carriers (in families, closed children's groups);

Medical personnel of hepatitis departments, hemodialysis centers, blood service departments, surgeons, dentists, pathologists;

Persons who have been accidentally injured by instruments contaminated with the blood of patients with hepatitis B or carriers of HBsAg.

Vaccination is carried out three times according to scheme 0; 1; 6 months Other schemes are also allowed: 0; 1; 3 months or 0; 1; 2; 12 months Revaccination is carried out every 5 years.

Only persons who do not have HBV markers detected in their blood (HBsAg, anti-HBc, anti-HBs) are subject to active immunization. If one of the markers of hepatitis B is present, vaccination is not carried out.

The effectiveness of vaccination is very high. Numerous studies show that when the vaccine is administered according to scheme 0; 1; After 6 months, 95% of individuals develop protective immunity, which provides reliable protection against HBV infection for 5 years or more.

There are no contraindications to vaccination against hepatitis B. The vaccine is safe and areactogenic.

Vaccination can reduce the incidence of hepatitis B by 10-30 times.

To prevent vertical transmission of HBV, the first phase of vaccines is administered immediately after birth (no later than 24 hours), then vaccinated after 1; 2 and 12 months For this purpose, combined passive-active immunization of newborns from mothers with hepatitis B or virus carriers can be used. Specific immunoglobulin is administered immediately after birth, and vaccination is carried out in the first 2 days, then at age 0; 1; 2 months with revaccination at 12 months. This passive-active immunization reduces the risk of infection of children from mothers with HBeAg from 90 to 5%.

Widespread implementation of vaccination against hepatitis B will reduce the incidence of not only acute but also chronic hepatitis B, as well as cirrhosis and primary liver cancer.

HEPATITIS DELTA

B16.0 - acute hepatitis B with delta agents (co-infection) and hepatic coma;

B16.1 - acute hepatitis B with delta agents (co-infection) without hepatic coma;

B17.0 - acute delta (super) - infection of the hepatitis B virus carrier.

Etiology. Hepatitis delta virus (HDV) is a spherical particle with a diameter of 35-37 nm, the outer shell of which is the HBV surface antigen (HBsAg). At the center of the particle is a specific antigen (AgD) containing small RNA (genome). For replication and expression, HDV requires the obligate HBV helper function, as a result of which it is one of the defective viruses with an incomplete genome. It has been established that delta antigen is located mainly in the nuclei of hepatocytes in the form of aggregates of individual particles 20-30 nm in size, localized in the chromatin zone and occasionally in the cytoplasm in association with ribosomes or in the hyaloplasm. The delta antigen is resistant to heat and acids, but is inactivated by alkalis and proteases. The experimental infection can be reproduced on chimpanzees.

Epidemiology. The source of the disease is patients with acute and especially chronic hepatitis delta, as well as healthy carriers of IOP and even carriers of antibodies to IOP.

IOP is transmitted exclusively by the parenteral route - through transfusion of virus-containing blood and its preparations, as well as through the use of needles, catheters, probes and other medical instruments contaminated with virus-containing blood. The risk of infection with IOP is especially high among regular recipients of donor blood or blood products (patients with hemophilia, hematological malignancies, and other chronic diseases), as well as among people serving hemodialysis centers, surgeons, and drug addicts.

Infection occurs through HBsAg-positive blood or its preparations containing antibodies to IOP. A donor of such blood usually has chronic hepatitis and delta antigen can always be detected in liver cells.

Transplacental transmission of IOP from mother to fetus is possible. However, more often newborns become infected during childbirth or immediately after birth as a result of contamination with maternal blood containing IOP through damaged skin and mucous membranes.

Persons who have not had hepatitis B, as well as carriers of HBV, are susceptible to IOP. The greatest susceptibility is observed in young children and in persons with chronic hepatitis B.

Pathogenesis. When infected with IOP, coinfection and superinfection can develop. Coinfection occurs in individuals who have not had viral hepatitis B and are not immune to HBV. Superinfection is possible when patients with chronic hepatitis B or carriers of HBV become infected. When coinfected, hepatitis B and hepatitis delta occur with corresponding serological responses to HBV and HDV. With superinfection, a clinical picture of acute hepatitis develops, accompanied by the appearance of antibodies to IOP with a simultaneous drop in the level of HBV markers in the blood and liver, which is explained by the influence of reproducing IOP on HBV. HDV superinfection usually manifests itself within a period of 3 weeks to 3 months after infection and, as a rule, ends in the formation of a joint chronic infection of HBV and HDV or the occurrence of chronic hepatitis delta against the background of ongoing carriage of HBV.

