Hepatitis: all types, signs, transmission, chronic, how to treat, prevention. Preventive measures for viral hepatitis A

Hepatitis C is an inflammation of the liver of viral origin, the clinical manifestations of which in most cases are significantly delayed in time or so little expressed that the patient himself may not even notice that a “gentle” killer virus, as the hepatitis C virus (HCV) is commonly called, has settled in his body.

Once upon a time, and this lasted until the end of the 80s of the last century, doctors knew about the existence of a special form of hepatitis, which does not fit into the concept of “Botkin’s disease” or jaundice, but it was obvious that this was hepatitis that affected the liver no less than its own “ brothers" (A and B). The unfamiliar species was called non-A, non-B hepatitis, since its own markers were still unknown, and the proximity of pathogenesis factors was obvious. It was similar to hepatitis A in that it was transmitted not only parenterally, but also suggested other routes of transmission. The similarity with hepatitis B, called serum hepatitis, was that it could also be contracted by receiving someone else's blood.

Currently, everyone knows that, called neither A nor B hepatitis, is open and well studied. This is hepatitis C, which in its prevalence is not only not inferior to the notorious one, but also far exceeds it.

Similarities and differences

Botkin's disease was previously called any inflammatory liver disease associated with a certain pathogen. The understanding that Botkin's disease can represent an independent group of polyetiological pathological conditions, each of which has its own pathogen and main route of transmission, came later.

Now these diseases are called hepatitis, but a capital letter of the Latin alphabet is added to the name according to the sequence of discovery of the pathogen (A, B, C, D, E, G). Patients often translate everything into Russian and indicate hepatitis C or hepatitis D. However, the diseases classified in this group are very similar in the sense that the viruses they cause have hepatotropic properties and, when they enter the body, affect the hepatobiliary system , each in its own way disrupting her functional abilities.

Different types of hepatitis are unequally prone to chronicity of the process, which indicates different behavior viruses in the body.

Hepatitis C is considered the most interesting in this regard., which long time remained a mystery, but even now, being widely known, it leaves mystery and intrigue, since it does not make it possible to give an accurate forecast (it can only be guessed).

Inflammatory processes of the liver caused by various pathogens do not differ in relation to gender, therefore affects men equally, and women. There was no difference in the course of the disease, however, it should be noted that in women during pregnancy, hepatitis can be more severe. In addition, the penetration of the virus in recent months or the active course of the process can negatively affect the health of the newborn.

Since liver diseases of viral origin still have obvious similarities, then when considering hepatitis C, it is advisable to touch on other types of hepatitis, otherwise the reader will think that only the “hero” of our article should be afraid. But through sexual contact you can become infected with almost every type, although this ability is attributed more to hepatitis B and C, and therefore they are often classified as sexually transmitted diseases. In this regard, other pathological conditions of the liver of viral origin are usually kept silent, since their consequences are not as significant as the consequences of hepatitis B and C, which are recognized as the most dangerous.

In addition, there are hepatitis of non-viral origin (autoimmune, alcoholic, toxic), which should also be touched upon, since one way or another, they are all interconnected and significantly aggravate each other.

How is the virus transmitted?

Depending on how the virus could “cross” to a person and what kind of things it will begin to “do” in the body of the new “host,” different types of hepatitis are distinguished. Some are transmitted in everyday life (via dirty hands, products, toys, etc.) appear quickly and pass, basically, without any consequences. Others, called parenteral, having the potential for chronicity, often remain in the body for life, destroying the liver to cirrhosis, and in some cases to primary liver cancer (hepatocarcinoma).

Thus, According to the mechanism and routes of infection, hepatitis is divided into two groups:

• Having an oral-fecal transmission mechanism (A and E);
• Hepatitis, for which blood contact (hemopercutaneous), or, more simply, the path through the blood, is the main one (B, C, D, G - group of parenteral hepatitis).

In addition to the transfusion of infected blood or flagrant non-compliance with the rules of medical procedures associated with damage to the skin (use of insufficiently processed instruments, for example, for acupuncture), The spread of hepatitis C, B, D, G is common and in other cases:

1. Various fashionable procedures (tattoos, piercings, ear piercings) performed by a non-professional at home or in any other conditions that do not meet the requirements of the sanitary and epidemiological regime;
2. By using one needle for several people, this method is practiced by syringe addicts;
3. Transmission of the virus through sexual intercourse, which is most likely for hepatitis B, hepatitis C in such situations is transmitted much less frequently;
4. There are known cases of infection through the “vertical” route (from mother to fetus). Active form illnesses, acute infection in the last trimester or being a carrier of HIV significantly increases the risk of hepatitis.
5. Unfortunately, up to 40% of patients cannot remember the source that gave them the hepatitis B, C, D, G virus.

The hepatitis virus is not transmitted through breast milk, so women who are carriers of hepatitis B and C can safely feed their baby without fear of infecting him.

We can agree that the fecal-oral mechanism, water, contact and household, being so interconnected, cannot exclude the possibility of transmission of the virus through sexual contact, just like other types of hepatitis transmitted through blood, they have the opportunity to penetrate into another body during sex.

Signs of an unhealthy liver

After infection, the first clinical signs different forms diseases appear at different times. For example, the hepatitis A virus makes itself known in two weeks (up to 4), the hepatitis B (HBV) pathogen is somewhat delayed and appears in the interval from two months to six months. As for hepatitis C, it the pathogen (HCV) can reveal itself after 2 weeks, after 6 months, or can “lurk” for years, turning a healthy person into a carrier and source of infection of a rather serious disease.

The fact that something is wrong with the liver can be guessed by the clinical manifestations of hepatitis:

• Temperature. Hepatitis A usually begins with it and the symptoms of influenza infection (headache, pain in bones and muscles). The beginning of HBV activation in the body is accompanied by a low-grade fever, and with hepatitis C it may not rise at all;
• Jaundice varying degrees of severity. This symptom appears a few days after the onset of the disease, and if its intensity does not increase, the patient’s condition usually improves. This phenomenon is most characteristic of hepatitis A, which cannot be said about hepatitis C, as well as toxic and alcoholic hepatitis. Here, a more saturated color is not considered a sign of future recovery; rather, on the contrary: with a mild form of liver inflammation, jaundice may be completely absent;
• Rashes and itching more characteristic of cholestatic forms of inflammatory processes in the liver, they are caused by the accumulation of bile acids in tissues due to obstructive lesions of the hepatic parenchyma and injury to the bile ducts;
• Decreased appetite;
• Heaviness in the right hypochondrium, possible enlargement of the liver and spleen;
• Nausea and vomiting. These symptoms are more typical for severe forms;
• Weakness, malaise;
• Joint pain;
• Dark urine similar to dark beer , discolored stool – typical signs of any viral hepatitis;
• Laboratory indicators: Liver function tests (AlT, AST, bilirubin), depending on the severity of the disease, can increase several times, and the number of platelets decreases.

During viral hepatitis, 4 forms are distinguished:

1. Light, more often characteristic of hepatitis C: jaundice is often absent, low-grade or normal temperature, heaviness in the right hypochondrium, loss of appetite;
2. Moderate: the above symptoms are more pronounced, joint pain, nausea and vomiting appear, appetite is practically absent;
3. Heavy. All symptoms are present in a pronounced form;
4. Lightning fast (fulminant), not found in hepatitis C, but very characteristic of hepatitis B, especially in the case of coinfection (HDV/HBV), that is, a combination of two viruses B and D that cause superinfection. The fulminant form is the most dangerous, since as a result of the rapid development of massive necrosis of the liver parenchyma, the death of the patient occurs.

Hepatitis, dangerous at home (A, E)

In everyday life, first of all, liver diseases that have a predominantly fecal-oral transmission route can lie in wait, and this, as is known, is hepatitis A and E, so you should dwell a little on their characteristic features:

Hepatitis A

Hepatitis A is a highly contagious infection. Previously, it was called simply infectious hepatitis (when B was serum, and others were not yet known). The causative agent of the disease is a small, but incredibly resistant virus containing RNA. Although epidemiologists note susceptibility to the pathogen as universal, it is predominantly children who are over one year of age who are affected. Infectious hepatitis, triggering inflammatory and necrobiotic processes in the liver parenchyma, giving symptoms of intoxication (weakness, fever, jaundice, etc.), as a rule, ends with recovery with the development of active immunity. The transition of infectious hepatitis to a chronic form practically does not occur.

Video: hepatitis A in the program “Live Healthy!”

Hepatitis E

Its virus also belongs to the RNA-containing type and feels good in the aquatic environment. Transmitted from a sick person or carrier (in the latent period), there is a high probability of infection through food that has not undergone heat treatment. Mostly young people (15-30 years old) living in countries are affected Central Asia and the Middle East. In Russia, the disease is extremely rare. The contact and household route of transmission cannot be excluded. Cases of chronicity or chronic carriage have not yet been established or described.

Hepatitis B and its dependent hepatitis D virus

Hepatitis virusB(HBV), or serum hepatitis, is a DNA-containing pathogen with a complex structure that prefers liver tissue for its replication. A tiny dose of infected biological material is enough to transmit the virus, why does this form so easily pass not only during medical procedures, but also during sexual intercourse or vertically.

Current viral infection multivariate. It may be limited to:

• Carriage;
• Give acute liver failure with the development of a fulminant (fulminant) form, often claiming the life of the patient;
• If the process becomes chronic, it can lead to the development of cirrhosis or hepatocarcinoma.

The incubation period of this form of the disease lasts from 2 months to six months, and the acute period in most cases has symptoms characteristic of hepatitis:

1. Fever, headache;
2. Decreased performance, general weakness, malaise;
3. Joint pain;
4. Function disorder digestive system(nausea, vomiting);
5. Sometimes rashes and itching;
6. Heaviness in the right hypochondrium;
7. Enlarged liver, sometimes spleen;
8. Jaundice;
9. A typical sign of liver inflammation is dark urine and discolored stool.

Combinations of HBV with the causative agent of hepatitis D (HD) are very dangerous and unpredictable., which was previously called delta infection - a unique virus that is obligatory dependent on HBV.

Transmission of two viruses can occur simultaneously, which leads to the development coinfections. If the D-pathogen later joined HBV-infected liver cells (hepatocytes), then we will talk about superinfections. The serious condition, which was the result of such a combination of viruses and the clinical manifestation of the most dangerous type of hepatitis (fulminant form), often threatens to be fatal within a short time.

Video: Hepatitis B

The most significant of parenteral hepatitis (C)

viruses of various hepatitis

The “famous” hepatitis C virus (HCV, HCV) is a microorganism with unprecedented heterogeneity. The pathogen contains single-stranded positively charged RNA encoding 8 proteins (3 structural + 5 non-structural), to each of which corresponding antibodies are produced during the disease process.

The hepatitis C virus is quite resistant to external environment, tolerates freezing and drying well, but is not transmitted in negligible doses, which explains the low risk of infection through vertical transmission and sexual intercourse. A low concentration of an infectious agent in secretions released during sex does not provide conditions for transmission of the disease, unless other factors are present that “help” the virus “move.” These factors include concomitant bacterial or viral infections (HIV primarily), which reduce immunity, and damage to the integrity of the skin.

The behavior of HCV in the body is difficult to predict. Having penetrated into the blood, it can circulate for a long time in minimal concentrations, forming in 80% of cases a chronic process that can, over time, lead to severe liver damage: cirrhosis and primary hepatocellular carcinoma (cancer).

The absence of symptoms or slight manifestation of signs of hepatitis is the main feature of this form of inflammatory liver disease, which remains unrecognized for a long time.

However, if the pathogen nevertheless “decided” to immediately begin damaging the liver tissue, then the first symptoms may already appear after 2-24 weeks and last 14-20 days.

The acute period often occurs in a mild anicteric form, accompanied by:

• Weakness;
• Joint pain;
• Digestive disorder;
• Minor fluctuations in laboratory parameters (liver enzymes, bilirubin).

The patient feels some heaviness on the side of the liver, sees a change in the color of urine and feces, however, pronounced signs of hepatitis, even in the acute phase, are generally not typical for this species and occur rarely. It becomes possible to diagnose hepatitis C by detecting the corresponding antibodies by the method (ELISA) and the RNA of the pathogen by conducting it (polymerase chain reaction).

Video: film about hepatitis C

What is hepatitis G

Hepatitis G is considered the most mysterious today. It is caused by a virus containing single-stranded RNA. The microorganism (HGV) has 5 types of genotypes and is structurally very similar to the causative agent of hepatitis C. One (the first) of the genotypes chose the west of the African continent for its habitat and is not found anywhere else, the second spread throughout the globe, the third and fourth “liked” Southeast Asia, and the fifth settled in southern Africa. Therefore, residents of the Russian Federation and the entire post-Soviet space have a “chance” of meeting a representative of type 2.

