Hepatitis, unspecified mcb. Chronic hepatitis C - symptoms, treatment and diagnosis Viral hepatitis C according to microbiology 10

29.08.2020

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Viral hepatitis (B15-B19)

Use additional code (Class XX) if required to indicate the cause of post-transfusion hepatitis.

Excluded:

cytomegalovirus hepatitis (B25.1)
herpesvirus hepatitis (B00.8)
sequelae of viral hepatitis (B94.2)

In Russia, the International Classification of Diseases of the 10th revision (ICD-10) has been adopted as a single normative document to take into account the incidence, reasons for the population's visits to medical institutions of all departments, and causes of death.

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Ministry of Health of Russia dated 05/27/97. No. 170

A new revision (ICD-11) is planned by WHO in 2017 2018.

As amended and supplemented by WHO

Processing and translating changes © mkb-10.com

Source: http://mkb-10.com/index.php?pid\u003d531

Classification of hepatitis according to ICD-10 - disease codes

As a rule, hepatitis (the ICD-10 code depends on the pathogen and is classified in the B15-B19 range), which is a polyetiologic inflammatory liver disease, has a viral origin. Today, in the structure of pathologies of this organ, viral hepatitis occupies the first place in the world. Infectionists-hepatologists treat such an ailment.

Etiology of hepatitis

The classification of the disease is complex. Hepatitis is divided into 2 large groups according to the etiological factor. These are non-viral and viral pathologies. The acute form includes several clinical variants with different causes.

In practice, the following types of non-viral ailment are distinguished:

Inflammatory-necrotic character has a progressive liver damage in the autoimmune variant, that is, if autoimmune hepatitis develops. Own immunity destroys the liver.
As a result of long-term irradiation at doses of more than 300-500 rad for 3-4 months, the radiation variant of inflammation of the liver tissue develops.
Often, necrosis occurs in toxic hepatitis (ICD-10 code K71). Cholestatic type - a very serious liver disease - is associated with the problems of bile flow.
In the structure of this pathology, unspecified hepatitis is determined. Such a disease develops imperceptibly. It is an ailment that has not evolved into cirrhosis. It also does not finish for 6 months.
Against the background of infectious diseases, gastrointestinal pathologies, damage to liver cells of an inflammatory-dystrophic nature develops. This is reactive hepatitis (ICD code K75.2).
Toxic jaundice is divided into a medicinal or alcoholic form, which occurs as a result of the abuse of harmful drinks or medicines. Drug or alcoholic hepatitis develops (ICD-10 code K70.1).
A disease of unknown etiology is cryptogenic hepatitis. This inflammatory process is localized and rapidly progresses in the liver.
The consequence of infection with syphilis, leptospirosis is bacterial inflammation of the liver tissue.

Diseases of viral origin

At the moment, the etiology of each of these pathogens is being studied in detail. In each type of ailment, genotypes were found - subspecies of viruses. Each of them always has its own distinctive features.

Viruses A and E are the least dangerous. Such infectious agents are transmitted through contaminated food and drink, and dirty hands. A month or a half is the period of cure for these types of jaundice. The most dangerous are viruses B and C. These insidious pathogens of jaundice are sexually transmitted, but more often through blood.

This leads to the development of severe chronic hepatitis B (ICD-10 code B18.1). Jaundice of C viral origin (CVHC) often develops asymptomatically before the age of 15. The destructive process gradually occurs in the patient's body with chronic hepatitis C (ICD code B18.2). Unspecified hepatitis lasts at least six months.

If a pathological inflammatory process develops for more than 6 months, a chronic form of the disease is diagnosed. Moreover, the clinical picture is not always pronounced. Chronic viral hepatitis occurs gradually. This form often leads to the development of liver cirrhosis if not properly treated. The described organ of the patient increases, the appearance of its pain is observed.

The mechanism and symptoms of the development of the disease

The main multifunctional cells of the liver are hepatocytes, which play a major role in the functioning of this excretory gland. It is they who become the target of hepatitis viruses and are affected by the causative agents of the disease. Functional and anatomical liver damage develops. This leads to severe disorders in the patient's body.

The rapidly developing pathological process is acute hepatitis, which is in the international classification of diseases of the tenth revision under the following codes:

acute form A - B15;
acute form B - B16;
acute form C - B17.1;
acute form E - B17.2.

The blood test is characterized by high numbers of liver enzymes, bilirubin. In short periods of time, jaundice appears, the patient has signs of intoxication of the body. The disease ends with recovery or chronicity of the process.

Clinical manifestations of the acute form of the disease:

Hepatolienal syndrome. The spleen and liver rapidly increase in size.
Hemorrhagic syndrome. Due to a violation of homeostasis, increased bleeding of blood vessels develops.
Dyspeptic symptoms. These problems are manifested by indigestion.
The color of urine and feces changes. The stool is grayish-white. The urine becomes dark. The mucous membranes and skin acquire a yellow tint. In the icteric or anicteric variant, the form of acute hepatitis, which is considered typical, may occur.
Asthenic syndrome is gradually formed. This is emotional instability, increased fatigue.

Danger of viral jaundice

Of all the pathologies of the hepatobiliary system, the viral type of the disease most often leads to the development of cancer or cirrhosis of the liver.

Due to the risk of the formation of the latter, hepatitis is especially dangerous. The treatment of these pathologies is extremely difficult. Fatal outcome in the case of viral hepatitis is often observed.

Diagnostic tests

Establishing the causative agent of the pathology, identifying the cause of the development of the disease are the purpose of the examination.

Diagnostics includes the following list of procedures:

Morphological studies. Puncture biopsy. A thin hollow needle is used to puncture the tissue for the purpose of examining biopsies.
Instrumental tests: MRI, ultrasound, CT. Laboratory tests: serological tests, liver function tests.

Therapeutic methods of exposure

Specialists, based on the results of the diagnostic examination, prescribe conservative treatment. Specific etiological therapy is aimed at eliminating the causes of the disease. In order to neutralize toxic substances, detoxification is mandatory.

Antihistamines are indicated for various types of ailment. Diet therapy is required. A balanced, sparing diet is essential for hepatitis.

At the first signs of trouble, it is important to contact an experienced specialist in a timely manner.

Source: http://ogepatite.ru/vidy/kod-po-mkb-10.html

Acute and chronic viral hepatitis

Chronic viral hepatitis (CVH) is a chronic inflammation of the liver caused by hepatotropic viruses, continuing without a tendency to improve for at least 6 months.

The vast majority of CVH cases are caused by hepatitis B, C and D viruses. The role of other hepatotropic viruses (virus G, TTV, SEN, etc.) has not yet been fully understood.

B18 Chronic hepatitis

B18.0 Chronic viral hepatitis B with delta agent

B18.1 Chronic viral hepatitis B without delta agent

B18.2 Chronic viral hepatitis C

B18.8 Other chronic viral hepatitis

B18.9 Chronic viral hepatitis, unspecified

Abbreviations: HBV - hepatitis B virus; HCV - hepatitis C virus; HDV - hepatitis D virus.

EXAMPLE FORMULATING A DIAGNOSIS

In the absence of data from a morphological study, it is possible to assess the activity of the process by the severity of the cytolysis syndrome (see the section "Classification").

Hepatitis B is one of the most common infections. In the world, there are approximately 300 million patients with CVH B (approximately 5% of the total population). Every year from liver damage associated with HBV-infection, at least people die (ninth place in the structure of total mortality). The prevalence of HBV infection in individual countries varies considerably.

■ Regions with a low prevalence (up to 2% of the population) include the USA, Canada, Western Europe, Australia, New Zealand.

■ Regions with medium prevalence (3-5%) include Eastern Europe, Mediterranean countries, Japan, Central Asia and the Middle East, and Central and South America.

■ Regions with a high prevalence (10–20%) (endemic areas) include South Asia, China, Indonesia, countries in tropical Africa, the Pacific Islands, and Alaska.

The causative agent of HBV infection is a DNA virus from the Hepadnaviridae family. The main route of transmission is parenteral (injection, blood transfusion), as well as through damaged mucous membranes and skin (perinatally, during sexual intercourse). Hepatitis B is characterized by high contagiousness - infection is possible if an insignificant amount of infected material (0.0001 ml of blood) gets on damaged skin or mucous membranes. The virus is stable in the external environment, at room temperature it retains its pathogenicity in dried blood for at least 7 days.

The frequency of individual transmission methods varies greatly from region to region. In countries with a low prevalence, infection most often occurs through sexual contact and parenteral (in risk groups). In contrast, in countries with medium and especially high prevalence, the leading route of infection is perinatal.

The main HBV Ags are surface (Australian) (HBsAg), medullary (HBcAg), which is found only in hepatocytes, and a viral replication marker (HBeAg). HBsAg, HBeAg, antibodies to them and to HBcAg (anti-HBs, anti-HBe, anti-HBc), as well as HBV DNA are the most significant serological markers of hepatitis B (for more details, see the Diagnostics section).