Pathomorphology. It is not possible to identify any specific morphological signs unique to hepatitis delta. Signs of a severe inflammatory process predominate.

Clinical manifestations. Depending on the mechanism of development, 4 forms of the disease are distinguished: mixed acute infection of HBV and HDV (co-infection); delta HDV superinfection; chronic concurrent hepatitis B and hepatitis delta; chronic hepatitis delta due to HBV carriage.

Coinfection. The incubation period ranges from 8 to 10 weeks. The disease manifests itself with the same clinical symptoms as acute hepatitis B, the initial period of the disease is often more defined: increased body temperature to 38-39 ° C, adynamia, decreased appetite, nausea, vomiting, abdominal pain, enlarged liver and spleen. In the blood serum, the content of total bilirubin is increased due to the direct fraction, the activity of hepatocellular enzymes is high, and dysproteinemia is noted.

With a favorable course, the duration of the disease is 1.5-3 months. Some children may develop protracted forms with clinically significant exacerbations, repeated increases in bilirubin levels and the activity of hepatocellular enzymes in the blood serum.

The formation of chronic hepatitis in the outcome of manifest clinical forms is not observed. In children in the first months of life, malignant hepatitis often occurs with a fatal outcome. The absence of chronicity of acute manifest forms of coinfection does not exclude the possibility of the formation of primary chronic hepatitis B and hepatitis delta, which occur latently, without an acute manifest phase.

IOP superinfection. When HDV infection is superimposed on chronic HBV infection, such as chronic hepatitis or as a healthy carrier, the incubation period is 3-4 weeks. In these cases, IOP infection is usually manifested by a clinical picture of acute hepatitis: increased body temperature to 38-39°C, malaise, general weakness, nausea, vomiting, abdominal pain. After 2-3 days, dark urine, discolored feces, icteric staining of the sclera and skin appear, and the liver and spleen become enlarged. At the same time, the content of total bilirubin in the blood serum increases 3-5 times, mainly due to the conjugated fraction, the activity of hepatic cellular enzymes increases 4-10 times, the thymol test indicators increase, the sublimate test and prothrombin index significantly decrease. The course of the disease is often severe, up to the occurrence of a malignant form with a fatal outcome in some patients. In other cases, chronic hepatitis delta is formed with high activity of the process.

Chronic active hepatitis B and hepatitis delta should be considered as a mixed chronic infection, since the pathological process is caused by actively occurring hepatitis B and hepatitis delta. In children, the disease manifests itself as severe symptoms of intoxication in the form of increased fatigue, emotional instability, decreased appetite, signs of dysfunction of the gastrointestinal tract (nausea, feeling of heaviness in the epigastric region, right hypochondrium, flatulence). Some patients have mild icterus of the skin, and all have enlarged liver and spleen. Multiple bruises on the extremities are constantly detected, nosebleeds are sometimes noted, telangiectasia, palmar erythema and other extrahepatic signs are common. In the blood serum of all patients, high activity of hepatocellular enzymes, a decrease in prothrombin, dysproteinemia, as well as HBsAg, HBeAg and markers of current hepatitis delta (HDV RNA and anti-HDV IgM) are detected. The course of the disease can be severe, with alternating short remissions and long-term exacerbations. After 5-6 years, the disease can already be interpreted as chronic active hepatitis delta with the formation of liver cirrhosis (see Fig. 77, 78, 79 on the color insert). These children have a pronounced hepatolienal syndrome with a sharp thickening of the liver, hemorrhagic manifestations, extrahepatic signs, high activity of hepatocellular enzymes, low levels of sublimate test, prothrombin index and the phenomenon of progressive dysproteinemia. Changes in the marker spectrum indicate continued HDV activity (anti-HDV IgM is detected) in the absence of HBV replicative activity (HBsAg and anti-HBe are detected).

Diagnosis hepatitis delta is established based on the detection of HDV RNA, HBV DNA, IgM and IgG antibodies in the blood by PCR method to HDV and HBV.