For comparison: hepatitis C distribution map

In epidemiological terms (sources of infection and routes of transmission), hepatitis G resembles other parenteral hepatitis. As for the role of HGV in the development of inflammatory liver diseases of infectious origin, it has not been determined, the opinions of scientists differ, and the data in the medical literature remain contradictory. Many researchers associate the presence of the pathogen with the fulminant form of the disease, and are also inclined to believe that the virus plays a role in the development of autoimmune hepatitis. In addition, a frequent combination of HGV with hepatitis C (HCV) and hepatitis B viruses (HBV) has been observed, that is, the presence of co-infection, which, however, does not aggravate the course of mono-infection and does not affect the immune response during interferon treatment.

HGV monoinfection usually occurs in subclinical, anicteric forms, however, as researchers note, in some cases it does not go away without a trace, that is, even in a latent state it can lead to morphological and functional changes in the liver parenchyma. There is an opinion that the virus, like HCV, can lie low and then strike no less, that is, transform into cancer or hepatocellular carcinoma.

When does hepatitis become chronic?

Chronic hepatitis is understood as a diffuse-dystrophic inflammatory process localized in the hepatobiliary system and caused by various etiological factors (viral or other origin).

The classification of inflammatory processes is complex, however, like other diseases, moreover, there is still no universal method, therefore, in order not to burden the reader with incomprehensible words, we will try to say the main thing.

Considering that in the liver, for certain reasons, a mechanism is triggered that causes degeneration of hepatocytes (liver cells), fibrosis, necrosis of the liver parenchyma and others morphological changes, leading to disruption of the functional abilities of the organ, began to be distinguished:

1. Autoimmune hepatitis, characterized by extensive liver damage, and, therefore, an abundance of symptoms;
2. Cholestatic hepatitis, caused by a violation of the outflow of bile and its stagnation as a result of an inflammatory process affecting the bile ducts;
3. Chronic hepatitis B, C, D;
4. Hepatitis caused by the toxic effects of drugs;
5. Chronic form hepatitis of unknown origin.

It is obvious that the classified etiological factors, associations of infections (co-infection, superinfection), phases of the chronic course do not fully provide a complete picture of inflammatory diseases of the main organ of detoxification. There is no information about the liver’s reaction to the damaging effects of adverse factors, toxic substances and new viruses, that is, nothing is said about very significant forms:

• Chronic alcoholic hepatitis, which is a source of alcoholic cirrhosis;
• Nonspecific reactive form of chronic hepatitis;
• Toxic hepatitis;
• Chronic hepatitis G, discovered later than others.

In this regard, it was determined 3 forms of chronic hepatitis based on morphological characteristics:

1. Chronic persistent hepatitis (CPH), which is usually inactive, takes a long time to manifest itself clinically, infiltration is observed only in the portal tracts, and only penetration of inflammation into the lobule will indicate its transition to the active phase;
2. Chronic active hepatitis (CAH) is characterized by the transition of the inflammatory infiltrate from the portal tracts into the lobules, which is clinically manifested varying degrees activity: slight, moderate, pronounced, pronounced;
3. Chronic lobular hepatitis, caused by the predominance of the inflammatory process in the lobules. The defeat of several lobules by multibular necrosis indicates a high degree of activity of the pathological process (necrotizing form).

Considering the etiological factor

Inflammatory process in the liver refers to polyetiological diseases, since it is caused by a number of reasons:

The classification of hepatitis has been revised many times, but experts have not come to a consensus. Currently, only 5 types of liver damage associated with alcohol have been identified, so it hardly makes sense to list all the options, because not all viruses have been discovered and studied, and not all forms of hepatitis have been described. Nevertheless, it may be worth introducing the reader to the most understandable and accessible division of chronic inflammatory liver diseases according to etiology:

1. Viral hepatitis, caused by certain microorganisms (B, C, D, G) and uncertain - poorly studied, unconfirmed by clinical data, new forms - F, TiTi;
2. Autoimmune hepatitis(types 1, 2, 3);
3. Liver inflammation (drug-induced), often detected in chronic patients, associated with long-term use of a large number of medications or the use of medications that exhibit pronounced aggression towards hepatocytes for a short time;
4. Toxic hepatitis caused by the influence of hepatotropic toxic substances, ionizing radiation, alcohol surrogates and other factors;
5. Alcoholic hepatitis, which, together with the drug-induced one, is classified as a toxic form, but in other cases is considered separately as a social problem;
6. Metabolic, occurring in congenital pathology - illnesses Konovalov-Wilson. The reason lies in a hereditary (autosomal recessive type) disorder of copper metabolism. The disease is extremely aggressive, quickly ending in cirrhosis and death of the patient in childhood or young age;
7. Cryptogenic hepatitis, the cause of which, even after a thorough examination, remains unknown. The disease is progressive and requires observation and control, as it often leads to severe liver damage (cirrhosis, cancer);
8. Nonspecific reactive hepatitis (secondary). It is often a companion to various pathological conditions: tuberculosis, renal pathology, pancreatitis, Crohn's disease, ulcerative processes in the gastrointestinal tract and other diseases.

Considering that some types of hepatitis are very related, widespread and quite aggressive, it makes sense to give a few examples that will likely be of interest to readers.

Chronic form of hepatitis C

An important question regarding hepatitis C is how to live with it and how many years people live with this disease. Upon learning of their diagnosis, people often panic, especially if they receive information from unverified sources. However, this is not necessary. Living with hepatitis C ordinary life, but they have it in mind in terms of some adherence to a diet (the liver should not be loaded with alcohol, fatty foods and substances toxic to the organ), increasing protective forces the body, that is, immunity, being careful in everyday life and during sexual intercourse. You just need to remember that human blood is contagious.

As for life expectancy, there are many cases where hepatitis, even in people who like to eat and drink well, has not shown itself in any way for 20 years, so you should not bury yourself prematurely. The literature describes both cases of recovery and the reactivation phase that occurs after 25 years. and of course, sad outcome– cirrhosis and cancer. Which of the three groups you can fall into sometimes depends on the patient, given that there is currently a medicine - synthetic interferon.

Hepatitis associated with genetics and immune response

Autoimmune hepatitis, which occurs in women 8 times more often than in men, is characterized by rapid progression with the transition to portal hypertension, renal failure, cirrhosis and ends in the death of the patient. According to the international classification, autoimmune hepatitis can occur in the absence of blood transfusions, liver damage from alcohol, toxic poisons, medicinal substances.

The cause of autoimmune liver damage is considered to be a genetic factor. Positive associations of the disease with antigens of the major histocompatibility complex (leukocyte HLA system), in particular, HLA-B 8, which is recognized as an antigen of hyperimmunoreactivity, have been identified. However, many may have a predisposition, but not everyone gets sick. Some medications (for example, interferon), as well as viruses, can provoke autoimmune damage to the liver parenchyma:

• Epstein-Barra;
• Corey;
• Herpes types 1 and 6;
• Gepatitov A, V, S.

It should be noted that about 35% of patients who were overtaken by AIH already had other autoimmune diseases.

The vast majority of cases of autoimmune hepatitis begin as acute inflammatory process(weakness, loss of appetite, significant jaundice, dark urine). After a few months, signs of an autoimmune nature begin to form.

Sometimes AIT develops gradually with a predominance of symptoms of asthenovegetative disorders, malaise, heaviness in the liver, slight jaundice, rarely the onset is manifested by a significant increase in temperature and signs of other (extrahepatic) pathology.

The following manifestations may indicate a full-blown clinical picture of AIH:

1. Severe malaise, loss of performance;
2. Heaviness and pain on the side of the liver;
3. Nausea;
4. Skin reactions (capillaritis, telangiectasia, purpura, etc.)
5. Itching of the skin;
6. Lymphadenopathy;
7. Jaundice (not constant);
8. Hepatomegaly (enlarged liver);
9. Splenomegaly (enlarged spleen);
10. In women – absence of menstruation (amenorrhea);
11. In men – enlargement of the mammary glands (gynecomastia);
12. Systemic manifestations (polyarthritis),

AIH is often a companion to other diseases: diabetes mellitus, blood, heart and kidney diseases, pathological processes localized in the organs of the digestive system. In a word, autoimmune - it is autoimmune and can manifest itself in any pathology that is far from liver.

Any liver “does not like” alcohol...

Alcoholic hepatitis (AH) can be considered as one of the forms of toxic hepatitis, because they have the same cause - the negative effect on the liver of irritating substances that have a detrimental effect on hepatocytes. Hepatitis of alcoholic origin is characterized by all the typical signs of liver inflammation, which, however, can occur in sharply progressive acute form or have a persistent chronic course.

Most often, the onset of an acute process is accompanied by signs:

• Intoxication: nausea, vomiting, diarrhea, aversion to food;
• Weight loss;
• Jaundice without itching or with itching due to the accumulation of bile acids in the cholestatic form;
• Significant enlargement of the liver with its thickening and pain in the right hypochondrium;
• Tremors;
• Hemorrhagic syndrome, renal failure, hepatic encephalopathy in the fulminant form. Hepatorenal syndrome and hepatic coma can cause the death of the patient.

Sometimes, during the acute course of alcoholic hepatitis, a significant increase in body temperature is observed, bleeding and the addition of bacterial infections are possible, causing inflammatory processes in the respiratory and urinary tract, gastrointestinal tract, etc.

Chronic persistence of hypertension is asymptomatic and often reversible if a person manages to stop in time. Otherwise the chronic form becomes progressive with transformation into cirrhosis.

...And other toxic substances

For the development of acute toxic hepatitis a single dose of a toxic substrate is sufficient, which has hepatotropic properties, or a large amount of substances that are less aggressive to the liver, for example, alcohol. Acute toxic inflammation of the liver manifests itself by its significant increase and pain in the right hypochondrium. Many people mistakenly believe that the organ itself hurts, but this is not the case. The pain is caused by stretching of the liver capsule due to an increase in its size.

With toxic liver damage, symptoms of alcoholic hepatitis are characteristic, but depending on the type of toxic substance, they can be more pronounced, for example:

1. Feverish state;
2. Progressive jaundice;
3. Vomiting with blood;
4. Nose and gum bleeding, hemorrhages on the skin due to damage to the vascular walls by toxins;
5. Mental disorders (excitement, lethargy, disorientation in space and time).

Chronic toxic hepatitis develops over a long period of time when exposed to small but constant doses of toxic substances. If the cause of the toxic effect is not eliminated, then after years (or only months) you can get complications in the form liver cirrhosis and liver failure.

Markers for early diagnosis. How to understand them?

Markers of viral hepatitis

Many people have heard that the first step in diagnosing inflammatory liver diseases is to test for markers. Having received a piece of paper with the test result for hepatitis, the patient is unable to understand the abbreviation unless he has special education.

Markers of viral hepatitis determined using and, inflammatory processes of non-viral origin are diagnosed by other methods, not excluding ELISA. In addition to these methods, biochemical tests, histological analysis (based on liver biopsy material) and instrumental studies are performed.

However, we should return to the markers:

• Infectious hepatitis A antigen can be determined only during the incubation period and only in feces. During the phase of clinical manifestations, class M immunoglobulins (IgM) begin to be produced and appear in the blood. HAV-IgG, synthesized somewhat later, indicates recovery and the formation of lifelong immunity, which these immunoglobulins will provide;
• The presence or absence of the causative agent of viral hepatitis B determined by the “Australian antigen” detected since time immemorial (though not by modern methods) - HBsAg (surface antigen) and inner membrane antigens - HBcAg and HBeAg, which became possible to identify only with the advent of ELISA and PCR in laboratory diagnostics. HBcAg is not detected in blood serum; it is determined using antibodies (anti-HBc). To confirm the diagnosis of HBV and monitor the course chronic process and to determine the effectiveness of treatment, it is advisable to use PCR diagnostics (detection of HBV DNA). The patient's recovery is indicated by the circulation of specific antibodies (anti-NVs, total anti-HBC, anti-HBe) in his blood serum in the absence of the antigen itselfHBsAg;
• Diagnosis of C-hepatitis without detection of virus RNA (PCR) is difficult. IgG antibodies, appearing at the initial stage, continue to circulate throughout life. The acute period and the reactivation phase are indicated by class M immunoglobulins (IgM), the titer of which increases. The most reliable criterion for diagnosis, monitoring and control over the treatment of hepatitis C is the determination of viral RNA by PCR.
• The main marker for diagnosing hepatitis D(delta infection) are considered immunoglobulins of class G (anti-HDV-IgG), which persist throughout life. In addition, to clarify monoinfection, super (association with HBV) or co-infection, an analysis is carried out to detect class M immunoglobulins, which remain forever in case of superinfection, and disappear after about six months in case of co-infection;
• The main laboratory test for hepatitis G is the determination of viral RNA using PCR. In Russia, specially developed ELISA kits that can detect immunoglobulins to the E2 envelope protein, which is a component of the pathogen (anti-HGV E2), help identify antibodies to HGV.