According to WHO, there are at least 170 million HCV infected in the world. The prevalence of HCV infection also varies considerably in different regions - from 0.01–0.02% in Western Europe to 6.5% in tropical Africa. CVH C is the most common form of chronic liver disease in most European countries and North America. The total number of HCV-infected in Russia is more than 1 million 700 thousand people. HCV infection is the cause in about 40% of cases of chronic liver disease.

The disease is caused by an RNA virus from the Flaviviridae family. The main route of transmission is parenteral. Sexual and perinatal transmission are also possible, but are of less importance due to the relatively low (compared to HBV) contagiousness of the virus. HCV is genetically heterogeneous - there are 6 main genotypes (1–6) and at least 50 subtypes. On the territory of the Russian Federation, genotypes 1b and 3a are most common.

The genotype of the virus is of fundamental importance for treatment: the effectiveness of antiviral drugs is significantly lower in infections associated with genotype 1 (no more than 50%), compared with genotypes 2 and 3 (up to 80–90%).

The main serological markers of hepatitis C are anti-HCV antibodies (anti-HCV) and viral RNA.

HDV infection is most common in southern Europe, North Africa, the Middle East, and Central and South America; in some regions, its prevalence can reach 47%. There are approximately 15 million patients with hepatitis D worldwide. The incidence of HDV infection in patients with CVH B averages approximately 10% (US data).

The disease is caused by an incomplete RNA virus (HDV, δ virus), which requires HBV for expression and pathogenicity. The routes of transmission are similar to those of HBV infection. The disease can occur in the form of acute infection with simultaneous infection with HBV and δ-virus (coinfection) or acute infection with HDV infection of HBV carriers or CVH B patients (superinfection). Hepatitis D is usually severe and is characterized by low efficacy of specific therapy and a poor prognosis. Serological markers - AT kAg HDV (anti-HDV) and viral RNA.

■ For screening for HBV infection, an ELISA test for HBsAg is used. The study is carried out in the following categories of the population.

✧All pregnant womenC on their first visit to the doctor. Re-examination (with negative results of the first) is carried out in the third trimester, if the woman is at risk. If the results are positive, urgent prophylaxis of infection in the newborn is required (see section "Prevention").

✧ In individuals at risk of HBV infection (however, no risk factors can be established in at least 30–40% of acute viral hepatitis B patients):

- homosexuals and men who practice bisexual sex;

- Persons using intravenous drugs;

- Persons leading a promiscuous sex life;

- victims of sexual violence;

- patients of hemodialysis departments;

- patients with other sexually transmitted diseases;

- migrants from regions endemic for HBV infection;

- sexual partners of patients with acute or chronic viral hepatitis B or persons who are in close household contact with them;

- medical workers (within the framework of annual preventive examinations);

- law enforcement officers;

- persons who are in places of deprivation of liberty.

✧ In patients with symptoms of acute or chronic hepatitis of unclear etiology, or when an increased activity of ALT and / or AST in the blood serum is detected, not associated with other diseases.

✧ Routine screening in the general population is economically feasible if the prevalence of HBV infection is 20% or higher.

■ For screening for HCV infection, anti-HCV ELISA is used (the sensitivity of this method reaches 98.8%, the specificity is 99.3%).

✧If positive results are obtained, it is necessary to confirm the infection by determining the HCV RNA in the blood using PCR. The presence of anti-HCV in the blood in the absence of viral RNA usually indicates that the patient has had a disease in the past. The exception is patients with immunodeficiency (including those on hemodialysis and after organ transplantation), in whom anti-HCV in the blood may be absent in the presence of HCV RNA.

✧The same populations are screened as for HBV infection (excluding pregnant women). Since in developed countries, the main route of transmission of the disease is parenteral, special attention should be paid to people who use drugs. Approximately 80% of drug-injecting drug users become infected with HCV within 1 year. Moreover, infection is possible with the use of drugs that are not administered parenterally. In particular, cases of HCV infection associated with the use of cocaine and other intranasally administered drugs (when using a common inhalation tube) have been described.

■ Routine screening for HDV infection (definition of anti-HDV) is usually not done and is possible in individuals who have migrated from areas endemic for hepatitis D.

Specific prophylaxis has been developed only for hepatitis B.

■ Since the main routes of transmission of HBV and HCV in developed countries are parenteral and sexual, measures to prevent drug addiction and promiscuity are of fundamental importance.

■ Blood products and organs for transplantation are subject to mandatory testing for markers of viral hepatitis (and other parenteral infections). To prevent iatrogenic infection, any medical instruments used for invasive medical and diagnostic procedures must be sterilized in accordance with established standards.

■ Health care workers should be extremely careful when handling infectious materials (blood and other body fluids) or medical instruments that have come into contact with them (especially syringes). When handling potentially infectious material, use personal protective equipment (gloves, mask, goggles, etc.). The risk of HBV / HCV infection from a single needle stick injection into a patient with HBV / HCV infection is 33% and 10%, respectively.

Vaccination against hepatitis B is indicated for all infants and children under 12 years of age, as well as adolescents and adults at risk of B. In the Russian Federation, genetically engineered recombinant vaccines are used for this purpose.

■ All newborns must be vaccinated.

✧ Newborns born to women with HBV infection should be vaccinated within the first 12 hours of life, while immunoglobulin against human hepatitis B (0.5 ml) is injected; these measures allow in most cases (80–98%) to prevent infection B. In the absence of specific prophylaxis, the risk of developing HBV infection is very high (from 30 to 90%), with CVH B developing in 90% of cases.

✧In other cases, the first dose is usually administered in the maternity hospital (or during the first 2 months of life), and the second and third doses 1 and 6 months after the first. Vaccination of newborns is cost-effective and can significantly reduce the incidence of CVH B and hepatocellular carcinoma in the pediatric population. The simultaneous administration of the hepatitis B vaccine and other vaccines is acceptable (but the injection sites must be different).

■ If vaccinations are not given in the first year of life, vaccinations should be given before age 12B (after this age, the incidence of hepatitis B increases significantly).

■ Compulsory vaccinations are also required for adolescents and adults at risk of HBV infection (see Screening section). Testing for HBsAg and anti-HBs is required prior to this. If HBsAg or HBsAg is detected in the blood and anti-HBs in diagnostic titers (i.e. signs of HBV infection), vaccination is not indicated. Also, there is no need for vaccination if only anti-HBs is detected in a protective titer (which indicates that the patient has already had acute hepatitis B).

■ Vaccination is also advisable in patients with CVH C and other chronic liver diseaseC, because HBV infection in such cases is severe and has a poor prognosis. However, the effectiveness of vaccination in patients with decompensated liver pathology is rather low.

Children of the first year of life are injected with the vaccine in the anterolateral region of the thigh, in other cases - in the deltoid muscle. The immunogenicity of the vaccine is lower in obesity, HIV infection, chronic diseases, smoking, as well as in the elderly. Patients on hemodialysis need large doses. The use of the vaccine is safe and does not lead to the development of neurological complications.

For emergency prevention of HBV infection, immunoglobulin against human hepatitis B and vaccination are used. If infected blood gets on damaged skin or mucous membranes, incidents associated with injections / cuts with infected medical instruments, sexual contact with a patient with HBV infection, immunoglobulin against human hepatitis B (0.06 ml / kg) is administered and a full course of vaccination is carried out. Immunoglobulin and vaccine can be given at the same time (but the injection sites must be different). Immunoglobulin administration should be carried out as soon as possible (no later than 7 days after the incident). If titrant-HBs is more than 10 million IU / ml, only vaccination can be limited. In case of household contact with a patient with HBV infection, vaccination is also sufficient.

The classification of chronic hepatitis, adopted at the International Congress of Gastroenterology in Los Angeles (USA) in 1994, is based on the etiological factor with additional information about the activity of the process and the stage of fibrosis (Tables 4-7).

Table 4-7. Classification of chronic hepatitis

Chronic viral hepatitis (not otherwise characterized)

Chronic hepatitis, not classified as viral or as autoimmune

Chronic drug hepatitis

Primary biliary cirrhosis

Primary sclerosing cholangitis

Liver disease due to α 1 -antitrypsin deficiency

Low (index of histological activity 4-8 points)

Moderate (index of histological activity 9-12 points)

High (index of histological activity 13-18 points)

1 - mild (periportal) fibrosis

2 - moderately pronounced fibrosis (port-portal septa)

3 - severe fibrosis (port-central septa)

4 - liver cirrhosis

The degree of activity of chronic hepatitis is established by the results of histological examination of liver tissue (Knodel system, Tables 4-8), as well as by the degree of increase in the activity of ALT and AST: 1.5–2 times more than the norm - minimal, 2–5 times - low, 5-10 times - moderate, more than 10 times - pronounced. The stage of fibrosis is determined on the basis of pathomorphological examination of liver biopsies (see table. 4-8).