Based only on clinical data, HDV infection can be assumed if a patient with chronic hepatitis B or a so-called healthy carrier of HBsAg experiences a clinically significant exacerbation with symptoms of intoxication, jaundice, a sharp enlargement of the liver and increased activity of hepatocellular enzymes.

Treatment for hepatitis, the delta is the same as for hepatitis B, and is built taking into account the severity of clinical manifestations and the course of the disease. Since the course of hepatitis delta is often unpredictable, all patients are subject to mandatory hospitalization in the hepatitis department of an infectious diseases hospital.

Prevention. In the prevention of hepatitis delta, the leading role is played by the prevention of hepatitis B. It is necessary to carefully protect HBV carriers and patients with chronic hepatitis B from superinfection with HDV. Such superinfection can occur not only during the transfusion of infected blood products or during parenteral manipulations, but also during close household contact through microtrauma of the skin and mucous membranes.

HEPATITIS C

Etiology. Hepatitis C virus (HCV) belongs to the flavivirus family. It has a diameter of 22 to 60 nm and is found both in blood and in liver extracts from humans or experimentally infected chimpanzees. Unlike other hepatitis viruses, it is found in the blood serum of patients in extremely low concentrations, and the immune response in the form of specific antibodies is very weak and late. The virus is sensitive to chloroform and formalin; when heated to 60°C it is inactivated within 10 hours, and when boiled - within 2 minutes. Sterilization of blood products using ultraviolet rays is effective.

Epidemiology. In Western Europe and the USA, up to 95% of all cases of post-transfusion and parenteral hepatitis are caused by HCV. The disease occurs after transfusion of virus-containing blood, plasma, fibrinogen, antihemophilic factor and other blood products. Outbreaks of hepatitis C have been reported among patients with immunodeficiencies after intravenous infusions of immunoglobulin drugs. Hepatitis C is the leading acute hepatitis in hemodialysis centers, among patients in organ transplant departments, in oncology hospitals, plasmapheresis centers, etc.

HCV is transmitted exclusively by the parenteral route, mainly with blood products and during various invasive interventions, including through microtrauma during household contact. The possibility of perinatal transmission of infection from mother to fetus transplacentally, as well as during childbirth and immediately after birth when the child is contaminated with mother’s blood through damaged skin has been shown. Sexual transmission of HCV is quite likely.

Pathogenesis. In the mechanism of damage to liver cells in hepatitis C, the leading role is played by immune cytolysis, realized by T-cell cytotoxicity directed against infected hepatocytes. The possibility of direct cytopathic effects of the virus on liver cells is possible. In the pathogenesis of the formation of chronic forms of the disease, the weakened ability of blood mononuclear cells to produce γ-interferon, as well as a change in the ratio of immunoregulatory subpopulations of T-helpers and T-suppressors with a predominance of the latter and the associated insufficiently effective T-cell and humoral immune response to the action, are of decisive importance pathogen and infected hepatocytes. The increased ability of the HCV antigen to masquerade into immune complexes is also of certain importance, which brings this disease closer to the immune complex.

Pathomorphology. Morphological changes in the liver with hepatitis C do not have strict specificity. However, in acute hepatitis C, portal inflammation is less pronounced, focal necrosis is less common, and steatosis is significantly more noticeable compared to that in hepatitis A and hepatitis B.

With the formation of chronic hepatitis, there is a significant increase in the portal and periportal inflammatory reaction with the accumulation of mononuclear elements, and mild fibrosis with a tendency to septal proliferation is detected. Diffuse dystrophic changes ranging from mild to severe, including balloon degeneration and necrosis, are observed in hepatocytes.

A chronic process in the liver may fit into the morphological picture of persistent hepatitis, but in most cases it is active hepatitis with relatively rare bridging necrosis and moderate lymphoid infiltration.

Clinical manifestations. The incubation period averages 7-8 weeks, with fluctuations from several days (with massive infection) to 26 weeks. The disease begins gradually with asthenovegetative and dyspeptic manifestations: lethargy, malaise, nausea, and sometimes low-grade body temperature. Abdominal pain and sometimes vomiting are possible. After a few days, dark urine and discolored feces appear. In all patients, the liver is enlarged, and sometimes the spleen is enlarged. Jaundice appears rarely, only in 15-40% of patients. In the absence of jaundice, the leading symptoms are malaise, asthenia and enlarged liver. In the blood serum of all patients, the activity of ALT and AST is increased, in some cases the content of total bilirubin is increased due to the direct fraction, a decrease in prothrombin, dysproteinemia, etc. are possible. The indicators of functional liver tests fully correspond to the severity of liver damage and the stage of the pathological process.