Markers of hepatitis of non-viral etiology

Diagnosis of AIH is based on the identification of serological markers (antibodies):

In addition, the diagnosis uses the determination of biochemical parameters: protein fractions (hypergammaglobulinemia), liver enzymes (significant transaminase activity), as well as the study of histological liver material (biopsy).

Depending on the type and ratio of markers, types of AIH are distinguished:

• The first most often manifests itself in adolescents or young adults, or “wait” until 50;
• The second most often affects children, has high activity and resistance to immunosuppressants, and quickly transforms into cirrhosis;
• The third type was previously identified as a separate form, but now it is no longer considered from this perspective;
• Atypical AIH, representing cross-hepatic syndromes (primary biliary cirrhosis, primary sclerosing cholangitis, chronic hepatitis of viral origin).

There is no direct evidence of alcoholic origin of liver damage, so there is no specific analysis for hepatitis associated with ethanol consumption, however, certain factors have been noted that are very characteristic of this pathology. For example, ethyl alcohol acting on the liver parenchyma promotes the release alcoholic hyaline called Mallory bodies, which leads to the appearance of ultrastructural changes in hepatocytes and stellate reticuloepitheliocytes, indicating the degree of negative effects of alcohol on the “long-suffering” organ.

In addition, some biochemical indicators (bilirubin, liver enzymes, gamma fraction) indicate alcoholic hepatitis, but their significant increase is typical for many pathological conditions of the liver when exposed to other toxic poisons.

Clarification of medical history, identification of a toxic substance that has affected the liver, biochemical tests and instrumental study are main criteria for diagnosing toxic hepatitis.

Can hepatitis be cured?

Treatment of hepatitis depends on the etiological factor that caused the inflammatory process in the liver. Of course , hepatitis of alcoholic or autoimmune origin usually requires only symptomatic, detoxification and hepatoprotective treatment .

Viral hepatitis A and E, although of infectious origin, are acute and, as a rule, do not become chronic. Human body in most cases is able to resist them, therefore it is not customary to treat them, unless sometimes used symptomatic therapy to eliminate headaches, nausea, vomiting, diarrhea.

The situation is more complicated with liver inflammation caused by viruses B, C, D. However, given that delta infection practically does not occur in its own form, but obligately follows HBV, it is necessary to treat B-hepatitis first, but with increased doses and an extended period of time. course.

It is not always possible to cure hepatitis C, although chances for a cure have appeared with the use of alpha interferons (a component of the immune defense against viruses). In addition, at present, to enhance the effect of the main drug, combination regimens are used, involving combinations of prolonged interferons with antiviral drugs, for example, ribavirin or lamivudine.

It should be noted that not every immune system adequately responds to the interference of immunomodulators introduced from the outside, therefore interferon, for all its advantages, can give undesirable effects. In this regard, interferon therapy is carried out under the close supervision of a doctor with regular laboratory monitoring of the behavior of the virus in the body. If it is possible to completely eliminate the virus, then we can consider this a victory over it. Incomplete elimination, but cessation of replication of the pathogen, is also a good result, allowing you to “lull the enemy’s vigilance” and long years delay the likelihood of hepatitis progressing to cirrhosis or hepatocellular carcinoma.

How to prevent hepatitis?

The expression “It is easier to prevent a disease than to treat it” has long become a hackneyed, but not forgotten, since many troubles can indeed be avoided if preventive measures are not neglected. As for viral hepatitis, special caution will not be superfluous here either. Compliance with the rules of personal hygiene, the use of specific means of protection when in contact with blood (gloves, finger caps, condoms) in other cases are quite capable of becoming an obstacle to the transmission of infection.

In the fight against hepatitis, medical workers specifically develop action plans and follow them to every point. Thus, in order to prevent the incidence of hepatitis and the transmission of HIV infection, as well as reduce the risk of occupational infection, the Sanitary and Epidemiological Service recommends adhering to certain rules of prevention:

1. Prevent “syringe hepatitis”, common among drug users. For this purpose, organize free syringe distribution points;
2. Prevent any possibility of transmission of viruses during blood transfusions (organization of PCR laboratories at transfusion stations and quarantine storage of drugs and components obtained from donated blood, in ultra-low temperatures);
3. Reduce to the maximum the likelihood of occupational infection by using all available personal protective equipment and complying with the requirements of sanitary and epidemiological authorities;
4. Pay special attention to departments with an increased risk of infection (hemodialysis, for example).

We should not forget about precautions when having sexual intercourse with an infected person. The likelihood of sexual transmission of the hepatitis C virus is negligible, but for HBV it increases significantly, especially in cases associated with the presence of blood, for example, menstruation in women or genital trauma in one of the partners. If you really can’t do without sex, then at least you shouldn’t forget about a condom.

There is a higher chance of becoming infected in the acute phase of the disease, when the concentration of the virus is especially high, so for such a period it would be better to abstain from sexual relations altogether. Otherwise, human carriers live normal lives, give birth to children, remembering their peculiarity, and be sure to warn doctors (ambulance, dentist, when registering with antenatal clinic and in other situations requiring increased attention) that they are at risk for hepatitis.

Increased immunity to hepatitis

Prevention of hepatitis also includes vaccination against viral infection. Unfortunately, a vaccine against hepatitis C has not yet been developed, but available vaccines against hepatitis A and B have significantly reduced the incidence of these types.

The hepatitis A vaccine is given to children aged 6-7 years (usually before entering school). A single use provides immunity for a year and a half, revaccination ( re-vaccination) extends the protection period to 20 years or more.

The HBV vaccine is mandatory for newborns in the maternity hospital; there are no age restrictions for children who have not been vaccinated for any reason, or for adults. To ensure a full immune response, the vaccine is administered three times over several months. The vaccine is developed based on the surface (“Australian”) antigen of HBs.

The liver is a delicate organ

Treating hepatitis yourself means taking full responsibility for the outcome of the inflammatory process in such important body on yourself, therefore, in the acute period or during the chronic course, it is better to coordinate any of your actions with your doctor. After all, anyone understands: if the residual effects of alcoholic or toxic hepatitis can be leveled folk remedies, then they are unlikely to cope with the rampant virus in the acute phase (meaning HBV and HCV). The liver is a delicate organ, albeit patient, so treatment at home should be thoughtful and reasonable.

Hepatitis A, for example, does not require anything other than following a diet, which is necessary, in general, in the acute phase of any inflammatory process. Nutrition should be as gentle as possible, since the liver passes everything through itself. In the hospital, the diet is called the fifth table (No. 5), which is followed at home for up to six months after acute period.

With chronic hepatitis, of course, it is not advisable to offer strict adherence to a diet for years, but it would be correct to remind the patient that it is still not necessary to irritate the organ again. It is advisable to try to consume boiled foods, exclude fried, fatty, pickled foods, and limit salty and sweet foods. The liver also does not accept strong broths, strong and weak alcoholic and carbonated drinks.

Can folk remedies save?

Folk remedies in other cases help the liver cope with the load that has fallen on it, raise natural immunity, strengthen the body. However They can't cure hepatitis, therefore, it is unlikely to be correct to engage in amateur activities and treat liver inflammation without a doctor, because each type has its own characteristics that must be taken into account in the fight against it.

"Blind" probing

Often the attending physician himself, when discharging a convalescent patient from the hospital, recommends simple home procedures. For example, “blind” probing, which is done on an empty stomach in the morning. The patient drinks 2 chicken yolks, discarding the whites or using them for other purposes, after 5 minutes he washes it all down with a glass mineral water without gas (or clean from the tap) and lay it on the right side, placing a warm heating pad under it. The procedure lasts an hour. You should not be surprised if after it a person runs to the toilet to give away everything unnecessary. Some people use magnesium sulfate instead of yolks, however, this is a saline laxative, which does not always provide the same comfort to the intestines as, say, eggs.

Horseradish?

Yes, some people use finely grated horseradish (4 tablespoons) as a treatment, diluting it with a glass of milk. It is not recommended to drink the mixture right away, so it is first heated (almost to a boil, but not boiling), and left for 15 minutes for a reaction to occur in the solution. Take the medicine several times a day. It is clear that such a remedy will have to be prepared every day if a person tolerates a product such as horseradish well.

Soda with lemon

They say that some people lose weight in the same way . But still, we have a different goal - to treat the disease. Squeeze the juice of one lemon and pour it into a teaspoon baking soda. After five minutes, the soda will extinguish and the medicine is ready. They drink three times a day for 3 days, then rest for 3 days and repeat the treatment again. We do not undertake to judge the mechanism of action of the medicine, but people do so.

Herbs: sage, mint, milk thistle

Some say that milk thistle, known in such cases, which helps not only with hepatitis, but also with cirrhosis, is absolutely ineffective against hepatitis C, but instead people offer other recipes:

• 1 tablespoon peppermint;
• Half a liter of boiling water;
• Leave for a day;
• Strained;
• Used throughout the day.

Or another recipe:

• Sage - tablespoon;
• 200 – 250 grams of boiling water;
• A tablespoon of natural honey;
• Honey is dissolved in sage with water and infused for an hour;
• The mixture should be drunk on an empty stomach.

However, not everyone shares a similar point of view regarding milk thistle and offers a recipe that helps with all inflammatory liver diseases, including hepatitis C:

1. The fresh plant (root, stem, leaves, flowers) is crushed;
2. Place in the oven for a quarter of an hour to dry;
3. Remove from the oven, lay out on paper and place in a dark place to complete the drying process;
4. Take 2 tablespoons of dry product;
5. Add half a liter of boiling water;
6. Leave for 8-12 hours (preferably at night);
7. Drink 50 ml 3 times a day for 40 days;
8. Take a break for two weeks and repeat the treatment.

Video: viral hepatitis at the “School of Doctor Komarovsky”

Symptoms of hepatitis A are characterized by a wide range of clinical signs: from inapparent subclinical forms that occur without clinical symptoms to clinically pronounced forms with clear symptoms of intoxication and rather severe metabolic disorders.

In the typical course of the disease, cyclicity is clearly expressed with a sequential change of four periods: incubation, pre-icteric, icteric and post-icteric. Considering that anicteric forms are often found, it is more correct to distinguish between the following periods of the disease: incubation, prodromal, or initial (pre-icteric), the peak period (full development of the disease) and the period of convalescence. The division into periods is to a certain extent schematic, since the line between them is not always clear. In some cases, the initial (prodromal) period may be unexpressed, and the disease begins as if immediately with jaundice. Determining the incubation period is very important, since its precise delimitation makes it possible to preliminarily differentiate hepatitis A from hepatitis B; studying the initial period determines the possibility of early diagnosis of the disease, precisely at the time when the patient is most contagious.

The period of convalescence, in accordance with its essence, can also be called restorative or reparation. This emphasizes its great clinical significance, since recovery from hepatitis A, although inevitable, still occurs in a multi-stage manner and has several options.

From a pathogenetic point of view, the incubation period corresponds to the phase of parenchymal diffusion and hepatic replication of the virus; the initial (prodromal) period - the phase of generalization of infection (viremia); the peak period - the phase of metabolic disorders (liver damage); the period of convalescence is the phase of persistent repair and elimination of the virus.

The first signs of hepatitis A

The incubation period for hepatitis A is from 10 to 45 days. Apparently only in in rare cases it can be shortened to 8 days or lengthened to 50 days. During this period, no clinical manifestations of the disease are observed. However, the activity of hepatocellular enzymes (ALT, AST, F-1-FA, etc.) increases in the blood and the hepatitis A virus is found in free circulation. These data are of great practical importance, since they justify the feasibility of conducting serum studies in foci of hepatitis A blood level of these enzymes if this disease is suspected.