Table 4-8. The index of histological activity (according to Knodell R. et al.) And the index of fibrosis (according to Sciot J., Desmet V.)

Note: The maximum score (excluding fibrosis) is 18.

The diagnosis of CVH is based on the data of the patient's clinical examination, biochemical blood tests (liver function tests) and studies for serological markers of hepatitis B viruses.

ANAMNESIS AND PHYSICAL EXAMINATION

ACUTE VIRAL HEPATITIS B

■ The duration of the incubation period for acute viral hepatitis B is from 30 to 180 days (usually 2–3 months). Depending on the presence and severity of the main symptoms of the disease, typical and atypical (anicteric, subclinical) forms are distinguished.

✧Typical form is characterized by a cyclical course with a sequential change of three periods: initial (preicteric), high (icteric) and convalescence.

–The preicteric period is 3–15 days and is characterized by symptoms of intoxication (fever, general weakness, lethargy, apathy, irritability, sleep disturbances, decreased appetite), arthralgia, pain in the right hypochondrium. In some cases, a skin rash (spotty, maculopapular or urticarial) is observed. In the last 1-2 days of the preicteric period, feces discoloration and urine darkening occur.

- The icteric period (the peak period) lasts from 10-14 to 30-40 days. The mucous membranes and sclera, and then the skin, acquire an icteric coloration. With the onset of jaundice, symptoms of intoxication usually worsen. In parallel with the growth of jaundice, the liver increases in size. In 30-50% of cases, an increase in the spleen is observed. At the height of the disease, bradycardia, a decrease in blood pressure, a weakening of heart sounds are found with great constancy. In severe forms, central nervous system depression of varying severity, dyspeptic and hemorrhagic syndromes develop. Separately, the fulminant form is distinguished due to massive necrosis of hepatocytes with the development of acute liver failure (frequency - 0.1-0.5%, which is approximately 10% of all cases of acute liver failure).

–The period of convalescence begins from the moment the jaundice disappears and ends after complete clinical and laboratory resolution of the disease, which usually occurs 3 months after its onset (in case of a prolonged course - after 6 months).

✧In the anicteric form, there is no icterus of the skin and mucous membranes, the rest of the symptoms are usually mild.

✧ The subclinical form is characterized by a complete absence of clinical manifestations. The diagnosis can only be made on the basis of laboratory tests.

■ The frequency of chronic HBV infection depends on many factors, but to the greatest extent on age and the state of the immune system.

■ After HBV infection, chronic hepatitis develops in 90% of newborns, 20–50% of children aged 1–5 years, and 5% of adolescents and adults.

■ The risk of chronicity is higher with immunodeficiency of any etiology (patients on hemodialysis, HIV-infected, receiving immunosuppressive therapy, etc.).

ACUTE VIRAL HEPATITIS C

■ The incubation period is usually 20–90 days. Acute viral hepatitis C is usually mild, predominantly anicteric or subclinical. It is diagnosed relatively rarely (no more than 20% of all cases of acute viral hepatitis), mainly in cases when the disease is accompanied by jaundice, or during dispensary observation of persons after incidents accompanied by the risk of infection. The most common symptoms are anorexia, nausea, vomiting, discomfort in the right hypochondrium, and sometimes jaundice (in less than 25% of patients). Symptoms usually persist for 2–12 weeks. Fulminant forms of acute viral hepatitis C are very rare.

■ The risk of chronic HCV infection is very high: more than 80% of patients who have had acute viral hepatitis C have HCV RNA in their blood. The risk of developing CVH C is slightly lower in children and patients with clinically manifest forms of acute viral hepatitis C.

ACUTE VIRAL HEPATITIS D

The clinical manifestations of coinfection (simultaneous infection with HBV and HDV) are generally identical to those in acute viral hepatitis B. Features include a shorter incubation period, the presence of prolonged fever with a body temperature of 39–41 ° C, the frequent appearance of skin rashes and migratory pain in large joints. The course is relatively favorable, the risk of chronicity practically does not exceed that of HBV infection. Acute viral hepatitis D due to superinfection (HDV infection of a person infected with HBV) is rarely observed, it is characterized by a severe course with frequent development of fulminant forms and a high risk of transformation into CVH (up to 90%).

CHRONIC VIRAL HEPATITIS

The clinical manifestations of CVH are quite polymorphic and include a wide range of symptoms associated with damage to both the liver and other organs and systems, mainly due to the formation of immune complexes and the development of autoimmune reactions. In many cases, CVH occurs with minimal clinical manifestations or generally asymptomatic.

■ Dyspeptic syndrome (nausea, aggravated after eating and taking drugs, vomiting, bitterness in the mouth, belching, diarrhea) is associated with impaired detoxification function of the liver, concomitant pathology of the duodenum, biliary system and pancreas.

■ Asthenic syndrome (weakness, fatigue, decreased performance, irritability, decreased mood) is more or less pronounced in most patients with CVH.

■ Signs of liver damage.

✧With an active process, the liver is usually enlarged, hardened and painful.

✧ Jaundice (parenchymal) is relatively rare.

✧Telangiectasias and palmar erythema are caused by an increase in estrogen concentration and a change in the sensitivity of vascular receptors (opening and expansion of arteriovenous shunts). Their severity correlates with the activity of the process and does not always indicate liver cirrhosis. Improvement of the functional state of the liver is accompanied by a decrease in the number of vascular "asterisks" or their disappearance, the hyperemia of the palms persists much longer (often until biochemical remission).

■ As liver cirrhosis progresses, portal hypertension develops (ascites, splenomegaly, esophageal varicose veins, etc.), signs of liver failure appear and intensify for the first time (see the article "Liver cirrhosis").

■ Amenorrhea, gynecomastia, decreased sex drive are associated with impaired metabolism of sex hormones in the liver (usually at the stage of cirrhosis).

■ Extrahepatic manifestations in CVH B are rare (in approximately 1% of patients) and are usually represented by kidney damage, polyarteritis nodosa, or cryoglobulinemia. Somewhat more often, extrahepatic manifestations develop in CVH C. Cryoglobulinemia, membranous glomerulonephritis, late cutaneous porphyria, autoimmune thyroiditis, less often - Sjogren's syndrome, lichen planus, seronegative arthritis, aplastic anemia, B-cell lymphoma are possible.

■ Clinical blood test: possible increased ESR, leukopenia, lymphocytosis, with fulminant form of acute viral hepatitis - leukocytosis.

■ General urine analysis: in acute viral hepatitis and exacerbation of CVH, the appearance of bile pigments, mainly direct bilirubin, urobilin, is possible.

■ Biochemical blood test.

✧Cytolysis syndrome: increased activity of ALT, AST. It is typical for all clinical variants of acute viral hepatitis and for most cases of CVH (ALT can be normal in 40% of patients with CVH C).

✧ Cholestasis syndrome: increased activity of alkaline phosphatase, GGTP, cholesterol content, total bilirubin (due to bound bilirubin). Usually seen with jaundice; it is necessary to exclude other causes of liver damage.

✧Syndrome of mesenchymal inflammation: an increase in the content of immunoglobulins, an increase in the thymol test, a decrease in the sublimate test. It is characteristic of all clinical variants of acute viral hepatitis and exacerbation of CVH.

✧Syndrome of hepatocellular failure: a decrease in the prothrombin index, serum albumin concentration, cholesterol, an increase in total bilirubin (due to indirect bilirubin); typical for severe forms of acute viral hepatitis and the transformation of CVH into cirrhosis of the liver with the development of liver failure.

■ Markers of hepatitis viruses (Table 4-9).

Table 4-9. Serologic markers of HBV infection

* A more correct term is "latent HBV infection".

✧HBV: HBsAg, anti-HBs, HBeAg, anti-HBe, anti-HBc IgM, anti-HBc IgG, HBV DNA.

–HBsAg can be detected in the blood 1–10 weeks after infection; its appearance precedes the development of clinical symptoms and an increase in ALT / AST activity. With an adequate immune response, it disappears 4–6 months after infection, approximately in the same period anti-HBs are detected (during the period of the “serological window”, when HBsAg has already disappeared, and antibodies to it have not yet appeared, the diagnosis can be confirmed by the detection of anti- HBc IgM). Anti-HBs are also produced during the vaccination process. It should be borne in mind that in the fulminant form of acute viral hepatitis B, HBsAg may be absent.

–HBeAg indicates viral replication in hepatocytes; detected in serum almost simultaneously with HBsAg, absent in HBV infection caused by a mutant virus strain (with a change in the genetic code in the "precore-region" and impaired HBeAg secretion). Anti-HBe (AT to e-Ag) is a serological marker of virus integration; in combination with anti-HBc IgG and anti-HBs indicates the complete completion of the infectious process.