Viral hepatitis C is classified in the same way as other viral hepatitis. There are typical and atypical variants of the disease.

Based on severity, they are divided into mild, moderate, severe and malignant, and according to their course - acute, protracted and chronic forms.

The characteristics of clinical forms and the criteria for their diagnosis are the same as for other hepatitis.

Flow. The acute course of hepatitis C occurs in 10-20% of cases, in other children the disease takes a chronic course. The transition to the chronic stage is manifested by persistent hyperfermentemia with a relatively satisfactory general condition, complete absence of complaints, slight enlargement and hardening of the liver. In the stage of established chronic hepatitis, patients may complain of increased fatigue, weakness, and dyspeptic symptoms. Upon examination, vascular changes can be detected (telangiectasia, palmar erythema), the liver is always enlarged, and often the spleen is enlarged. Despite the low severity of clinical symptoms, the pathological process in the liver morphologically in most cases corresponds to chronic active hepatitis, often with signs of developing cirrhosis.

Diagnostics. The diagnosis of hepatitis C is established when specific antibodies to the structural and non-structural proteins of the virus are detected in the blood serum by ELISA, as well as viral RNA by PCR.

Treatment. The general principles of treatment for patients with acute and chronic hepatitis C are the same as for other viral hepatitis. Prescribe bed rest, diet, and symptomatic medications. For malignant forms, corticosteroid hormones are used, and in patients with chronic hepatitis, recombinant interferon preparations (viferon, intron A, roferon A, etc.) are successfully used.

To relieve the toxic load on the liver, it is necessary to carry out enterosorption therapy (enterosgel, enterodesis). For long-term enterosorption, a selective enterosorbent with pronounced hydrophobic properties is recommended. In children with chronic viral liver damage (HBV and HCV), combination therapy using drugs with antiviral activity with a different mechanism of action is indicated: for chronic viral hepatitis B - lamivudine and cycloferon or viferon and cycloferon.

As a means of pathogenetic therapy for chronic hepatitis C, ursodeoxycholic acid (ursosan) is prescribed, which has a corrective effect on the main links of pathogenesis that predetermine the chronic course of the infection (anticholestatic, immunomodulatory, antifibrotic, antioxidant, antiapoptotic). The drug Ursosan is prescribed at a dose of 10-15 mg/kg. days both during treatment with interferons and as monotherapy with a course duration of 3-6 months to one year.

Prevention. The principles of preventing hepatitis C are the same as for hepatitis B. The use of disposable syringes, infusion systems, catheters, as well as compliance with the rules of sterilization of surgical, dental and other instruments lead to a significant reduction in the incidence of not only hepatitis B, but also hepatitis C.

Testing blood products for anti-HCV and transaminase activity and then excluding positive samples leads to a significant reduction in the incidence of hepatitis C among blood product recipients.

HEPATITIS G

Based on the composition of nucleotide and amino acid sequences, the G virus, together with HCV, forms a group of hepatitis-associated viruses within the flavivirus family (Flaviviridae). In this case, the HCV RNA is constructed according to a scheme characteristic of the entire flavivirus family: at the 5th end there is a zone encoding structural proteins, at the 3rd end there is a zone encoding non-structural proteins.

The RNA molecule contains one open reading frame; encodes the synthesis of a precursor polyprotein consisting of approximately 2900 amino acids. The virus has constant regions of the genome (used to create primers used in PCR), but is also characterized by significant variability, which is explained by the low reliability of the reading function of the viral RNA polymerase. The virus is believed to contain a core protein (nucleocapsid protein) and surface proteins (supercapsid proteins). Various variants of HCV nucleotide sequences in different isolates are regarded as different subtypes within a single genotype or as intermediate between genotypes and subtypes. There are several genotypes of GBV (GBV-C and GBV-prototype, etc.).