The disease, as a rule, begins acutely with a rise in body temperature to 38-39 C, less often to higher values, and the appearance of symptoms of intoxication (malaise, weakness, loss of appetite, nausea and vomiting). From the first days of the illness, patients complain of weakness, headache, bitter taste and bad breath, a feeling of heaviness or pain in the right hypochondrium, epigastrium, or without a specific localization. The pain is usually dull or colicky in nature. They can be strong and give the impression of an attack of appendicitis, acute cholecystitis and even cholelithiasis. The prodromal period is characterized by a noticeable change in mood, expressed in irritability, increased nervousness, moodiness, and sleep disturbance. In 2/3 of patients in the pre-icteric period of the disease, repeated vomiting is observed, not associated with the intake of food, water and medications; less often, repeated vomiting occurs. Transient dyspeptic disorders often occur: flatulence, constipation, and less commonly, diarrhea.

In rare cases (10-15%) in the initial period, catarrhal phenomena are observed in the form of nasal congestion, hyperemia of the mucous membranes of the oropharynx, slight cough. These patients usually have a high temperature reaction. Until recently, catarrhal symptoms in hepatitis A were attributed to the underlying disease, which gave rise to some authors to identify a flu-like variant of the pre-icteric period. According to modern concepts, the hepatitis A virus does not affect the mucous membranes of the oropharynx and respiratory tract. The occurrence of catarrhal symptoms in some patients in the initial period of hepatitis A should be regarded as manifestations of an acute respiratory viral disease.

After 1-2, less often - 3 days from the onset of the disease, the body temperature normalizes, and the symptoms of intoxication weaken somewhat, but general weakness, anorexia, nausea still persist, vomiting occurs, and abdominal pain usually increases.

The most important objective symptoms in this period of the disease are an increase in the size of the liver, sensitivity and pain on palpation. An increase in the size of the liver is observed in more than half of the patients and from the first days of the disease; in isolated cases, the edge of the spleen is palpated. The liver usually protrudes from under the edge of the costal arch by 1.5-2 cm, of moderate density,

By the end of the pre-icteric period, as a rule, there is darkening of urine (the color of beer in 68% of patients), less often - partial discoloration of feces (the color of clay in 33%). In some patients, the clinical manifestations of the initial period are mild or absent altogether, and the disease begins as if immediately with a change in the color of urine and feces. This type of onset of hepatitis A occurs in 10-15% of patients, usually with mild or mild forms of the disease.

The described typical symptom complex of the initial (pre-icteric) period of hepatitis A is in full accordance with the characteristics of the pathogenesis of the disease. The generalization of infection (viremia) that occurs during this period is reflected in the manifestations of infectious toxicosis in the first days of the disease with a clinical picture that is uncharacteristic in terms of specificity; after this, already on the 3rd - 4th day of the disease, along with the subsidence of the infectious toxic syndrome, and symptoms of hepatitis A gradually increase, indicating an ever-increasing disorder functional state liver.

Symptoms of intoxication in the initial period are correlated with the concentration of the virus in the blood. The highest concentration of viral antigen is detected precisely in the first days of the initial period, when the symptoms of intoxication are most pronounced. At the end of the prodromal period, the concentration of the virus in the blood begins to decrease, and already from 3-5 days after the onset of jaundice, the viral antigen in the blood, as a rule, is not detected.

Manifestations of the initial (pre-icteric) period of hepatitis A are polymorphic, but this cannot serve as a basis for identifying individual clinical syndromes (asthenovegetative, dyspeptic, catarrhal, etc.), as many authors do. In children, such a distinction between syndromes seems impractical, since syndromes are mostly observed in combination, and it is difficult to identify the leading significance of any of them.

Despite the heterogeneity of clinical manifestations and the absence of pathognomonic symptoms of hepatitis A in the pre-icteric period, hepatitis A can be suspected in this period on the basis of a characteristic combination of symptoms of intoxication with signs of incipient liver damage (enlargement, hardening and pain). The diagnosis is greatly simplified in the presence of dark colored urine and discolored feces, an epidemic situation and can be supported by laboratory tests. The most important among them in this period of the disease is hyperenzymemia. The activity of almost all hepatic cellular enzymes (ALT, AST, F-1-FA, sorbitol dehydrogenase, glutamate dehydrogenase, urocaninase, etc.) turns out to be sharply increased in the first days of the disease in all patients. The indicators of thymol test and beta-liloproteins also increase.

Determination of bilirubin in blood serum during this period of the disease has less diagnostic value compared to enzymatic tests and sediment samples. The total amount of bilirubin at the onset of the disease has not yet increased, but it is still often possible to detect an increased content of its bound fraction. From the first days of the disease, the amount of urobilin in the urine increases, and at the end of the pre-icteric period, bile pigments are detected with great regularity,

Changes in peripheral blood are not typical. Red blood is not changed, ESR is not increased, and sometimes there is a transient slight leukocytosis.

The duration of the prodromal period, according to various authors, varies within quite significant limits: from several days to 2 and even 3 weeks. In children, for the most part it does not exceed 5-8 days, only in 13% of patients the pre-icteric period ranges from 8 to 12 days.

Most authors believe that the duration of the prodromal period depends on the severity of the disease. In adults, the shorter the prodromal period, the milder the disease. According to our data, which is consistent with the data of most pediatricians, the severity of viral hepatitis is greater, the shorter the pre-icteric period. In mild forms of hepatitis A, jaundice usually appears on the 4-7th day, and in moderate forms - on the 3-5th day. At the same time, in mild forms, 2 times more often than in moderate forms, the disease begins immediately with the appearance of jaundice. This is apparently explained by the fact that in mild forms the symptoms of intoxication in the pre-icteric period are so weakly expressed that they can go unnoticed.

Symptoms of hepatitis A in the icteric period

The transition to the peak period (icteric period) usually occurs when there is a clear improvement in the general condition and a decrease in complaints. With the appearance of jaundice, the general condition in 42% of patients with hepatitis A can be assessed as satisfactory, and in the rest - as moderate for another 2-3 days of the icteric period. In the following days, in these patients, the symptoms of intoxication are practically undetectable or mild, and the general condition can be assessed as satisfactory.

First, yellowness of the sclera, hard and soft palate appears, then - the skin of the face, torso, and later - the limbs. Jaundice grows quickly, within 1-2 days; often the patient turns yellow as if “overnight.”

The intensity of jaundice with hepatitis A can be mild or moderate. Having reached the peak of development, jaundice due to hepatitis A begins to decrease after 2-3 days and disappears after 7-10 days. In some cases, it may be delayed for 2-3 weeks. Jaundice lasts the longest in the folds of the skin, on the ears, the mucous membrane of the soft palate, especially under the tongue and on the sclera - in the form of “marginal icterus.” Itching of the skin is not typical for hepatitis A, but in some cases it is possible at the height of jaundice, especially in prepubertal or pubertal children, as well as in adults.

Skin rashes are not typical for hepatitis A; only a few patients have an urticarial rash, which can always be associated with food allergies.

With the appearance of jaundice, a further increase in the size of the liver occurs, its edge becomes denser, rounded (less often sharp), painful on palpation. The increase in the size of the liver corresponds mainly to the severity of hepatitis: in a mild form of the disease, the liver usually protrudes from under the edge of the costal arch by 2-3 cm, and in a moderate form - by 3-5 cm.

The increase in the size of the liver is mostly uniform, but often the lesion of one lobe predominates, usually the left one.

An increase in the size of the spleen in hepatitis A is observed relatively rarely - no more than 15-20% of patients, but still this symptom of hepatitis A can be classified as a typical or even pathognomonic sign of the disease. Usually the spleen protrudes from under the edge of the costal arch by no more than 1-1.5 cm, its edge is rounded, moderately compacted, painless on palpation. An increase in the size of the spleen, as a rule, is noted during the acute period: with the disappearance of jaundice, the spleen is palpable only in a few patients. Most authors do not recognize a definite connection between an enlarged spleen and the severity of the disease, as well as the intensity of jaundice.

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

Cardiovascular changes in hepatitis A never play a significant role in the course of the disease. Electrocardiographic changes, expressed mainly in flattening and reduction of the T wave, a slight acceleration of the QRS complex, and sometimes a slight decrease in the ST interval, should be interpreted as the result of extracardiac influences, that is, as an “infectious heart”, and not as an indicator of myocardial damage.

Changes in the nervous system in the clinical picture of hepatitis A are not significant. However, at the onset of the disease, some general depression of the central nervous system can be detected, expressed in changes in mood, decreased activity, lethargy, and dynamics, sleep disturbance and other manifestations.

With hepatitis A, in typical cases, urine is intensely dark in color (especially foam), and its amount is reduced. At the height of clinical manifestations, traces of protein, single red blood cells, hyaline and granular casts are often found in the urine.

Excretion of bilirubin in urine is one of the characteristic symptoms all hepatitis. Clinically, this is expressed by the appearance of dark colored urine. In hepatitis A, the intensity of bilirubin excretion in the urine strictly correlates with the content of conjugated (direct) bilirubin in the blood - the higher the level direct bilirubin in the blood, the darker the color of the urine. During this period of the disease, liver function tests are maximally changed. The content of bilirubin in the blood serum is increased, mainly due to the conjugated fraction, the activity of hepatic cellular enzymes is always increased, and changes in each of their types of metabolism increase.

Hematological changes in hepatitis A are ambiguous; they depend on the stage of the disease, the age of the patient and the severity of the pathological process.

At the height of the disease, there is some thickening of the blood with a simultaneous increase in the amount of intracellular fluid. The hematocrit increases. The volume of erythrocytes increases with an almost unchanged average hemoglobin content. The number of red blood cells does not change significantly. The percentage of reticulocytes at the height of the disease is often increased. The sternum punctate reveals an increase in the number of erythroblastic elements, bone marrow erythropenia, mild eosinophilia, and maturation (to a small extent) of granuloblastic elements. There is also a slight increase in the number of differentiated cellular elements and a pronounced plasma cell reaction. All these changes can be explained by the state of irritation of the erythropostic apparatus of the bone marrow by the virus that causes the disease.

ESR in hepatitis A is normal or slightly slow. Its increase is observed when a bacterial infection is associated. In white blood, normocytosis or moderate leukopenia, with relative and absolute neutropenia, is more common. monocytosis and lymphocytosis. only in some cases there is mild leukocytosis. In some cases, an increase in plasma cells is noted.

For the initial (pre-jaundice) period, a slight leukocytosis with a shift to the left is typical; with the appearance of jaundice, the number of leukocytes is normal or below normal; in the period of convalescence, the number of leukocytes is normal.

The phase of reverse development occurs on the 7-14th day from the onset of the disease and is characterized by the complete disappearance of symptoms of intoxication, improved appetite, reduction and disappearance of jaundice, a significant increase in diuresis (polyuria), bile pigments are not detected in the urine and urobilin bodies appear, feces are colored.

In the normal course of the disease, the decline in clinical manifestations lasts 7-10 days. From this moment on, patients feel completely healthy, but in addition to an increase in the size of the liver and sometimes the spleen, their liver function tests remain pathologically altered.

The recovery or convalescent (pre-icteric) period is characterized by normalization of the size of the liver and restoration of its functional state. In some cases, patients may still complain of rapid fatigue after physical activity, possible abdominal pain, an increase in liver size, symptoms of dyslroteinemia, and an episodic or constant increase in the activity of hepatic cellular enzymes. These symptoms of hepatitis A are observed in isolation or in various combinations. The duration of the convalescence period is about 2-3 months.

Course of hepatitis A

The course of hepatitis A in duration can be acute and protracted, and in nature - smooth without exacerbations, with exacerbations, as well as with complications from the biliary tract and with a layer of intercurrent diseases.

The basis for distinguishing acute and protracted course is the time factor. In an acute course, complete restoration of the structure and function of the liver occurs after 2-3 months, while in a protracted course - after 5-6 months from the onset of the disease.

Acute course

An acute course is observed in 90-95% of patients with verified hepatitis A. As part of the acute course, there may be a very rapid disappearance of the clinical symptoms of hepatitis A, and by the end of the 2-3rd week of the disease, complete clinical recovery occurs with normalization of the functional state of the liver, but may There may also be a slower reverse dynamics of clinical manifestations with a slower recovery of liver function. In these patients, the total duration of the disease fits within the time frame of acute hepatitis (2-3 months), but for 6-8 weeks after the disappearance of jaundice, certain complaints may remain (impaired appetite, discomfort in the liver, etc.), as well as enlargement, hardening or tenderness of the liver, rarely - an increase in the size of the spleen, incomplete normalization of liver function (according to the results of functional tests), etc.