–Anti-HBc (AT to nuclear Ag) is an important diagnostic marker of infection. Anti-HBc IgM is one of the earliest serum markers of CVH B; sensitive marker of HBV infection. Indicates viral replication and activity in the liver. Its disappearance is an indicator of either the sanitation of the organism from the pathogen, or the development of the integrative phase of HBV infection. Anti-HBc IgG persists for many years, indicating an existing or previous infection.

–HBV-DNA (HBV DNA) and DNA polymerase are diagnostic markers of viral replication.

✧The diagnosis of acute viral hepatitis B is confirmed by the detection of HBsAg and anti-HBc IgM in the blood. With the elimination of the virus (recovery), HBsAg should disappear from the blood no later than 6 months after the onset of the disease (in rare cases, it can persist up to 12 months).

✧ With chronic HBV infection (CVH B or virus carriage), HBsAg from the blood does not disappear (persists for more than 6 months).

✧HCV: anti-HCV, HCV-RNA.

–HCV RNA is the earliest biochemical marker of infection; it occurs within a few days to 8 weeks after infection. In cases of recovery from acute viral hepatitis C, viral RNA disappears from the blood within 12 weeks (no later than 20 weeks) after the first symptoms appear. The likelihood of spontaneous elimination of the virus while maintaining HCV RNA beyond the specified time frame is doubtful.

–Anti-HCV is determined in the blood no earlier than 8 weeks after infection. About half of patients with clinically manifest acute viral hepatitis C have anti-HCV in their blood at the onset of the disease. In subclinical infection, AT is usually detected much later - on average, 41 weeks after the appearance of the virus RNA in the blood.

✧НDV: anti-HDV IgM, HDV RNA (HDV replication marker).

ADDITIONAL EXAMINATION METHODS

■ Stool analysis: a decrease in the content or absence of stercobilin due to the cessation of the flow of bile into the intestine. The appearance of stercobilin in the feces during the icteric period of acute viral hepatitis is evidence of the resolution of jaundice.

■ Concentration in blood of α-fetoprotein (screening for hepatocellular carcinoma).

■ Additional laboratory tests are necessary for differential diagnosis with other chronic liver diseases (markers of autoimmune hepatitis, ceruloplasmin concentration and daily urinary copper excretion, ferritin concentration, transferrin saturation, etc., see the article "Liver cirrhosis").

MANDATORY EXAMINATION METHODS

■ Ultrasound of the liver and spleen: characterized by increased echogenicity of the parenchyma, induration along the vessels of the liver, with cirrhosis of the liver, splenomegaly is possible.

■ Liver biopsy: Although diagnosis is possible without this test, liver biopsy is advisable in most CVH cases to assess the extent of liver damage and to plan specific antiviral therapy C.

ADDITIONAL RESEARCH METHODS

■ CT scan of the abdominal organs: in case of difficulties in establishing a diagnosis or the need for differential diagnosis, for example, with volumetric processes in the liver.

■ FEGDS: to exclude concomitant pathology of the upper gastrointestinal tract, to identify varicose veins of the esophagus (usually in liver cirrhosis).

It is necessary to carry out differential diagnosis of CVH with other chronic liver diseases: alcoholic liver disease, autoimmune hepatitis, hemochromatosis, Wilson-Konovalov disease, etc. Detection of markers of hepatitis viruses is of the greatest diagnostic value, and in doubtful cases - the results of liver biopsy. The issues of differential diagnosis of chronic liver diseases are described in detail in the article "Liver cirrhosis".

INDICATIONS FOR CONSULTATION OF OTHER SPECIALISTS

■ Related specialists (nephrologist, hematologist, dermatologist, rheumatologist): with the development of extrahepatic manifestations of CVH.

■ Psychiatrist: with the development of severe depression or other mental disorders associated with therapy with interferon drugs.

■ Acute viral hepatitis: relief of the main symptoms of the disease and prevention of chronicity of the process and the development of complications.

■ CVH: stable suppression of viral replication, and, as a result, the achievement of remission of the disease.

INDICATIONS FOR HOSPITALIZATION

All patients with acute viral hepatitis are hospitalized in an infectious diseases hospital. In the case of a mild course of acute viral hepatitis and compliance with sanitary and anti-epidemic measures, treatment at home is possible (the question is decided by the attending physician). In CVH, hospitalization is indicated in case of an exacerbation of the disease or the development of complications (bleeding from varicose veins of the esophagus, spontaneous bacterial peritonitis, hepatorenal syndrome, hepatic encephalopathy, ascites, etc.).

■ In acute viral hepatitis and exacerbations of CVH, it is necessary to adhere to bed or semi-bed (depending on the severity of the condition) regimen.

■ A balanced diet is essential. The intake of proteins, sodium and fluids is limited only for decompensated liver cirrhosis.

■ It is advisable to vaccinate against hepatitis A. Hepatitis A in patients with chronic liver disease, including CVH, is difficult. Vaccination against hepatitis A for CVH B is safe and effective.

■ In acute viral hepatitis, treatment is mainly symptomatic - detoxification infusion therapy, enterosorbents, ursodeoxycholic acid for severe cholestasis, in severe cases - proteolysis inhibitors and glucocorticoids, but their effectiveness is questionable.

■ Specific antiviral therapy is indicated for acute viral hepatitis C. Usually, interferon alfa is used 5 million IU subcutaneously daily for 4 weeks, then 5 million IU subcutaneously 3 times a week for 20 weeks, which can significantly reduce the risk of CVH C. Alternative option - the appointment of peginterferon alfa2a (180 mg / week) or peginterferon alfa2b (1.5 μg / kg per week for 6 months). The transition to the use of peginterferon alfa2b in combination with ribavirin is indicated in the absence of the effect of monotherapy with interferon alfa for 3 months (preservation of HCV RNA in the blood). In patients with clinically manifest forms of acute viral hepatitis C, treatment is started when HCV RNA remains in the blood 12 weeks after the onset of the disease (if it is absent, repeated triple studies with an interval of 3 months are required). When diagnosing asymptomatic forms of acute viral hepatitis C, treatment should be started immediately.

CHRONIC VIRAL HEPATITIS B

■ Antiviral therapy for CVH B is indicated for patients at high risk of developing progressive liver damage B. Interferon alfa and lamivudine are used. Their effectiveness is approximately the same, the choice of a particular drug is carried out on an individual basis (portability, availability, etc.). The criteria for the effectiveness of therapy are the normalization of the activity of ALT, HBV DNA and HBeAg (with or without the appearance of anti-HBe), a decrease in necrotic and inflammatory changes in the liver (according to biopsy data).

✧The drug of choice - interferon alpha A. Treatment is carried out with CVH B, accompanied by an increase in ALT activity (with an initially normal ALT level, it is possible to induce an increase in ALT with glucocorticoids), an HBV DNA titer of 108 / l or more, signs of chronic hepatitis according to liver biopsy in the absence of liver decompensation.

–Doses of interferon alfa in the treatment of HBeAg-positive patients are 9-10 million IU 3 times a week for 4-6 months. If HBeAg is absent in the blood serum (“precore” mutant variant), the course of treatment should be long - 12 months.

- Persistent disappearance of HBeAg / HBV DNA occurs in 25–40% of patients receiving interferon alpha therapy.

- The most common side effects are flu-like symptoms, myelotoxicity, depression and other mental disorders. With the development of severe side effects, it is necessary to reduce the dose (in 10–40% of patients) or to cancel the drug (in 10%). With prolonged therapy, the need for prophylactic antidepressants should be considered.

✧Lamivudine is prescribed 100 mg / day orally. In HIV-infected patients, the dose is increased to 150 mg / day (other antiretroviral drugs are prescribed at the same time). The duration of the course of treatment is 1 year. In the absence of effect, longer courses are acceptable, which is also shown in HBeAg-negative variant. After 1 year of treatment, persistent disappearance of HBeAg and HBV DNA is observed in 16-18% of cases, histological improvement - in 46-56%. At 24 and 36 months, HBeAg seroconversion was observed in 27 and 33%. The probability of occurrence of mutant strains resistant to lamivudine is 14, 38 and 49% after 1, 2 and 3 years of treatment, respectively (clinical signs of exacerbation of hepatitis develop). Tolerance to lamivudine is usually good (side effects occur no more often than with placebo). After the end of the course of treatment, an exacerbation of the disease is possible, so the patient must be observed for at least 1 year.

–Severe heart disease;

–Pregnancy or impossibility of effective contraception;

–After organ transplantation (except liver) or red bone marrow;

–Decompensated liver cirrhosis or hepatocellular carcinoma;

–Granulocytopenia less than 1.5 109 / l or thrombocytopenia less than 90 109 / l;

–Active or difficult to treat autoimmune diseases (ulcerative colitis, psoriasis, hyperthyroidism, systemic lupus erythematosus);

CHRONIC VIRAL HEPATITIS C

■ Antiviral therapy for CVH C is indicated in patients with high disease activity (serum HCV RNA, elevated ALT activity, signs of moderate or severe chronic hepatitis in liver biopsies) and compensated liver functions A. Child-Pugh Class B cirrhosis should be treated by a physician experienced in treating such patients.