Epidemiology. CHG is found everywhere. The frequency of HCV RNA detection clearly correlates with blood transfusions and multiple parenteral interventions. HCV is very common among drug addicts who inject drugs intravenously, people receiving hemodialysis, blood donors, and also among patients with chronic hepatitis C.

Sexual and vertical transmission of infection cannot be excluded.

Pathogenesis. HCV RNA begins to be detected in blood serum 1 week after transfusion of infected blood components. More than 9 years of observation of individuals with persistent HCV infection showed both high (up to 10 7 /ml) and low (up to 10 2 /ml) RNA titers; titers may remain constant during the observation period or they fluctuate widely (up to 6 orders of magnitude), as well as periodic disappearance of HCV RNA in serum samples. HCV RNA is also found in liver tissue. During experimental infection (chimpanzees), liver damage, intralobular necrotic-inflammatory changes and inflammatory infiltration along the portal tracts are found, similar to those with hepatitis C.

Pathomorphology. Pathological changes in liver tissue with hepatitis G correspond to those with hepatitis C.

Clinical manifestations. The disease manifests itself in a wide range of liver lesions - from acute cyclic hepatitis and chronic forms to asymptomatic carriage.

In acute monoinfection, a slight increase in body temperature, asthenodyspeptic symptoms in the form of lethargy, nausea, abdominal pain, and vomiting may be observed. At the height of the disease, the liver enlarges, and less often, the spleen. In the blood serum, the activity of ALT and AST is always increased, and the level of bilirubin, as a rule, is within normal limits, HGG RNA is detected. The course of the disease can be acute, protracted and chronic. The clinical manifestations of these forms are practically indistinguishable from those of viral hepatitis C.

Diagnostics. Specific diagnosis of hepatitis G is based on detection of HCV RNA in blood serum using PCR. The primers used for PCR are specific to the 5NCR, NS3 and NS5a regions of the viral genome as the most conserved ones.

Another way to diagnose HCV infection is to test for the detection of antibodies to the surface protein E2 of HGV using ELISA.

Treatment. The principles of therapy for hepatitis G are the same as for hepatitis C.

Prevention. A set of the same measures is being carried out as to prevent other viral hepatitis with pyrexial infection.

At the International Symposium in Los Angeles in 1994, definitions of hepatitis of various etiological origins were given, in particular, a formulation of the concept of what viral hepatitis is.

Viral hepatitis is a set of diseases caused by viruses that damage the liver in the form of cytolytic, cholestatic and immunoinflammatory syndromes.

Based on etiology (named after the virus that caused them), 7 nosological units of hepatitis are distinguished: A, B. C. D. E. F. G.

• They belong to anthroponotic diseases.
• Routes of infection – fecal-oral, parenteral
• Pathogens are viruses that remain highly virulent in the environment.
• All viruses are hepatotropic.
• The same pathogenesis links: cytolysis, cholestasis and immunoinflammatory reaction.
• Symptoms are common to all types of viral hepatitis.
• Biochemical and pathological changes are similar due to the same effect on the liver
• Pathogenetic therapy is carried out according to the same rules.
• Laboratory diagnosis of viral hepatitis is based on the detection of specific viral antigens and antibodies to them in the patient’s biological material (blood, saliva, feces).

Nonspecific laboratory parameters are characteristic of all types of hepatitis: an increase in blood serum transaminases (ALT, AST), alkaline phosphatase, thymol test. They are one of the first to be examined, as they help to suspect hepatitis in inapparent forms.

Viral hepatitis A

In Russia, hepatitis A accounts for 70% of the structure of viral hepatitis. Children 3-14 years old, mainly those in organized groups (kindergartens, schools, boarding schools), are especially sensitive to the disease.

It belongs to the picornovirus family and contains only RNA. It differs from other enteroviruses in its increased resistance to environmental conditions. Retains its virulence at positive temperatures close to zero - for several months. When boiled, it is destroyed in 5 minutes, under ultraviolet radiation in a minute, in a dry-heat oven (180 degrees) in an hour. Vulnerable when exposed to bleach, chloramine, formaldehyde.

Epidemiology

Main epidemiological features: it spreads everywhere, is characterized by cyclicity, the greatest intensity is noted in the cold season (autumn, winter), small children, schoolchildren, and young people predominate among the sick. The degree of morbidity is directly dependent on the sanitary condition of the territories.