Among the 1158 children we examined who had hepatitis A, by the time of discharge from the hospital (25-30th day of illness), 2/3 had completely absent clinical symptoms of hepatitis A and normalization of most liver function tests occurred. At the same time, symptoms of intoxication in 73% of children disappeared by the 10th day of illness. The jaundice of the skin in 70% of children disappeared by the 15th day of illness, in the remaining 30% it persisted in the form of slight icterus of the sclera for up to 25 days. Complete normalization of pigment metabolism indicators in 2/3 of the children occurred by the 20th day, in the rest - by the 25-30th day of illness. The activity of liver cell enzymes reached normal values ​​by this time in 54% of patients; In 41% of children, the size of the liver normalized by this period; in the remaining 59%, the edge of the liver protruded from under the costal arch (no more than 2-3 cm), but in most of them this increase could be associated with age characteristics. After 2 months from the onset of the disease, only 14.2% of children who had hepatitis A had slight hyperenzymemia (ALT activity exceeded normal values ​​by no more than 2-3 times) in combination with a slight increase in liver size (the edge of the liver protruded from under costal arch by 1-2 cm), an increase in the thymol test and symptoms of dysproteinemia. We regarded the pathological process in these cases as prolonged convalescence. The further course of the disease in most of these patients is also benign.

Protracted current

According to modern concepts, prolonged hepatitis should be understood as a pathological process characterized by persistent clinical, biochemical and morphological signs of active hepatitis, lasting from 3 to 6-9 months. With hepatitis A, prolonged hepatitis is relatively rare. S.N. Sorinsoi observed a protracted course of hepatitis A in 2.7% of patients, I.V. Shakhgildyan - 5.1%, P.A., Daminov - 10%. The relatively wide range of fluctuations in the frequency of protracted hepatitis A can be explained not only by the different composition of patients, but primarily by the different approach to diagnosis. Prolonged hepatitis is considered to include all cases of the disease lasting from 3 to 9 months. In hepatitis A, prolonged hepatitis should be diagnosed when the disease lasts more than 2 months.

In the observed patients with prolonged hepatitis A, the initial manifestations of the disease differed little from those in acute hepatitis. The disease, as a rule, began acutely, with a rise in body temperature to 38-39 °C and the appearance of symptoms of intoxication. The average duration of the pre-jaundice period was 5+2 soup. With the appearance of jaundice, the symptoms of intoxication usually weakened. Jaundice reached its maximum severity on days 2-3 of the icteric period. In most cases, the symptoms of intoxication and jaundice disappeared within a period corresponding to the acute course of the disease. Disturbances in cyclicity were detected only in the period of early convalescence. At the same time, the size of the liver and, rarely, the spleen remained enlarged for a long time. In the blood serum, the activity of hepatic cellular enzymes did not show a tendency towards normalization, and remained high performance thymol test. In a quarter of patients with clear initial positive dynamics of clinical and biochemical parameters in the period of convalescence, the activity of ALT and F-1-PA increased again and the results of the thymol test increased, while only in isolated cases did insignificant (the amount of bilirubin not higher than 35 μmol/l) and short-term jaundice.

It is important to emphasize that prolonged hepatitis A always ends in recovery.

Morphological data obtained from liver puncture biopsy 4-6 months after the onset of the disease indicated the continuation of the acute process in the absence of signs of chronic hepatitis.

The presented evidence shows that the recovery process for prolonged hepatitis A can be significantly delayed and last more than 6 months. However, this does not give grounds to consider such forms as chronic hepatitis. The occurrence of protracted hepatitis A is based on the characteristics of the immunological response. Indicators of cellular immunity in such patients throughout the entire acute period are characterized by a slight decrease in the number of T-lymphocytes and an almost complete absence of changes in immunoregulatory subpopulations. At the same time, the T-helper/T-suppressor ratio does not deviate from normal values. The absence of redistribution of immunoregulatory subpopulations, presumably, does not contribute to globulin production. In patients with prolonged hepatitis A, the number of B-lymphocytes and the concentration of serum IgG and IgM at the height of the acute period are usually within normal values, and the level of specific anti-HAV class IgM, although it increases, but only slightly, only at the end of the 2nd month from the beginning disease, there is a slight decrease in the number of T-suppressors, which ultimately leads to an increase in the number of B-lymphocytes, an increase in the concentration of serum immunoglobulins by 1.5-2 times and an increase in the level of specific anti-HAV class IgM. Such immunological changes led to delayed, but still complete elimination of the virus and recovery.

Thus, in terms of the nature of the immunological response, protracted hepatitis A is close to acute hepatitis, with the only peculiarity that with it slow specific immunogenesis is observed and an extended cycle of the infectious process is formed.

Course with exacerbation

An exacerbation should be understood as an increase in the clinical signs of hepatitis and a deterioration in the performance of functional liver tests against the background of a persistent pathological process in the liver. Exacerbations should be distinguished from relapses - the re-occurrence (after a period of absence of visible manifestations of the disease) of the main syndrome of the disease in the form of an increase in the size of the liver, often the spleen, the appearance of jaundice, increased body temperature, etc. Relapses can also occur in the form of an anicteric variant. Both exacerbations and relapses are always accompanied by an increase in the activity of hepatocellular enzymes. Corresponding changes in sediment protein samples and other laboratory tests are detected. In some cases, only abnormal liver tests are noted without any clinical manifestations of the disease. These are so-called biochemical exacerbations.

The causes of exacerbations and relapses have not yet been precisely established. Considering that relapses occur in most cases 2-4 months after the onset of hepatitis A, one can assume superinfection with viruses of another type of hepatitis. According to the literature, in half of the cases, during a relapse, transient HBs antigenemia is detected, which indicates in favor of layered hepatitis B. It has been shown that when hepatitis B is layered, the course of hepatitis A is wave-like due to enzymatic exacerbations, or relapses occur with a typical clinical picture hepatitis B. Studies conducted in our clinic confirm the leading role of superinfection in the occurrence of relapses in hepatitis A. In almost all patients with the so-called relapse of hepatitis A, we documented superinfection with the HB virus or could not exclude the layering of viral hepatitis “neither A nor B” .

However, if the question of the genesis of relapses of hepatitis A is resolved by most researchers unambiguously - the layering of another type of hepatitis, then understanding the cause of exacerbations is not always easy. Very often, exacerbations of hepatitis A occur in patients with the so-called prolonged convalescence, then the network against the background of still remaining activity of hepatocellular enzymes and deviations from the norm in other liver tests. An increase in the activity of the pathological process in the liver in such cases occurs without visible reasons and, as a rule, against the background of circulation in the blood of specific anti-NAV class IgM. One can, of course, assume that in these cases infection occurs with another antigenic variant of the hepatitis A virus, but there is still more reason to believe that the main cause of exacerbation is the activation of the virus in a patient with functional immune deficiency and a delay in a full immunological response, which can result in low level specific antibodies about the genesis and repeated breakthrough of the virus into free circulation. In a number of cases, in the period preceding the exacerbation, we observed a decrease in the titer of anti-HAV class IgA in the blood serum.

Course with damage to the bile ducts

With hepatitis A, damage to the biliary tract is usually accompanied by dyskinetic phenomena, which can be diagnosed at any period of the disease. The predominant type of dyskinesia is hypertensive, characterized by hypertension of the constrictor muscle, increased tone cystic duct and gallbladder. These changes are observed in any form of hepatitis A, but are more pronounced in the moderate form, especially in patients with cholestatic syndrome.

In most sick foxes, kinetic phenomena in the biliary tract disappear without any treatment as the symptoms of viral liver damage are eliminated, which allows their occurrence in the acute period of the disease to be associated directly with HAV infection. Damage to the bile ducts in the acute period of hepatitis A does not significantly affect the nature of the pathological process in the liver. The total duration of the disease in most cases falls within the framework of acute hepatitis. Only in rare cases is damage to the biliary tract accompanied by cholestatic syndrome. Often, damage to the biliary tract is detected during the period of convalescence. In this case, patients complain of periodic abdominal pain, nausea, and sometimes vomiting. They often belch on an empty stomach. An objective examination reveals pain in the liver, mainly in the projection of the gallbladder. In some cases, positive “bubble” symptoms of hepatitis A and hepatomegaly are noted without clear subjective complaints.

Course with layering of intercurrent diseases

It is generally accepted that the combination of two infectious diseases always affects their clinical course. Many people also consider intercurrent diseases as one of the possible reasons exacerbations, relapses and protracted course of hepatitis A.

The literature expresses an opinion about the aggravating influence on the course of the disease of such intercurrent infections as dysentery, pneumonia, typhoid fever, ARVI, measles, whooping cough, as well as helminthic infestation, gastroduodenitis, ulcerative colitis and many others.

It should be noted, however, that most of the literature data on the problem of mixed hepatitis is unconvincing, since observations were carried out on verified hepatitis A and, therefore, did not exclude hepatitis B, C and “neither A nor B” in this group of patients.

Among the 987 patients with verified hepatitis A we observed, in 33% of cases the disease occurred in combination with other infections, including 23% with ARVI and 4% with a urinary tract infection.

There is no significant influence of intercurrent diseases on the severity of clinical manifestations, the degree of functional impairment, as well as the nature of the course, immediate and long-term outcomes of hepatitis A. Only in some patients, with the development of an intercurrent disease, an increase in the size of the liver, a revival of the activity of hepatopulmonary enzymes, an increase in the thymol test, and even a slower rate of functional recovery of the liver were again noted. However, even in these patients, it was not possible to associate the noted changes solely with superimposed infection. Obviously, the issue of the mutual influence of hepatitis A and concomitant diseases cannot be considered completely resolved; In our opinion, there are no sufficient grounds to exaggerate the importance of intercurrent diseases for the severity, nature of the course and outcomes of hepatitis A.

Classification of hepatitis A

Hepatitis A is classified by type, severity and course.

Severity indicators:

• clinical - increased body temperature, vomiting, decreased appetite, hemorrhagic manifestations, intensity of jaundice, enlarged liver;
• laboratory tests - the content of bilirubin, prothrombin, sublimate titer, etc.

Typical forms include all cases accompanied by the appearance of icteric staining of the skin and visible mucous membranes; atypical forms include anicteric, erased and subclinical. Typical hepatitis A can be mild, moderate or severe in severity. Atypical cases are usually mild.

As with other infectious diseases, the severity of hepatitis A can only be assessed at the height of the disease, when all the symptoms of hepatitis A have reached their maximum development, and the severity of the pre-icteric period must also be taken into account.

Clinical forms of hepatitis A

Symptoms of general intoxication (fever, vomiting, adynamia, decreased appetite) in the initial, pre-icteric period are more pronounced, the more severe the form of the disease. A short pre-icteric period is typical for more severe forms. Differences in intoxication depending on the severity of the disease are especially clearly revealed in the icteric period. In mild and moderate forms of the disease with the appearance of jaundice, the symptoms of intoxication significantly weaken or even disappear completely. In severe forms with the appearance of jaundice, the patient’s condition, on the contrary, worsens due to the appearance of “metabolic” or secondary toxicosis. Patients complain of headache, dizziness, general weakness, and lack of appetite.

Objective criteria for the severity of viral hepatitis in patients are the degree of increase in liver size and the intensity of jaundice.

Moderate form of hepatitis A

Occurs in 30% of patients. Characterized by moderately severe symptoms of intoxication. In the pre-icteric period, body temperature rises to 38-39 °C for 2-3 days. Characterized by lethargy, mood changes, and dyspeptic symptoms. Symptoms (nausea, vomiting), abdominal pain, and sometimes upset bowel movements. The duration of the pre-icteric period is on average 3.3±1.4 days. that is, it is shorter than in mild forms of the disease. With the appearance of jaundice, the symptoms of intoxication, although weakened, persist; lethargy and loss of appetite - in all, nausea, sometimes vomiting - in a third, low-grade body temperature - in half of the patients. Jaundice ranges from moderate to severe; in isolated cases, itching of the skin is possible. The liver is painful, its edge is dense, protrudes from under the costal arch by 2-5 cm. The spleen is enlarged in 6-10% of patients, palpated at the edge of the costal arch. Bradycardia and often hypotension are often observed. The amount of urine is reduced.

In the blood serum, the level of total bilirubin is from 85 to 150 µmol/l. rarely up to 200 µmol/l, including free (indirect) up to 50 µmol/l. A decrease in the prothrombin index (up to 70%) and sublimate titer (up to 1.7 units) is possible. The activity of organ-specific enzymes exceeds normal values ​​by 15-25 times.

The course of the disease is usually cyclical and benign. Symptoms of intoxication usually persist until the 10-14th day of illness, jaundice - 2-3 weeks. Complete restoration of the structure and function of the liver occurs on the 40-60th day of illness. A prolonged course is observed in only 3% of patients.

Severe form of hepatitis A

With hepatitis A it is extremely rare, not more often than 5% of patients. It seems that severe forms of hepatitis A occur much more often through waterborne infection.