✧ Usually, a combination therapy is carried out: peginterferon alfa2b 1.5 μg / kg subcutaneously once a week or peginterferon alfa2a 180 μg / kg subcutaneously once a week in combination with ribavirin, the dose of which depends on body weight (less than 65 kg - 800 mg / days, 65–80 kg - 1000 mg / day, 86–105 kg - 1200 mg / day, more than 105 kg - 1400 mg / day).

–With CVH C caused by HCV genotype 1, combination therapy with a low level of viremia is carried out for 6 months, with a high level - 12 months.

–In CVH C caused by HCV genotypes 2 or 3, treatment is continued for 6 months (longer courses are necessary only for liver cirrhosis).

–Early virological response (HCV RNA control) is determined after 3 months. If the test remains positive, further treatment should be changed.

–The effectiveness of combination therapy (persistent disappearance of HCV RNA) is on average 40-50% (20-30% for HCV genotype 1, 60-70% for HCV genotypes 2 and 3).

✧ Monotherapy with peginterferon alfa2b (1 μg / kg subcutaneously 1 time per week) or peginterferon alfa2a (180 μg / kg subcutaneously 1 time per week) is performed if there are contraindications to ribavirin (most often renal failure). The effectiveness of therapy is assessed in the same way as in combination therapy, but after 6 months. When the HCV RNA titer disappears or decreases, treatment is continued for up to 1 year, otherwise the therapy is stopped. The effectiveness of monotherapy is 23-25%. Even if elimination of HCV RNA is not achieved, treatment with interferons slows the progression of the disease and reduces the risk of developing hepatocellular carcinoma.

✧ Side effects are similar to those with interferon alpha; in addition, the development of hemolysis and dysfunction of the thyroid gland are possible (in 5-10% of cases). With the development of pronounced side effects, the doses of drugs are reduced or canceled. Short-term (less than 2 weeks) drug withdrawal does not affect the effectiveness of therapy.

■ Antiviral therapy is not justified in patients with low disease activity B (in particular, with a long course of the disease with minimal histological activity and normal ALT levels).

■ Contraindications to ribavirin treatment.

–The presence of severe heart disease;

- renal failure in the terminal stage;

–Pregnancy or impossibility of effective contraception.

–Uncontrolled arterial hypertension;

Once infected with the hepatitis C virus, most people who are infected develop chronic hepatitis C. The probability is about 70%.

Chronic hepatitis C develops in 85% of patients with an acute form of infection. During the development of the disease, a chain of acute viral hepatitis → chronic hepatitis → liver cirrhosis → hepatocellular cancer is quite likely.

Please note that this article contains only general current understanding of chronic hepatitis C.

Chronic viral hepatitis C - symptoms Much more dangerous is the chronic form - the disease lasts for a long time asymptomatically, only chronic fatigue, lack of energy and lack of energy signal the disease.

CHRONIC HEPATITIS C

Chronic hepatitis Cis an inflammatory liver disease caused by the hepatitis C virus, which has not improved for 6 months or more. Synonyms: Chronic viral Hepatitis C (HCV), Chronic HCV infection (from the English hepatitis C virus), chronic hepatitis C.

Viral hepatitis C was discovered only in 1989. The disease is dangerous to those, it is practically asymptomatic and does not manifest itself clinically. Acute viral hepatitis C only in 15-20% of cases ends with recovery, the rest become chronic.

Depending on the degree of activity of the infectious process, chronic viral hepatitis with minimal, mild, moderate, pronounced activity, fulminant hepatitis with hepatic encephalopathy are isolated.

Chronic viral hepatitis C with a minimal degree of activity (chronic persistent viral hepatitis) occurs in conditions of a genetically determined weak immune response.

ICD-10 CODE B18.2 Chronic viral hepatitis C.

Epidemiology of hepatitis C

The prevalence of chronic HCV infection in the world is 0.5-2%. Areas with a high prevalence of viral hepatitis C are distinguished: isolated settlements in Japan (16%), Zaire and Saudi Arabia (\u003e 6%), etc. In Russia, the incidence of acute HCV infection is 9.9 per 100,000 population (2005) ...

Chronic viral hepatitis C over the past 5 years has come out on top in terms of morbidity and severity of complications.

There are 6 main genotypes of the hepatitis C virus and over 40 subtypes. This is the reason for the high incidence of chronic viral hepatitis C.

PREVENTION OF HEPATITIS C

Non-specific prophylaxis - see "Chronic hepatitis B".
Research results indicate a low probability of sexual transmission of HCV infection. A vaccine to prevent hepatitis C is under development.

Chronic hepatitis C is one of the main causes of liver transplants.

SCREENING

Determine the total antibodies to the hepatitis C virus (anti-HCV). Confirmation of a positive ELISA result by recombinant immunoblotting is recommended.

ROUTES OF HEPATITIS C INFECTION, ETIOLOGY

The causative agent is an enveloped RNA-containing virus with a diameter of 55 nm of the Flaviviridae family. The virus is characterized by a high frequency of mutations in the genome regions encoding the E1 and E2 / NS1 proteins, which determines the significant variability of HCV infection and the possibility of simultaneous infection with different types of the virus.

Transmission of infection occurs by hematogenous route, less often through sexual contact or from an infected mother to the fetus (3-5% of cases).

The hepatitis C virus is transmitted through blood. Sexual transmission is not relevant and sexual transmission of the hepatitis C virus is rare. Transmission of the virus from the mother during pregnancy is also extremely rare. Breastfeeding is not prohibited for hepatitis C, but caution should be exercised when blood appears on the nipples.

You can get infected with the virus when getting tattoos, piercing, visiting a manicure room, medical manipulations with blood, including blood transfusion, administration of blood products, operations, at the dentist. It is also possible to become infected with the general use of toothbrushes, shaving razors, and manicure supplies.

It is impossible to become infected with the hepatitis C virus through household contacts. The virus is not transmitted by airborne droplets, shaking hands, hugging and sharing utensils.

After the virus enters the human blood, it enters the liver with the blood stream, infects the liver cells and multiplies there.

SYMPTOMS OF HEPATITIS C - CLINICAL PICTURE

Chronic viral hepatitis FROM proceeds, as a rule, with a poor clinical picture and a transient level of transaminases.

In most cases, the disease is asymptomatic. Asthenic syndrome is detected in 6% of patients. Dull, intermittent pain or heaviness in the right hypochondrium is often observed (these symptoms are not directly related to HCV infection), less often - nausea, decreased appetite, pruritus, arthralgia and myalgia.

Extrahepatic clinical manifestations of viral hepatitis C:

often mixed cryoglobulinemia - manifested by purpura, arthralgia.
damage to the kidneys and rarely the nervous system;
membranous glomerulonephritis;
sjogren's syndrome;
lichen planus;
autoimmune thrombocytopenia;
late cutaneous porphyria.

DIAGNOSTICS OF HEPATITIS C

Anamnesis allows you to get information about the possible route of infection and sometimes about the previous acute hepatitis C.

Physical examination for hepatitis C

At the pre-cirrhotic stage, it is not very informative, there may be minor hepatomegaly. The appearance of jaundice, splenomegaly, telangiecasia indicates decompensation of liver function or the addition of acute hepatitis of a different etiology (HDV, alcoholic, drug hepatitis, etc.).

Laboratory tests for hepatitis C

Biochemical blood test for hepatitis C:Cytolytic syndrome reflects the activity of transaminases (ALT and AST). However, their normal values \u200b\u200bdo not exclude the cytological activity of hepatitis. In chronic hepatitis C, ALT activity rarely reaches high values \u200b\u200band is subject to spontaneous fluctuations. Constantly normal activity of transaminases and 20% of cases does not correlate with the severity of histological changes. Only with increased ALT activity 10 times or more is it possible (with a high degree of probability to assume the presence of bridging liver necrosis)

According to prospective studies, in about 30% of patients with chronic viral hepatitis C (CVHC), aminotransferase activity remains within the normal range.

Serological testswith hepatitis C: the main marker of the presence of hepatitis C virus in the body is HCV-RNA. Aichi-HCV may not be detected in people with congenital or acquired immunodeficiency, in newborns from carrier mothers, or when using insufficiently sensitive diagnostic methods.

Before starting antiviral therapy, it is necessary to determine the HCV genotype and viral load (the number of copies of viral RNA in 1 ml of blood; the indicator can also be expressed in ME). For example, genotypes 1 and 4 are less responsive to interferon treatment. The value of the viral load is especially high in case of HCV infection with genotype 1, because if it is below 2x10 ^ 6 copies / ml or 600 IU / ml, a reduction in the course of treatment is possible.