The route of transmission is fecal-oral. The source of infection is a sick person.

Patients with erased forms are especially contagious at the end of incubation and in the pre-icteric period, when there is a massive release of the virus along with feces. When jaundice appears, the virus content of feces decreases significantly. Routes of infection - water, food, contact and household.

Water transmission occurs when a water supply becomes infected with the feces of a sick person. Epidemics are common in regions with poor sanitation and hygiene conditions, inaccessibility of clean water and lack of medical care.

The food route is possible in the event of food contamination by sick employees of public catering establishments or food sellers.

The household contact route is implemented if there is a sick person in the family. The disease is facilitated by crowded living conditions (military barracks, prisons, orphanages). Epidemic outbreaks and epidemics are likely.

When a patient is identified, anti-epidemic measures are taken to quickly localize the outbreak and prevent the spread of infection.

Nonspecific prevention

• Drinking water safety.
• Anti-epidemic measures at water intake and water treatment stations.
• Early identification of patients, timely hospitalization, disinfection of disease foci.

Particular attention is paid to sick people performing work related to food products (catering workers, dairy workers, salespeople).

In the outbreak, to prevent the disease, contacts are given immunoglobulin containing antibodies to hepatitis A.

Specific prevention is carried out by vaccination. Vaccines are highly immunogenic and protection lasts for 6-10 years.

Recognition of virus A during the incubation period is carried out by finding the virus A antigen in the patient's feces. IgM antibodies are the first to be detected in the blood and saliva. The presence of specific IgM antibodies proves the presence of virus A in the body. This test is often practiced at the site of infection to recognize asymptomatic forms.
IgG antibodies are produced a month after the onset of the disease and circulate for a long time, which makes it possible to compare the immunity levels of the population.

Hepatitis B

The genome of virus B contains two DNA strands surrounded by a lipoprotein envelope. Due to its structural features, the virus is invulnerable to many disinfection methods. It persists in whole blood and its preparations for years. Virus disinfection is carried out by autoclaving for 45 minutes at T o + 125 C, in a dry-heat oven for 1 hour. Kills when exposed to phenol, hydrogen peroxide, chloramine, formaldehyde.

The significant virulence of the virus and its resistance under the influence of chemical and physical factors determines the massive expansion of hepatitis B in society. To reduce the infection of infants from virus-carrying mothers, early screening to detect carriage and special preventive measures are necessary. A scheme for emergency prevention of newborns born to mothers with the presence of HBeAg in the blood has been developed.

Epidemiology

The source of infection is patients or virus carriers. All age categories are susceptible to the disease.

Routes of transmission

• Hematogenous.
• Sexual.
• Peri, intranatally - from an infected mother to a child.
• Contact-household - when blood and other biological secretions of a patient enter through the skin, mucous membranes into the blood of a healthy person.

The implementation of the contact-household route is possible due to the high level of the virus in the blood, and its partial transfer into all other human biological fluids: saliva, sperm, and menstrual secretions, urine, sweat.

Causes of infection

• Violation of basic hygiene standards - the use of individual items (combs, brushes, scissors, powder, lipstick) by several people.
• Neglect of barrier contraception (condoms) during casual sexual intercourse.
• Failure to comply with the rules of asepsis and antisepsis during surgical interventions and various medical procedures.
• In hairdressing salons when performing procedures that damage the skin (tattoo, piercing, manicure, pedicure, ear piercing), when instruments are not properly disinfected.
• During blood transfusions.
• From mother to child transplacentally or during childbirth.
• Infection of medical personnel through contact with blood in violation of personal protective measures.
• Homosexual contacts with different partners.
• In injection drug addicts.

The epidemiological significance of specific prevention comes down to the creation of a high immune layer of residents. Children are vaccinated from the neonatal period. This is especially important, given that when newborns are infected, hepatitis B transforms into a chronic course with 100% probability. Chronic forms are dangerous due to rapid progression to cirrhosis and liver cancer. Most of the adult population has no protection against this disease.

At-risk groups

• Patients with blood and liver diseases.
• Children of all ages who were not vaccinated in infancy.
• Persons with multiple sexual relationships, including homosexual ones.
• Persons who have close household contact with the patient (family, closed institutions).
• Patients forced to resort to ongoing invasive medical procedures.
• Persons visiting areas affected by hepatitis B.