Distinctive signs of the severe form are intoxication and pronounced biochemical changes in the blood serum. The disease always begins acutely with a rise in body temperature to 39-40 °C. From the first days, weakness, anorexia, nausea, repeated vomiting, abdominal pain are characteristic, dizziness, and stool upset are possible. The pre-icteric period is often short - 2-3 days. With the onset of jaundice, the condition of the patients remains serious. Patients complain of general weakness, headache, dizziness, complete absence appetite. Jaundice grows quickly, over the course of a day, and is usually bright, but there is no itching. Hemorrhagic rashes on the skin are possible, usually appearing on the neck or shoulders after applying a tourniquet in connection with intravenous manipulations. Heart sounds are muffled, pulse is rapid, blood pressure tends to decrease. The liver is sharply enlarged, its palpation is painful, the spleen is enlarged.

The content of total bilirubin in the blood serum is more than 170 µmol/l. The level of conjugated bilirubin is predominantly increased, but 1/3 of the total bilirubin is the free fraction. The prothrombin index decreases to 40%, the sublimate titer - to 1.4 BD, the activity of organ-specific liver-cellular enzymes is sharply increased, especially in the pre-icteric period and in the first days of jaundice. The disease proceeds smoothly. A protracted course practically does not occur.

Anicteric form of hepatitis A

A distinctive feature of this form of the disease is the complete absence of hysteria of the skin and sclera throughout the entire disease. During a targeted examination of groups in epidemic foci of hepatitis A, anicteric forms are diagnosed 3-5 times more often than icteric forms.

Clinical manifestations of the anicteric form are practically no different from those with mild typical forms.

Anicteric forms of hepatitis A are characterized by a combination of dyspeptic and asthenovegetative symptoms with an increase in the size of the liver, as well as a change in the color of urine due to an increase in the concentration of urobilin and bile pigments. In the blood serum, increased activity of hepatic cellular enzymes (ALT, AST, F-1-FA, etc.) is always detected, the thymol test is significantly increased, the content of conjugated bilirubin often increases, but the level of total bilirubin does not exceed 35 µmol/l. The prothrombin level and mercuric titer are always within normal values. Clinical symptoms of hepatitis A, with the exception of an increase in liver size, as well as disturbances in biochemical parameters, last for a short time in anicteric forms. General state the patient is practically not disturbed, and therefore, with insufficiently careful observation, the patient can endure the disease on his feet, remaining in the team.

Erased form

The erased form includes cases of viral hepatitis with mild main symptoms of the disease. Distinctive feature erased form - barely noticeable yellowness of the skin, visible mucous membranes and sclera, disappearing after 2-3 days. In the erased form, the symptoms of hepatitis A in the initial (prodromal) period are mild or absent. A short-term (1-2 days) increase in body temperature, lethargy, weakness, loss of appetite are possible: the increase in liver size is slight. Dark urine and discolored feces are observed with great consistency, but for a short time. Moderately increased activity of hepatocellular enzymes is detected in the blood. The content of total bilirubin is slightly increased due to the conjugated (direct) fraction. The thymol test indicators increased 1.5-2 times. In general, clinical and biochemical manifestations in the erased form can be characterized as lightweight, rudimentary light option a typical form with an abortive course. Its significance, like the anicteric form, lies in the difficulty of recognition, with the ensuing epidemiological consequences.

Subclinical (inapparent) form

In this form, in contrast to anicteric and erased forms, clinical manifestations are completely absent. The diagnosis is made only through laboratory examination of those in contact with patients with viral hepatitis. Of the biochemical tests, the most important for the diagnosis of such forms are indicators of enzymatic activity and, above all, an increase in the activity of ALT and F-1-FA in the blood serum; less often, AST activity increases and a positive thymol test is detected. All patients with subclinical hepatitis A have specific antibodies in their blood - anti-HAV class IgM, which is crucial for making a diagnosis. It is widely believed that in the focus of hepatitis A, most patients become infected and suffer a predominantly inapparent form of the disease. In hepatitis A foci, per disease diagnosed clinically and using biochemical tests, an average of 5-10 patients are identified with the presence of hepatitis A virus in their feces. It has been shown that if contacts in foci of hepatitis A are examined using only biochemical tests, the disease is detected on average in 15%, while when using virological methods - in 56 and even 83% of contacts.

ABOUT widespread Subclinical forms of hepatitis A are evidenced by the fact that among patients with anti-HAV class IgM, only 10-15% suffer the icteric form of the disease. The significance of inapparent subclinical forms of hepatitis A is that, while remaining unrecognized, they, like anicteric forms, serve as an invisible link that constantly supports the chain of the epidemic process.

Viral hepatitis A with cholestatic syndrome

With this variant of viral hepatitis, the 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. Cholestasis syndrome can occur in both mild and more severe forms of the disease. Its development is based on bile retention at the level of the intrahepatic bile ducts. It has been suggested that bile retention occurs due to damage to the cholangioles directly by the virus itself. Many authors point to the involvement of intrahepatic bile ducts in the pathological process in viral hepatitis. In this case, swelling and granularity of the cytoplasm of the epithelium, damage to the plasma membranes of bile capillaries, and karyolysis of the nuclei of ductular epithelial cells are observed. Inflammatory changes in the intrahepatic bile ducts, their increased permeability, bile diapedesis, and an increase in its viscosity lead to the formation of blood clots and large bilirubin crystals; Difficulties arise in the movement of bile through the bile capillaries and cholangioles. To a certain extent, intracanalicular bile retention is associated with pericholangiolytic and periportal infiltration, which occurs as a consequence of hyperergic disorders. It is also impossible to exclude the participation in this process of damage to the hepatocytes themselves, namely increased permeability cell membranes with the development of direct communications between the bile capillaries and the space of Disse, which presumably entails the appearance of excess protein in the bile, its thickening and the formation of blood clots.

In relation to the cholestatic form of viral hepatitis, the point of view of past authors is not without foundation. According to it, the main cause of cholestasis is a mechanical obstruction that occurs at the level of the bile ducts, gallbladder and even the constrictor muscle of the common bile duct.

In the literature, these forms of the disease are described under different names: “acute icteric form with cholestatic syndrome”, “cholestatic or cholangiolytic hepatitis”, “hepatitis with intrahepatic choletasis”, “cholangiolytic hepatitis”, “viral hepatitis with prolonged bile retention”, etc.

Literature data on frequency cholestatic form viral hepatitis are very inconsistent: from 2.5 to 10%.

The leading clinical symptom of hepatitis A with cholestatic syndrome is more or less pronounced congestive jaundice for a long time (up to 30-40 days or more) and itching of the skin. Often jaundice has a greenish or saffron tint, but sometimes skin jaundice can be mild, and the clinical picture is dominated by itchy skin. There are no symptoms of intoxication in the cholestatic form or they are mild. The size of the liver increases slightly. The urine is usually dark and the mouth guard is discolored. In the blood serum, the bilirubin content is usually high, exclusively due to the conjugated fraction. The activity of liver cell enzymes increases moderately from the first days, and then, despite the high content of bilirubin in the blood serum, decreases to almost normal values. Characteristics of the cholestatic form can be considered a high content of beta-lipoproteins, total cholesterol, as well as a significant increase in the activity of alkaline phosphatase and leucine aminopeptidase in the blood serum. Indicators of other functional tests (sublimate test, level of coagulation factors, thymol test, etc.) change slightly or remain within normal values.

The course of hepatitis A with cholestatic syndrome, although long-term, is always favorable; complete restoration of the functional state of the liver occurs. Chronic hepatitis does not develop.

Outcomes of hepatitis A

The outcomes of hepatitis A are recovery with complete restoration of the structure and function of the liver, recovery with an anatomical defect (residual fibrosis) or the formation of various complications from the biliary tract and gastroduodenal zone.

Recovery with complete restoration of liver structure and function

According to one of the clinic’s clinics, out of 1,158 children who had hepatitis A, by the time of discharge from the hospital (25-30 days of illness), clinical recovery and normalization of biochemical tests were observed in 50% of cases, after 2 months - in 67.6% , after 3 months - in 76%, after 6 months - in 88.4%; in the remaining 11.6% of children, 6 months from the onset of the disease, various consequences of hepatitis A were detected, including in 4.4% - enlargement and hardening of the liver with complete preservation of its functions, in 7.2% - abdominal pain due to dyskinesia biliary tract (3%), cholecystitis or cholangitis 0.5%), gastroduodenitis (2.5%), pancreatopathy (0.2%). In no case was the formation of chronic hepatitis observed.

Recovery with anatomical defect, post-hepatitis hepatomegaly (residual fibrosis).

A long-term or lifelong increase in liver size is possible after hepatitis A in the complete absence of clinical symptoms and laboratory changes. The morphological basis of hepatomegaly is residual liver fibrosis. Wherein dystrophic changes on the part of hepatocytes are completely absent, but proliferation of Kupffer cells and coarsening of the stroma are possible. It should be noted, however, that not any enlargement of the liver after acute hepatitis can be regarded as residual fibrosis. An increase in the size and hardening of the liver 1 month after discharge from the hospital is observed in 32.4% of children, after 3 months - in 24, and after 6 months - in 11.6% of patients. In all these patients, the liver protruded from under the edge of the costal arch by 1.5-2.5 cm and was painless, and biochemical tests indicated a complete restoration of its functional activity. According to formal criteria, such an increase in liver size could be interpreted as residual liver fibrosis as a result of hepatitis A. However, with a careful study of the anamnesis and as a result of targeted examination (ultrasound, immunological tests, etc.), in most of these patients, an increase in liver size was regarded as a constitutional feature or as a result of previously suffered other diseases. Only 4.5% of patients had documented residual fibrosis as a result of hepatitis A.

Biliary tract damage

Damage to the biliary tract is more correctly interpreted not as an outcome, but as a complication of hepatitis A, resulting from combined damage to the biliary tract by the virus and secondary microbial flora. By its nature, it is a diekinetic or inflammatory process. It is often combined with damage to other parts of the gastrointestinal tract, gastroduodenitis, pancreatitis, enterocolitis.

Clinically, damage to the biliary tract is manifested by various types of complaints (pain in the right hypochondrium or epigastrium, more often periodic or paroxysmal, associated with eating food, sometimes a feeling of heaviness or pressure in the right hypochondrium, nausea, vomiting). As a rule, abdominal pain appears 2-3 months after hepatitis A.

Among the observed 1158 patients with hepatitis A, abdominal pain 6 months after the onset of the disease was observed in 84 cases, which is 7.2%. All of these patients, along with moderate hepatomegaly, had complaints of abdominal pain, nausea, sometimes vomiting, belching on an empty stomach or associated with food intake. Palpation revealed pain in the epigastric region. Some patients showed positive “vesical” symptoms and hepatomegaly without clear subjective complaints. A comprehensive clinical and laboratory examination made it possible to exclude the formation of chronic hepatitis in all these patients. To clarify the diagnosis, they were examined in depth in a gastroenterological center using modern research methods (fibrogastroduodenoscopy, colonoscopy, irrigoscopy, fractional study of gastric juice, duodenal intubation, etc.).

When analyzing anamnestic data, it turned out that half of the patients had complaints of abdominal pain and dyspeptic disorders before contracting hepatitis A. Some patients were treated in somatic hospitals for chronic gastroduodenitis, biliary dyskinesia, chronic colitis etc. The duration of these diseases before the onset of hepatitis A was 1-7 years. In the early stages of convalescence (2-4 weeks after discharge from the hepatitis hospital), all these patients again developed abdominal pain and dyspeptic symptoms of hepatitis A. Upon examination, the majority were diagnosed with exacerbation of chronic gastroduodenitis. FEGDS revealed changes in the mucous membrane of the stomach and duodenum in 82% of cases. In some cases, in the absence of endoscopic signs of damage, functional disorders acid and secretion-forming functions of the stomach. Often, combined pathology of the gastroduodenal system, intestines and biliary tract was detected.

A retrospective analysis of anamnestic data showed that the majority of these patients (62%) had a family history of gastroenterological pathology, manifested by food or polyvalent allergies, bronchial asthma, neurodermatitis, etc.

38% of patients had no complaints of abdominal pain or any dyspeptic disorders before contracting hepatitis A. Their pain appeared 2-3 months after the onset of hepatitis and was of a different nature, more often in the early stages after eating, less often in the late stages, or were constant. As a rule, pain arose in connection with physical activity and was paroxysmal or aching in nature. Dyspeptic symptoms usually included nausea, less commonly vomiting, unstable chair, belching, heartburn, constipation.