Chronic Hepatitis C Treatment

Patients with a high risk of developing cirrhosis of the liver, determined by biochemical and histological signs, are subject to treatment of chronic hepatitis C. Therapy for chronic hepatitis C is aimed at achieving a stable virological response, that is, elimination of serum HCV-RNA 6 months after the end of antiviral therapy, since in this case relapses of the disease are rare.

The virological response is accompanied by biochemical (normalization of ALT and ACT) and histological (decrease in the index of histological activity and index of fibrosis) changes. The histological response may be delayed, especially in high-grade baseline fibrosis. The absence of a biochemical and histological response when virologic is achieved requires careful exclusion of other causes of liver damage.

Hepatitis C Treatment Goals

Normalization of serum transaminase activity.
Elimination of serum HCV-RNA.
Normalization or improvement of the histological structure of the liver.
Prevention of complications (cirrhosis, liver cancer).
Reduced mortality.

Medication for chronic hepatitis C

Antiviral therapy for chronic hematitis C involves the use of interferons alfa (simple or pegylated) in combination with ribavirin.

The pharmacotherapy regimen for hepatitis C depends on the HCV genotype and the patient's body weight.

The drugs are used in combination.

Ribavirin orally 2 times a day with meals at the following dose: with a body weight of up to 65 kg - 800 mg / day, 65-85 kg - 1000 mg / day, 85-105 kg - 1200 mg / day. above 105 kg - 1400 mg / day.

Interferon alpha at a dose of 3 million IU 3 times a week in the form of intramuscular or subcutaneous injections. Or peginterferon alfa-2a subcutaneously at a dose of 180 mcg once a week. Or peginterferon alfa-2b subcutaneously at a dose of 1.5 mcg / kg once a week.

For HCV infection with genotype 1 or 4, the duration of the combined treatment course is 48 weeks; for HCV infection with a different genotype, this treatment regimen is used for 24 weeks.

Currently, the development of new antiviral drugs inhibitors of HCV enzymes (proteases, helicases, polymerases) is underway. With compensated cirrhosis of the liver in the outcome of chronic hepatitis C, antiviral treatment is carried out according to general principles. At the same time, the likelihood of reducing a sustained virological response is lower, and the frequency of side effects of drugs is higher than in the treatment of patients without cirrhosis.

Prognosis for chronic hepatitis C

The incidence of cirrhosis of the liver in its typical course of chronic hepatitis C reaches 20-25%. However, fluctuations in this indicator within significant limits are possible, because the development of liver cirrhosis depends on the individual characteristics of the course of the disease and additional damaging factors (especially alcohol). The process of formation of liver cirrhosis lasts from 10 to 50 years (on average - 20 years). With infection at the age of 50 and older, the progression of the disease is accelerated.

The risk of developing hepatocellular carcinoma in patients with liver cirrhosis ranges from 1.4 to 6.9%. Antiviral therapy is the only way to prevent severe complications of chronic hepatitis C in patients at high risk of disease progression.

Even with decompensated cirrhosis, it reduces the risk of developing gelatocellular carcinoma to 0.9-1.4% per year, and the need for liver transplantation - from 100 to 70%.

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Viral hepatitis C (hepatitis C) is an infectious disease that mostly affects the liver tissue and other organs such as the thyroid gland and bone marrow. The features of the disease are characterized by the code of chronic hepatitis C according to ICD 10.

It is under the heading of varieties of hepatitis B15-B19. The code for the general concept of chronic liver disease according to the documents of the international classification of diseases looks like B18, and chronic hepatitis C, in turn, is under the code B18.2.

A virus that has entered the human body is in it for a long time and may not manifest itself in any way, but the fact is that it is such a chronic course that is destructive, since lost time can lead to irreversible processes in the liver.

The virus kills the cells of the liver tissue, and connective tissue and fibrous connections appear in their place, which will further lead to cirrhosis or cancer of a vital organ.

Infection routes

Infection with viral hepatitis C occurs by parenteral, instrumental, sexual routes and from mother to child. In local protocols, the hepatitis C code describes the most common factors:

blood transfusion from donor to recipient;
multiple use of a disposable injection needle for different people is considered the most common route of infection;
sexual contact;
during pregnancy, the fetus can become infected only in the case of an acute form of the disease in the mother;
nail salons and hairdressing salons are a threat of infection if all the rules of asepsis, antiseptics and sterilization are not observed by the service personnel.

40% of cases of infection in modern practice are still unknown.

Typical symptoms

Some symptoms may appear, but their inconsistency and blurring does not cause most people anxiety and the need to see a doctor.

Subjective complaints can be as follows:

periodic nausea;
aches in muscles and joints;
decreased appetite;
instability of the stool;
apathetic states;
soreness in the epigastric region.

In contrast to the acute form of the disease, the chronic course is quite difficult to determine without a specific analysis for markers of hepatitis. Usually, the identification of a progressive agent occurs when the body is randomly examined for a completely different pathology.

Hepatitis C in ICD 10 has code B18.2, which determines the types of diagnostic measures and the use of standard treatment, which consists in the appointment of antiviral therapy. For the targeted treatment of this pathology, specialists use the following diagnostic methods: biochemical blood test for AST, ALT, bilirubin and protein, complete blood count, ultrasound of the abdominal organs, blood test for antibodies to the virus, liver biopsy.

Treatment of an acute form of the disease in a medical institution is carried out by an infectious disease doctor, and a gastroenterologist or hepatologist deals with chronic pathology.

The course of treatment in both cases lasts at least 21 days.

Our liver is subjected to serious stress every day. Improper nutrition, alcohol, medication - all this has an extremely negative effect on the state of such an important organ. Chronic hepatitis is considered one of the most serious liver diseases.

Chronic hepatitis, ICD-10 code

Specialists call chronic hepatitis an inflammatory hepatic pathology that occurs with characteristic and, at the same time, there are no signs and structural disorders of the lobules.

Usually, patients with such a pathology note disturbing discomfort in the right hypochondrium and a decrease in working capacity, and stool disorders, itching sensations and yellowness of the skin.

According to ICD-10, chronic hepatitis is classified as K73. In this form of hepatitis, healthy liver tissue is replaced by connective tissue. It can act as a complication of other pathologies or as an independent disease.

Forms and classification

Chronic hepatitis is classified according to a variety of principles. Depending on the etiological factor, the following varieties are distinguished:

A, B, D, C;
Cryptogenic;
Autoimmune;
Toxic, medicinal.

Depending on the activity of the pathological process, chronic hepatitis is inactive (persistent) or progressive (active or aggressive).

Depending on the stage of development, another classification of pathology is used:

Stage 0 - there is no tissue fibrosis, there is no pronounced clinic, sometimes dyspepsia worries;
Stage 1 - fibrosis is insignificant, connective tissue grows around the cellular structures of the organ and bile ducts;
Stage 2 - moderate hepatic fibrosis;
Stage 3 - fibrosis becomes pronounced;
Stage 4 - significant connective tissue growths with irreversible structural changes in the organ. Irreversible pathology is present.

Only at the initial stages can forecasts be favorable, because the disease can still be controlled

The reasons

Hepatitis is formed for a variety of reasons. The main reason is the penetration of a certain virus into the body. Also, the following factors can provoke hepatic pathology:

Uncontrolled intake of medications;
Decreased immune defenses;
Unfavorable environmental conditions, environmental pollution, hazardous production;
Autoimmune pathologies;
Frequent stress, other adverse factors.

An improper lifestyle, malaria and infectious pathologies, liver diseases, etc., can provoke the development of chronic hepatitis.

Symptoms

The clinical picture of chronic hepatitis can differ according to the specific etiology. But the disease also has general symptoms, which include:

Physical weakness and periodic depression;
Itchy skin, yellowing of the epidermis;
Hands turn red, purple vessels appear on the surface, resembling anemia;
Changes in feces that are not related to diet;
Painful sensations under the ribs of the encircling nature;
The appearance of capillary stars on the surface of the neck and face, chest;
Feeling of bitterness in the mouth, a sharp-smelling belching, heaviness in the abdomen.

These signs indicate the development of pathology, therefore, if they are detected, it is necessary to urgently consult a specialist.

Diagnostics

To diagnose chronic hepatitis, patients are usually assigned studies:

Ultrasound, which shows signs of an inflammatory process;
When carrying out, a characteristic increase in bilirubin and enzyme substances produced by the liver is revealed;
To detect antibodies to viruses C and B, patients undergo a serological blood test;
An immunological study is shown, which will help detect the presence of antibodies to the components of the cellular hepatic structures;
It is also carried out, which allows you to get more accurate information about the severity of the inflammatory process, as well as a biopsy helps to timely detect signs and even determine the etiology of hepatitis;
To determine the exact virus that caused inflammatory processes in the liver tissues, patients are assigned virological diagnostics;
If necessary, rheohepatography is performed, aimed at examining the blood supply to the hepatic organ, studies are carried out to identify various blood markers, etc.