Emergency specific prevention is carried out using immunoglobulin containing antibodies against virus B. The circle of people subject to emergency prevention coincides with people at risk.

At different stages of the disease, markers are determined: antigens - HBsAg, HBeAg and antibodies - anti-HBc, anti-HBe, anti-HBs.

In the acute form, viral DNA, HBsAg, HbeAg, and hepatitis B virus IgM antibodies are present.

The appearance of IgG antibodies confirms the degree of immunity intensity.

Prolonged presence in the blood of HBsAg and HBeAg together with IgM antibodies is evidence of the disease becoming chronic.

When carrying the virus, the blood contains the HBsAg antigen. To detect antigens and antibodies, serological methods are used: passive hemagglutination reaction (RPH), enzyme-linked immunosorbent assay (ELISA), radioimmunoassay (RIA).

Hepatitis C

Virus C belongs to the flavivirus family, contains one strand of RNA, and has up to 6 serotypes. Tends to transform the antigenic structure. A large infectious dose is required for infection. 2% of Russian residents are infected with low-manifest forms. In 60% of those infected, the disease has a chronic course, and 20% of them develop cirrhosis of the liver.

Epidemiology

• Hematogenous route of transmission.
• From mother to child (in 4% of cases).
• Sexually.

The disease is characterized by an asymptomatic course, when a person, unaware of the disease, is unsafe for others. The patient is contagious during incubation and throughout the period of persistence of the virus in the blood.

Risk groups for hepatitis C infection

• Young people using injection drugs.
• Persons suffering from blood diseases, renal failure, tuberculosis, receiving multiple blood transfusions.
• Medical staff.
• Blood and plasma donors.

The diagnosis is based on the detection of antibodies to the C virus by RIA and ELISA methods. The detection of virus RNA eliminates the possibility of false positive results, since it is detected during replication in hepatocytes.

Hepatitis D

The hepatitis D virus is defective, small in size, and contains single-stranded RNA. The outer shell contains HBsAg. The D virus is not able to reproduce individually in hepatocytes, it needs support - virus B. The addition of virus D aggravates the pathological process. There is a rapid transition to a chronic form and transformation into cirrhosis and liver cancer. Mechanism of infection and ways distribution identical to hepatitis B: hematogenous, sexual, from a sick mother to a child. At the end illness is set tense immunity.

Protection against hepatitis D is carried out by the hepatitis B vaccine, since this virus alone is not capable of causing the disease.

A diagnostic criterion indicating the addition of virus D to hepatitis B is the presence of HBsAg, IgM, delta antigen. Throughout the course of the disease, IgM antibodies are present in the blood.

Hepatitis E

Caused by the E virus, the genome consists of single-stranded RNA, without a supercapsid. The route of transmission is fecal-oral. The source of infection is the patient from the end of the incubation period and after the end of the disease. Spread occurs by water through contaminated water sources, through consumption of seafood cultivated in contaminated water bodies. If hygiene standards are not observed and the sanitary condition is poor, epidemic outbreaks occur in the regions where the population lives. Distributed in hot tropical climates. The disease is characterized by a mild course, with minor liver damage, and ends with recovery. It is severe only in pregnant women and leads to miscarriages. Every fifth pregnant woman dies from hepatitis E.

Chronicization of the pathological process does not occur; persistent immunity remains after the disease.

The marker of the E virus is the RNA of the virus and IgM antibodies. Specific IgM antibodies are found in the second week after infection. Virus RNA is detected from the first days of illness using polymerase chain reaction (PCR). IgG antibodies to the hepatitis E virus appear after recovery, which proves the existence of a high level of immunity.

Hepatitis G

Caused by an RNA virus from the flavivirus class. Several genotypes have been identified. The route of transmission is parenteral. According to the duration of the course - acute and chronic forms. Markers are often detected, especially after kidney implantation, hemodialysis, and in drug addicts.

Hepatitis F

The properties and characteristics of the F virus are being studied.

The epidemiological prognosis for viral hepatitis is disappointing. Despite advances in hepatology, the creation of vaccines, and the introduction of new diagnostic and treatment methods, the incidence continues to increase worldwide. In terms of the number of cases, viral hepatitis is second only to influenza.