Clinical examination revealed pain upon palpation in the epigastric and pyloroduodenal region, in the right hypochondrium and at the point of the gallbladder. In all these patients, there was an increase in the size of the liver (the lower edge protruded from under the costal arch by 2-3 cm) and positive “vesicles” were detected. » symptoms of hepatitis A. During endoscopy, 76.7% of patients showed signs of damage to the mucous membrane of the stomach and duodenum. In 63% the pathology was combined (gastroduodenitis), and in 16.9% it was isolated (gastritis or duodenitis). Only in 17.8% of patients no changes in the mucous membrane of the stomach and duodenum were visually detected. However, during a fractional study of gastric juice, some of them were found to have disturbances in the acid- and secretion-forming functions of the stomach.

In the vast majority of cases (85.7%), along with damage to the gastro-duodenal zone, dyskinetic disorders of the gallbladder were detected. In some patients they were combined with an anomaly in the development of the gallbladder or with symptoms of sluggish cholecystitis.

Thus, the so-called residual effects or long-term consequences detected in hepatitis A convalescents in the form of long-lasting symptoms of general asthenia, vague abdominal pain, enlarged liver, dyspeptic complaints and other manifestations that practical work usually interpreted as “post-hepatitis syndrome”, with a thorough targeted examination in most cases they are deciphered as chronic gastroduodenal or hepatobiliary pathology, revealed or arising in connection with hepatitis A. That is why, if there are complaints of abdominal pain, heartburn; nausea or vomiting during the period of convalescence of hepatitis A, it is necessary to conduct an in-depth examination of the patient in order to identify pathology from the gastroduodenal and biliary systems. Such convalescents should be observed by a gastroenterologist and receive appropriate therapy.

Posthepatitis hyperbilirubinemia

Post-hepatitis hyperbilirubinemia can only be conditionally associated with viral hepatitis. According to modern concepts, this syndrome is caused by a hereditary defect in bilirubin metabolism, leading to impaired transformation of unconjugated bilirubin or impaired excretion of conjugated bilirubin and, as a consequence, to the accumulation in the blood of an indirect fraction of bilirubin (Gilbert's syndrome) or a direct fraction (Rotor, Dabin-Johnson syndromes, etc. ). This is a hereditary disease, and viral hepatitis in such cases is a provoking factor that reveals this pathology in the same way as, for example, physical or emotional stress, ARVI, etc.

As a result of hepatitis A, Gilbert's syndrome develops in 1-5% of patients, usually within the first year after the acute period of the disease. More often it occurs in boys during puberty. The leading clinical symptom of hepatitis A is mild jaundice due to a moderate increase in unconjugated bilirubin in the blood (usually no more than 80 µmol/l) in the complete absence of signs characteristic of hemolytic jaundice and viral hepatitis. The same can be said in relation to Rotor and Dabin-Johnson syndromes, with the only peculiarity that in these cases the blood content of exclusively conjugated bilirubin is increased.

RCHR (Republican Center for Health Development of the Ministry of Health of the Republic of Kazakhstan)
Version: Clinical protocols of the Ministry of Health of the Republic of Kazakhstan - 2013

Hepatitis A without hepatic coma (B15.9)

Infectious diseases in children, Pediatrics

general information

Short description

Approved by the minutes of the meeting
Expert Commission on Health Development of the Ministry of Health of the Republic of Kazakhstan
No. 23 from 12/12/2013

Viral hepatitis A- an acute, cyclical infectious disease characterized by short-term symptoms intoxication, quickly passing disorders of liver function, benign course.

I. INTRODUCTORY PART

Protocol name: Viral hepatitis A in children
Protocol code:

ICD-10 code(s):
Code: At 15.9
B 15 acute hepatitis A
B15.0 hepatitis A with hepatic coma
B15.9 hepatitis A without hepatic coma

Date of development of the protocol: 22.08.2013

Abbreviations used in the protocol:
1. ALT - alanine transferase
2. AST - aspartate transferase
3. Anti-HAV - JgM, JgG - immunoglobulins M, G against the CAA.
4. HAV - viral hepatitis A
5. ELISA - enzyme immunoassay
6. AVH - acute viral hepatitis
7. APE - acute hepatic encephalopathy
8. PTI - prothrombin index
9. PCR - polymerase chain reaction
10. RIA - radioimmunoassay
11. ALP - alkaline phosphatase
12. GPs - doctors general practice
13. IV - intravenous administration

Protocol users: pediatricians, infectious disease specialists, GPs.

Classification

Clinical classification

Viral hepatitis with enteral transmission

Acute viral hepatitis A

OVG forms:

I. Typical icteric form- a combination of jaundice with cytolytic syndrome with a clear distinction between 3 periods of the disease: pre-icteric, icteric, convalescence.
Typical icteric form with cholestatic component- more intense jaundice, high bilirubinemia, slight transaminasemia, there is a tendency to increase alkaline phosphatase. The icteric period of the disease is longer.

The typical form is divided according to severity:
- light,
- medium-heavy,
- severe severity.

II. Atypical anicteric form- complete absence of jaundice. Clinical symptoms are not pronounced and are close to the pre-icteric period, hepatomegaly. Specific markers of viral hepatitis in combination with elevated ALT levels.

There is a malignant form- fulminant hepatitis. Fulminant (malignant) hepatitis with massive and submassive liver necrosis.
The hyperacute variant corresponds to a truly fulminant course of acute hepatitis with the development of hepatic coma and death on days 1-8 of illness. Fulminant course of hepatitis A occurs in 0.01 - 0.5 cases. Mortality is high: 80-100%.

Along the OVG current
Acute cyclic course - within 1-1.5 months, the replication (multiplication) of the virus stops, it is eliminated (removed) from the body and complete sanitation occurs. For hepatitis A and E, this is a typical course of the disease.
With CAA, a protracted course is sometimes observed in children with a burdened premorbid background, but ends with complete recovery.

Diagnostics

II. METHODS, APPROACHES AND PROCEDURES FOR DIAGNOSIS AND TREATMENT

List of diagnostic measures

Basic laboratory tests:



4. Blood for markers of HAV A (anti-HAV IgM)

Additional laboratory tests:
1. Proteinogram and coagulogram according to indications
2. Alkaline phosphatase study

Examinations before planned hospitalization:
1. General blood and urine analysis
2. Urine analysis for bile pigments and urobilin
3. Blood for total bilirubin and its fractions, ALT and AST (their ratios)
4. Blood for HAV markers A (anti-HAV Ig M)

Specific diagnostic methods:
Blood for markers of viral hepatitis A - anti-HAV IgM, IgG:
- Blood ELISA with determination of anti-HAV IgM, IgG
- PCR of blood with determination of RNA HAV (if diagnosis is difficult)

Complaints and anamnesis

A) pre-icteric period - increased temperature (70-80%), weakness, malaise, loss of appetite, nausea, may be vomiting, abdominal pain, hyperemia of the oropharyngeal mucosa, objective symptom - hepatomegaly;

B) icteric period - improvement of well-being with the appearance of jaundice, yellowness of the sclera, skin, darkening of the color of urine, acholic stool, hepatomegaly;

C) in the anamnesis - contact with a patient with CHA, indirectly the autumn-winter period of the year, violation of sanitary and hygienic standards;

G) Criteria for assessing the severity of acute viral hepatitis

1. Mild severity :
- mild intoxication phenomena or their complete absence;
- appetite is moderately reduced, nausea is intermittent;
- vomiting is not typical;
- the degree of increase in liver size usually does not correlate with the severity of the disease and is more related to age characteristics, previous and concomitant diseases;
- the intensity and persistence of jaundice is minimal.

2. Moderate severity:
- symptoms of intoxication are moderately expressed;
- poor appetite, severe nausea without vomiting;
- hepatomegaly is moderate, the edge is dull, elastic in consistency, the spleen is not enlarged;
- severe and persistent jaundice.

3. Severe severity:
- pronounced increase in signs of intoxication;
- hemorrhagic syndrome, tachycardia, pain in the liver area, a tendency to fluid retention, “aseptic fever” with neutrophilic leukocytosis may occur;

Fulminant hepatitis. In VH A it is very rare. Clinical syndrome with sudden development severe liver dysfunction with encephalopathy, coagulopathy and other metabolic disorders.

Physical examination:
a) Yellowness of the skin and visible mucous membranes, darkening of the color of urine, acholic stools, possible traces of scratching;
b) Determine the edge, consistency, tenderness and size of the liver.

Laboratory research

At mild degree severity:
- Total bilirubin (due to the direct fraction) in the blood does not exceed 4 times the normal parameters, the coagulogram indicator (prothrombin index) is without deviations from the norm.

For moderate severity:
- The level of total bilirubin in the blood serum reaches up to 160 µmol/l with a predominance of direct fractions, the most informative is the level of prothrombin index, which decreases to 60-70%.

For severe cases:
- bilirubinemia over 160-180 µmol/l with a tendency to rapidly increase.
- prothrombin index decreases to 40-60%;
- with increasing severity, bilirubin-enzyme dissociation is noted (a drop in the level of aminotransferases with an increase in the level of blood bilirubin, which may indicate a threat of developing acute liver failure , especially with an increase in the indirect fraction of bilirubin)
- it is necessary to remember that in children of the first year of life, even with the most severe liver damage, the bilirubin content may be low and not exceed 4 norms (SI system).

Instrumental studies
Ultrasound of the abdominal organs with determination of the size, structure of the tissues of the liver, spleen in severe cases, cholestatic variant, prolonged course of CAA.

Indications for consultation with specialists
Depending on the condition, background and concomitant diseases of the patient (surgeon, oncologist).

Differential diagnosis

Differential diagnosis of HAV

Diagnosis or cause of disease	In favor of diagnosis
1. Acute respiratory disease	Differential diagnosis is necessary only in the initial period of the VH disease, in which catarrhal manifestations are not expressed and the child’s well-being does not improve after a decrease in temperature. An objective symptom of CH is early liver enlargement
2. Gilbert's syndrome	Occurs in adolescence and young adulthood. The disease is characterized by a relative deficiency of the UDPHT enzyme and an increase in the level of indirect bilirubin in the blood.
3. Acute intestinal infection	Differential diagnosis is required in the initial period of VH disease, when there may be a diarrheal syndrome that is not severe and resolves without treatment. The objective symptom is hepatomegaly
4. Hemolytic jaundice - Prehepatic jaundice	They are characterized by an increase in indirect bilirubin due to increased hemolysis, as well as jaundice due to anemia. Hemolytic jaundice is not characterized by syndromes of parenchymal liver damage (mesenchymal-inflammatory, cytolysis and cholestasis).
5. Acute abdomen: appendicitis, mesadenitis, pancreatitis	With VH A, as a rule, there is no pronounced pain in the entire abdomen, only moderate pain in the area of ​​the right hypochondrium. The objective symptom of VH is hepatomegaly
6. Mechanical jaundice:	They arise due to blockage of the bile ducts with stones, a ball of helminths, or a tumor. In such conditions, total bilirubin increases due to the direct fraction as in CH, but transaminase activity is usually normal or slightly increased and pain is more often expressed
7. Hepatitis in a number of infections, for example: yersiniosis, listeriosis, leptospirosis, infectious mononucleosis, cytomegalovirus infection	In addition to the clinical and laboratory data characteristic of hepatitis, such diseases have many other symptoms, including fever, which is usually prolonged than with HAV A and, in addition to hepatomegaly, there is damage to other systems and organs
8. Toxic lesions liver while taking medications (for example, anti-tuberculosis drugs), toxic substances	Clinic of parenchymal liver damage. A differential diagnostic sign is the disappearance of signs of the disease after the elimination of the causing cause.

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Treatment

Treatment Goals: relief of intoxication, icteric syndrome, cytolysis of hepatocytes.

Treatment tactics

Non-drug treatment (basic therapy):
1. Regimen - bed during the pre-icteric, icteric periods of CAV, regardless of the severity, throughout the entire acute period of the disease.
2. Diet - table No. 5a.5, the ratio of proteins, fats and carbohydrates is 1: 1: 4.5, their quantity corresponds to age standards.
3. Detoxification therapy - taking liquids through the mouth.

Drug treatment:
1. Treatment of patients with mild and moderate severity of CAA is carried out at home.

2. The main means of pathogenetic therapy used for severe severity of HAV:
- means of detoxification therapy: 5%-10% dextrose solutions, crystalloids (sodium chloride, potassium chloride, sodium bicarbonate), rheopolyglucin, refortan;
- anticholestatic agents - ursodeoxycholic acid;
- choleretic drugs cholekinetic action (during the period of reduction of icteric syndrome) -5-10% solution of magnesium sulfate through the mouth, holosas;
- proteolysis inhibitors (contrical, trasylol, etc.);
- antioxidants and hepatoprotectors (ascorbic acid, tocopherol, essential phospholipids, silymarin preparations;
- hemostatic therapy (fresh frozen plasma, aminocaproic acid, etc.);
- syndromic therapy.