Additional diagnostic techniques are determined by the clinical picture of the pathological process. Diagnostic procedures are prescribed by a gastroenterologist, and after obtaining accurate results, the specialist makes a final diagnosis.

Treatment

Therapy of chronic hepatitis is extremely complex, regardless of the etiology of the inflammatory process. The recommendations of a specialist should be followed by the patient constantly, because the pathology is chronic.

First you need to get rid of the root cause of the pathology, remove toxins or eliminate viruses. Then therapy is directed to the restoration of the hepatic organ. Throughout and after treatment, the patient must follow dietary recommendations.

Drug therapy involves the use of hepatoprotectors, multivitamins, interferons and glucocorticoids, immunomodulators, and with long problematic constipation - laxatives.

If the pathology is severe, then detoxification therapy is indicated. If conservative methods do not give results, then surgery is performed aimed at.

Diet

Regardless of the type of drug treatment, the patient must follow a strict dietary regimen in the diet. This is necessary to reduce the load on the organ. Diet therapy involves the complete elimination of such products:

Salty, seasoned, fatty;
Products containing oxalic acid;
Coffee, cocoa, strong tea;
Cholesterol-rich foods
Surrogates and alcohol;
Fatty types of meat and fish.

Onions, baked goods and legumes, mushrooms and nuts, canned food and radishes, smoked meats and garlic are banned. Drink plenty of fluids, at least 2 liters per day. In this case, soups and other liquid food are not included here.

The food should be high in calories, but light. You need to steam it, bake it or boil it. Eaten food should have a grated, liquid or puree-like consistency. Any food should be consumed exclusively warm. In this case, you need to eat every 2.5 hours.

With an exacerbation of chronic hepatitis in the first 2 days, you should limit yourself only to the use of green tea or non-carbonated mineral water.

Forecast and prevention

Primary prevention of hepatitis of viral etiology consists in compliance with hygiene standards, sanitary and epidemiological measures and supervision at enterprises. It is also necessary to vaccinate.

For the prevention of hepatitis of other etiological forms, moderate consumption of alcohol is recommended, taking medications solely as prescribed by a doctor, as well as avoiding contact with toxic substances.

Secondary preventive measures include:

Compliance with the diet, regimen and lifestyle, according to the recommendations of the doctor.
It is necessary to undergo regular examinations, monitor blood counts.
Such patients are recommended sanatorium-resort treatment, periodically undergo laboratory diagnostics.
It is necessary to exclude casual unprotected sex, timely treat infectious pathologies and observe personal hygiene.
You also need to eat right and undergo gastroenterological consultations.

As for the prognosis, it will be favorable with the timely diagnosis of hepatitis. The patient will have to take some medications for life, as well as follow the dietary recommendations of the gastroenterologist.

Alcoholic and toxic forms of pathology in 10% of cases are fatal.

With an unfavorable course of the pathological process, irreversible hepatic lesions develop. Sometimes complications of hepatitis are manifested in the form of anemia, diabetes, liver oncology. Only timely diagnosis will ensure a favorable outcome for hepatitis.

Video lecture about chronic hepatitis:

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Ministry of Health of Russia dated 05/27/97. No. 170

A new revision (ICD-11) is planned by WHO in 2017 2018.

As amended and supplemented by WHO

Processing and translating changes © mkb-10.com

Viral hepatitis C mkb 10 code

HEPATITIS B (ICD-10 code - B16

Acute (or chronic) liver disease caused by a parenteral DNA virus. Hepatitis B (HB) often proceeds in moderate and severe form, often protracted and chronic (5-10%). The problem of hepatitis B is gaining special relevance in connection with the growing drug addiction among older children and adolescents.

Figure: 1. Hepatitis B. Electronogram of the virus

The incubation period is 2 to

6 months. The characteristic features of the clinical manifestations of a typical acute hepatitis B are a gradual onset, pronounced hepatolienal syndrome, persistence and even an increase in symptoms of intoxication in the icteric period of the disease, a gradual increase in jaundice followed by stabilization at altitude (“icteric plateau”), in connection with which the icteric period can tighten to 3-

Figure: 2. Histology of the liver in acute hepatitis B. Staining with hematoxylin eosin

5 weeks, occasionally maculopapular skin rash (Gianotti-Crosty syndrome), prevalence of moderate and severe forms of the disease, and in children 1 year of age, the possible development of a malignant form of hepatitis B.

For the diagnosis, the detection in the blood serum of the surface antigen of the hepatitis B virus - HB $ Ag - using the ELISA method is of decisive importance. It is important to take into account that in the acute course of the disease, HB $ Ag usually disappears from the blood by the end of the first month after the onset of jaundice. Long-term, more than 6 months, detection of HB $ Ag indicates a chronic course of the disease. Active replication of the hepatitis B virus is confirmed by detection in blood by ELISA HBeAg and HBV DNA using PCR. Among other serum markers, detection of anti-HBc IgM in the blood by ELISA in the preicteric period, during the entire icteric period and in the initial stage of convalescence is of great diagnostic value. High titers of anti-HBc IgM are observed in all patients regardless of the severity of the disease at the earliest and throughout the entire acute phase of the disease, including in those cases when HB $ Ag is not detected due to a decrease in its concentration. as is the case with fulminant hepatitis or late admission to the hospital. On the other hand, the absence of anti-HBc IgM in patients with clinical signs of acute hepatitis reliably excludes HB viral etiology of the disease.

When diagnosing mild and moderate forms of the disease, patients are on

3. Hepatitis. Hepatitis B rash

half-bed mode and receive symptomatic treatment. Prescribe a hepatic table, abundant drinking, a complex of vitamins (C, Bp B2, B6) and, if necessary, choleretic drugs: sandy immortelle (flamin), berberine, choleretic collection, etc. calculation of 3-5 mg / kg for 3 days, followed by a decrease by 1/3 of the dose that is given

2-3 days, then decreases by another 1/3 of the initial and is given for 2-3 days with subsequent cancellation), as well as intravenous drip infusions of a multicomponent antioxidant solution of Reamberin 1.5%

Figure: 6. Liver necrosis. Liver histology

and a metabolic cytoprotectant of iitofavin, dextran (rheopolyglucin), dextrose (glucose) solution, human albumin; liquid is administered at the rate of no more than 50 ml / kg per day. In case of a malignant form, the patient is transferred to the intensive care unit, where he is sequentially prescribed prednisolone up to 10-15 mg / kg intravenously in equal doses after 4 hours without a night break, intravenously dropwise albumin (10-15 ml / kg), 10% glucose solution, cytof - avalanches (no more than 100 ml / kg of all infusion solutions per day, with diuresis control), inhibitors of olis: aprotinin (trasil lol), gordox, kontrikal in an age dosage, as well as furosemid (lasix) 1-2 mg / kgimannitol

1.5 g / kg jets but, slowly, heparin 100-300 BD / k g with the threat of D B C-syndrome a, broad-spectrum antibiotics. If therapy is ineffective (coma TT), plasmapheresis is performed in the amount of 2-3 volumes of circulating blood (BCC) 1-2 times a day until coming out of coma.

Important measures are interrupting the transmission of infection: the use of disposable syringes and other medical instruments, proper sterilization of dental and surgical instruments, testing of blood and blood products for hepatitis viruses using highly sensitive methods, the use of rubber gloves by medical staff and strict adherence to personal hygiene rules. Specific prophylaxis is of decisive importance, which is achieved by active immunization with recombinant monovaccines and combined vaccine preparations, starting from infancy, according to the scheme according to the national immunization schedule.

In our country, vaccines Kombiotech (Russia), Regevak B (Russia), Engerix B (Russia), H-V-Wah II (USA), Shanvak B (India), etc. are used for hepatitis B vaccination.

B 18.1 - "Chronic hepatitis B without delta agent";

B 18.0 - "Chronic hepatitis B with a delta agent."

Natural history of chronic HBV infection

In patients with CVHB, the cumulative incidence of CP development within 5 years is from 8 to 20%, in the next 5 years the possibility of decompensation is 20%. With compensated cirrhosis, the probability of patient survival within 5 years is 80–86%. With decompensated CP, the chance of survival within 5 years is extremely low (14–35%). The annual incidence of hepatocellular carcinoma in patients with an established diagnosis of cirrhosis in the outcome of CHB is 2–5% and differs in a number of geographic regions.

There are 4 phases of the natural course of chronic HBV infection:

phase of immune tolerance,

phase of immune clearance,

phase of immune control.