List of essential medicines: No.

List of additional medicines:
1. 5-10% dextrose solutions
2. crystalloids
3. fresh frozen plasma
4. protease inhibitors
5. ursodeoxycholic acid
6. silymarin preparations
7. antioxidants
8. holosas

Other types of treatment: not shown

Surgical intervention: not required.

Preventive measures for viral hepatitis A

Prevention and control strategy:
- Provide the population with good quality drinking water;

Ensure proper sanitary and hygienic conditions in preschool organizations, schools and other educational institutions to prevent contact and household transmission of infection, paying special attention to the creation drinking regime and basic conditions for personal hygiene (soap, toilet paper);

Laboratory examinations of contact persons for biochemical blood tests are prescribed by a doctor if there are clinical indications;

Final disinfection is carried out in kindergartens and closed children's organizations, provided that children eat, stay and sleep together after isolating the patient from the team (On approval of the Sanitary Rules "Sanitary and epidemiological requirements for the organization and implementation of sanitary and anti-epidemic (preventive) measures to prevent infectious diseases” Decree of the Government of the Republic of Kazakhstan dated January 12, 2012 No. 33;

Specific prevention of HAV is vaccination.

Contingents subject to vaccination:
1. Children from 2 years of age;
2. Contacts in HAV foci under the age of 14 years inclusive in the first 2 weeks from the date of contact;
3. Children under 14 years of age with chronic viral hepatitis B and C in remission.

Vaccination is carried out 2 times with an interval of 6 months. Adverse reactions to the vaccine are not typical. It is allowed to administer the HAV vaccine simultaneously with other vaccines, provided they are administered separately.

Further management
Dispensary observation:
The first examination is 15-30 days after discharge from the hospital, repeated – after 3 months. In the absence of residual effects and complete normalization of liver tests, convalescents are removed from the register. In the presence of residual effects, clinical observation is carried out until complete recovery.

Indicators of treatment effectiveness:
- disappearance of intoxication (restoration of appetite, improvement of well-being);
- normalization of pigment metabolism, liver size;
- complete clinical and laboratory recovery.

Hospitalization

Indications for hospitalization:
1. Planned- severe form of CAA, prolonged course, cholestatic variant.
2. Emergency- with severe severity of CAA.

Information

Sources and literature

1. Minutes of meetings of the Expert Commission on Health Development of the Ministry of Health of the Republic of Kazakhstan, 2013
   1. 1. Treatment of viral hepatitis A.A. Klyuchareva, N.V. Goloborodko, L.S. Zhmurovskaya and others / Ed. A.A. Klyucharevoy – Minsk: Doctor Design LLC, 2003. – 216 p. 2. Mayer K.-P. Hepatitis and consequences of hepatitis: Practical. Hand: Translated from German. / edited by A.A. Sheptulina. // M.: Gzotar medicine, 1999. – 432 p. 3. Uchaikin V.F. Guide to infectious diseases in children // M.: Gzotar Medicine, 2001. - 809 p. 4. Sherlock S., Dooley J. Diseases of the liver and biliary tract: Practical manual: translation from English. / Edited by Z.G. Aprosina, N.A. Mukhina - M.: Geotar Medicine, 1999. - 864 p. 5. Kuntz E., Kuntz H. Hepatology: Principles and practice: history, morphology, biochemistry, diagnosis, clinic, therapy. – Springer – Verlag Berlin, Heidelberg, 2002.- 825 p. 6. Lok A.S., Heathcote E.J., Hoofnagle J.H. Management of Hepatitis B 2000, Summary of a Workshop. Gastroenterology 2001;120:1828-53. 7. Zhang L, Miao L, Liu JF, Fu HC, Ma L, Zhao GZ, Dou XG. Study on the relationship between the serum levels of Th1/Th2 cytokines and the clinical manifestations of chronic hepatitis C and the outcome of interferon therapy // Zhonghua Shi Yan He Lin Chuang Bing Du XueZaZhi. 2009 Oct;23(5):352-4. 8. Al-Ali J, Al-Mutari N, Ahmed el-SF. Hepatitis C virus and the skin //

Information

III. ORGANIZATIONAL ASPECTS OF PROTOCOL IMPLEMENTATION

List of developers:
1. Kuttykozhanova G.G. - Doctor of Medical Sciences, Professor, Head of the Department of Children's Infectious Diseases of KAZ NMU named after. Asfendiyarov.
2. Efendiev I.M. - Candidate of Medical Sciences, Associate Professor, Head of the Department of Children's Infectious Diseases and Phthisiology of Semey State Medical University.
3. Atkenov S. B. - Candidate of Medical Sciences, Associate Professor, Department of Children's Infectious Diseases of JSC " Medical University Astana"

Reviewers:
1. Baesheva D.A. - Doctor of Medical Sciences, Head of the Department of Children's Infectious Diseases of Astana Medical University JSC.
2. Kosherova B. N. - Vice-Rector for Clinical Work and Continuing Professional Development, Doctor of Medical Sciences, Professor of Infectious Diseases of KarSMU

Indication of no conflict of interest: No.

Specifying the conditions for reviewing the protocol:
- changes legal framework Republic of Kazakhstan;
- revision of WHO clinical guidelines; (with completed justification form) coming until March 29, 2019:[email protected] , [email protected] , [email protected]

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Hepatitis is an inflammatory disease of the liver. According to the nature of the course, acute and chronic hepatitis are distinguished. Acute cases occur with severe symptoms and have two possible outcomes: complete cure, or transition to a chronic form.

Different types of hepatitis differ from each other different ways infection, rate of progression, severity of clinical manifestations, treatment methods and prognosis for the patient. Hepatitis is characterized by a specific set of symptoms, which, depending on the type of disease, may be more severe than others.

What is hepatitis?

Hepatitis is an acute or chronic inflammatory disease of the liver that occurs due to infection with specific viruses or the influence of toxic substances on the parenchyma of the organ (for example, alcohol, drugs, drugs, poisons).

Viral hepatitis is a group of common and dangerous infectious diseases for humans, which differ quite significantly from each other, are caused by different viruses, but still have a common feature - it is a disease that primarily affects the human liver and causes its inflammation.

The main signs of hepatitis are– abdominal pain, loss of appetite with frequent nausea and vomiting, headache, general weakness and increased body temperature up to 38.8°C, and in severe cases, yellowing of the skin and eyes.

Types of viral hepatitis

Hepatitis is classified:

• due to development - viral, alcoholic, medicinal, autoimmune hepatitis, specific (tuberculosis, echinococcal, etc.), secondary hepatitis (as complications of other pathologies), cryptogenic (of unclear etiology);
• along the course (acute, chronic);
• according to clinical signs (icteric, anicteric, subclinical forms).

According to the mechanism and routes of infection, they are divided into two groups:

• Having an oral-fecal transmission mechanism (A and E);
• Hepatitis, for which blood contact (hemopercutaneous), or, more simply, the path through the blood, is the main one (B, C, D, G - group of parenteral hepatitis).

Depending on the form of hepatitis, the disease can bother the patient for a long time, and in 45–55% of cases complete recovery occurs. The chronic (permanent) form of viral hepatitis can bother the patient throughout his life.

Hepatitis A or Botkin's disease is the most common form of viral hepatitis. His incubation period(from the moment of infection to the appearance of the first signs of the disease) ranges from 7 to 50 days.

During this period, a person can infect others. Most symptoms usually disappear after a few days or weeks, but the feeling of fatigue may last for months as the liver returns to normal. It takes several months to fully recover.

Viral hepatitis B

Jaundice occurs as a result of a disorder in the metabolism of bilirubin, which is toxic to the body. When liver function is impaired, it accumulates in the blood, spreads throughout the body, depositing in the skin and mucous membranes and giving them a yellowish color.

Most often, as a result of a violation of the outflow of bile from the liver, some of which enters the blood and spreads throughout the body, itching appears: bile acids, deposited in the skin, greatly irritate it.

In some cases, patients develop so-called fulminant acute hepatitis. This is an extremely severe form of the disease, in which there is massive tissue death and extremely rapid development of symptoms. If left untreated, such acute hepatitis ends in death.

Forms of development

During viral hepatitis, 4 forms are distinguished:

1. Mild, more often characteristic of hepatitis C: jaundice is often absent, low-grade or normal temperature, heaviness in the right hypochondrium, loss of appetite;
2. Moderate severity: the above symptoms are more pronounced, joint pain, nausea and vomiting appear, appetite is practically absent;
3. Heavy. All symptoms are present in a pronounced form;
4. Fulminant (fulminant), not found in hepatitis C, but very characteristic of hepatitis B, especially in the case of coinfection (HDV/HBV), that is, a combination of two viruses B and D that cause superinfection.

Complications and consequences for the body

Both acute and chronic hepatitis can lead to very serious consequences. Among them it is worth especially noting:

• inflammatory diseases of the biliary tract;
• hepatic coma (ends in death in 90% of cases);
• Liver cirrhosis – occurs in 20% of patients with viral hepatitis. Hepatitis B and its derivatives most often lead to cirrhosis;
• liver cancer;
• dilation of blood vessels and subsequent internal bleeding;
• accumulation of fluid in the abdominal cavity - ascites.

Treatment of hepatitis

Treatment of hepatitis depends on the etiological factor that caused the inflammatory process in the liver. Of course, hepatitis of alcoholic or autoimmune origin usually requires only symptomatic, detoxification and hepatoprotective treatment.

Standard treatment tactics for hepatitis include:

• eliminating the cause of the disease by destroying the virus and detoxifying the body;
• treatment of concomitant diseases;
• restoration of liver function;
• maintaining normal functioning of the organ;
• compliance special diet and certain sanitary and hygienic protection measures.

Treatment of acute hepatitis

Treatment must be carried out in a hospital. Besides:

• diet No. 5A is prescribed, semi-bed rest (with severe course– bed);
• For all forms of hepatitis, alcohol and hepatotoxic drugs are contraindicated;
• intensive detoxification infusion therapy is performed to compensate for this
• liver function;
• prescribe hepatoprotective drugs (essential phospholipids, silymarin, milk thistle extract);
• prescribe a daily high enema;
• carry out metabolic correction - potassium, calcium and manganese preparations, vitamin complexes.

Diet

Except drug therapy, the patient must follow a diet. Nutrition should be based on the following rules:

• complete exclusion of alcohol (including beer);
• ban on marinades, smoked meats, spicy and fatty foods;
• lean meat and fish are recommended;
• You can consume low-fat dairy products.

Antiviral therapy in tandem with diet and bed rest may lead to complete recovery. However, it should be noted that adherence to dietary nutrition and therapy is required even after recovery. Otherwise, relapse and transition of the disease to chronic viral hepatitis are practically not excluded.

What to eat:

• various teas based on herbs and berries, juices and compotes with a small sugar content;
• ground, well-cooked porridge;
• various soups and vegetable purees;
• low-fat dairy products;
• meat and fish must be low-fat varieties steamed;
• steam omelette;
• bran bread, rye bread, biscuits.

For sweets, you can eat dried fruits, not too sweet jam, honey. Baked apples, bananas and berries in small quantities are useful.

What not to do:

• very strong tea, chocolate, coffee;
• legumes, mushrooms;
• sour, salty, too sweet;
• baked goods, puff pastry products, pancakes, pies;
• sausages and canned meats;
• pork;
• hard-boiled and fried eggs.

Prevention

Prevention is necessary so that viral hepatitis does not return, and in the case of chronic manifestations, it does not worsen or become complicated. Prevention consists of observing the following rules:

• exclusion of alcohol from the diet (completely);
• compliance with all doctor’s recommendations (do not skip appointments, take prescribed medications correctly);
• diet (exclude fried and fatty, salty and spicy foods, canned food and preserves);
• exercise caution when in contact with contaminated biomaterials (applies to healthcare workers), namely, use PPE (protective equipment).

How to protect yourself from hepatitis?

Viral hepatitis often leads to serious and dangerous complications, and their treatment is not only lengthy, but also expensive.

Prevention is as follows:

• Wash your hands before eating
• Boil water before drinking
• Always wash fruits and vegetables and heat-treat food
• Avoid contact with biological fluids other people, including those with blood
• Protect yourself during sexual intercourse (including oral)
• Do piercings and tattoos only with sterile instruments in trusted centers
• Get vaccinated against hepatitis.