Immune Tolerance Phase ... as a rule, it is registered in young people infected in childhood. These are patients with a high viral load, HBeAg positive, with normal liver enzyme activity, absence of liver fibrosis, and minimal necroinflammatory activity.

Immunoactive phase chronic HBeAg-positive hepatitis can develop in three scenarios.

I– Possible spontaneous HBeAg seroconversion. and the transition of the disease to the phase of inactive carriage of HBsAg.

II - ongoing course of chronic HBeAg-positive hepatitis B with a high risk of LC.

III - transformation of HBeAg-positive hepatitis into HBeAg-negative chronic hepatitis as a result of the development of mutations in the core HBV zone, and the termination of the production of “classic HBeAg.” Mutant forms of HBV gradually begin to dominate in the population, followed by the complete predominance of this variant of the virus.

Immune control phase - persistent HBV infection without pronounced necro-inflammatory process in the liver and fibrosis.

In 15% of patients, reactivation of HBV infection and the development of a pronounced inflammatory necrotic process in the liver is possible. It is possible (0.06%) the formation of cirrhosis and the development of hepatocellular carcinoma, which justifies the need for lifelong dynamic monitoring of this group of patients. At the same time, spontaneous elimination of HBsAg occurs in “inactive HBsAg carriers” (1-2% per year), and anti-HBs are subsequently recorded in the blood in most of these patients.

Reactivation phase HBV infection is possible with immunosuppression. In this case, high viremia, increased ALT activity and active hepatitis B, confirmed histologically, are again revealed. In some cases, anti-HBe / HBeAg reversion is possible.

Threat factors for the transformation of acute HBV into chronic:

protracted course of hepatitis (more than 3 months);

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Classification of hepatitis according to ICD-10 - disease codes

Etiology of hepatitis

The classification of the disease is complex. Hepatitis is divided into 2 large groups according to the etiological factor. These are non-viral and viral pathologies. The acute form includes several clinical variants with different causes.

In practice, the following types of non-viral ailment are distinguished:

Inflammatory-necrotic character has a progressive liver damage in the autoimmune variant, that is, if autoimmune hepatitis develops. Own immunity destroys the liver.
As a result of long-term irradiation at doses of more than 300-500 rad for 3-4 months, the radiation variant of inflammation of the liver tissue develops.
Often, necrosis occurs in toxic hepatitis (ICD-10 code K71). Cholestatic type - a very serious liver disease - is associated with the problems of bile flow.
In the structure of this pathology, unspecified hepatitis is determined. Such a disease develops imperceptibly. It is an ailment that has not evolved into cirrhosis. It also does not finish for 6 months.
Against the background of infectious diseases, gastrointestinal pathologies, damage to liver cells of an inflammatory-dystrophic nature develops. This is reactive hepatitis (ICD code K75.2).
Toxic jaundice is divided into a medicinal or alcoholic form, which occurs as a result of the abuse of harmful drinks or medicines. Drug or alcoholic hepatitis develops (ICD-10 code K70.1).
A disease of unknown etiology is cryptogenic hepatitis. This inflammatory process is localized and rapidly progresses in the liver.
The consequence of infection with syphilis, leptospirosis is bacterial inflammation of the liver tissue.

Diseases of viral origin

The mechanism and symptoms of the development of the disease

The rapidly developing pathological process is acute hepatitis, which is in the international classification of diseases of the tenth revision under the following codes:

acute form A - B15;
acute form B - B16;
acute form C - B17.1;
acute form E - B17.2.

Clinical manifestations of the acute form of the disease:

Hepatolienal syndrome. The spleen and liver rapidly increase in size.
Hemorrhagic syndrome. Due to a violation of homeostasis, increased bleeding of blood vessels develops.
Dyspeptic symptoms. These problems are manifested by indigestion.
The color of urine and feces changes. The stool is grayish-white. The urine becomes dark. The mucous membranes and skin acquire a yellow tint. In the icteric or anicteric variant, the form of acute hepatitis, which is considered typical, may occur.
Asthenic syndrome is gradually formed. This is emotional instability, increased fatigue.

Danger of viral jaundice

Of all the pathologies of the hepatobiliary system, the viral type of the disease most often leads to the development of cancer or cirrhosis of the liver.

Diagnostic tests

Establishing the causative agent of the pathology, identifying the cause of the development of the disease are the purpose of the examination.

Diagnostics includes the following list of procedures:

Morphological studies. Puncture biopsy. A thin hollow needle is used to puncture the tissue for the purpose of examining biopsies.
Instrumental tests: MRI, ultrasound, CT. Laboratory tests: serological tests, liver function tests.

Therapeutic methods of exposure

Antihistamines are indicated for various types of ailment. Diet therapy is required. A balanced, sparing diet is essential for hepatitis.

At the first signs of trouble, it is important to contact an experienced specialist in a timely manner.

Chronic hepatitis C encoding in ICD

The virus kills the cells of the liver tissue, and connective tissue and fibrous connections appear in their place, which will further lead to cirrhosis or cancer of a vital organ.

Infection routes

Infection with viral hepatitis C occurs by parenteral, instrumental, sexual routes and from mother to child. In local protocols, the hepatitis C code describes the most common factors:

blood transfusion from donor to recipient;
multiple use of a disposable injection needle for different people is considered the most common route of infection;
sexual contact;
during pregnancy, the fetus can become infected only in the case of an acute form of the disease in the mother;
nail salons and hairdressing salons are a threat of infection if all the rules of asepsis, antiseptics and sterilization are not observed by the service personnel.

40% of cases of infection in modern practice are still unknown.

Typical symptoms

Some symptoms may appear, but their inconsistency and blurring does not cause most people anxiety and the need to see a doctor.

Subjective complaints can be as follows:

periodic nausea;
aches in muscles and joints;
decreased appetite;
instability of the stool;
apathetic states;
soreness in the epigastric region.

Treatment of an acute form of the disease in a medical institution is carried out by an infectious disease doctor, and a gastroenterologist or hepatologist deals with chronic pathology.

The course of treatment in both cases lasts at least 21 days.

Chronic viral hepatitis C in adults

The incidence of hepatitis C in the Russian Federation is steadily increasing. A feature of chronic hepatitis C is that it has little symptoms for many years. More often, such patients are discovered by chance, when contacting medical institutions for other diseases, before operations, when undergoing a planned medical examination. Sometimes patients only go to the doctor if they have serious complications from the disease. Therefore, it is so important to diagnose viral hepatitis C on time and begin treatment.

Viral hepatitis C is an infectious disease. It is characterized by a mild (up to asymptomatic) course in acute form. Most often, the disease acquires the status of chronic, which entails the development of severe complications - cirrhosis and liver carcinoma.

The only source of hepatitis C virus is a sick person.

HCV in the world are considered to be infected approximately 170 million people.

In the international classification of diseases of the last revision (ICD-10), viral hepatitis C has the codes:

B17. 2 - acute hepatitis C.
B18. 2 - chronic hepatitis C.

The causative agent of the pathology is the hepatitis C virus (HCV). The peculiarity of this virus is its high mutation capacity. The variability of the genotype allows the hepatitis C virus to adapt to the conditions in the human body and to function for a long time in it. There are 6 varieties of this virus.

Establishment of the genetic variety of the virus in a specific case of infection does not determine the result of the disease, but identification of the genotype makes it possible to predict the effectiveness of the treatment and affects its duration.

Hepatitis C is characterized by a blood-contact mechanism of transmission of the pathogen. The implementation of the mechanism occurs naturally (when the virus is transmitted from mother to fetus - vertical, contact - when using household items and during sexual intercourse) and artificially.

The artificial route of infection occurs through the transfusion of contaminated blood and its components, during medical and non-medical procedures, which are accompanied by a violation of the integrity of the skin and mucous membranes, when manipulating instruments containing contaminated blood.

Human susceptibility to the virus is high. The occurrence of infection largely depends on how much of the pathological agent has entered the body.

Acute hepatitis C is asymptomatic, making diagnosis difficult. Therefore, in almost 82% of cases, chronic hepatitis C occurs.

A feature of the chronic course of the disease in adults is smoothed symptoms or even the absence of symptoms. Increased activity of liver enzymes, detection of virus markers in blood serum for a period of six months or more are indicators of this disease. Often, patients go to the doctor only after the onset of liver cirrhosis and when its complications appear.

Chronic HCV infection can be accompanied by completely normal activity of liver enzymes when repeatedly examined during the year.

In some patients (15% or more), liver biopsy reveals serious violations of the organ structure. Extrahepatic manifestations of this disease occur, according to the scientific medical community, in more than half of patients. They will determine the prognostic data of the disease.

The course of the disease is complicated by such extrahepatic disorders as the production of abnormal blood proteins, lichen planus, glamerulonephritis, skin porphyria, rheumatism. The role of the virus in the development of B-cell lymphoma, thrombocytopenia, damage to the internal glands (thyroiditis) and external secretion (salivary and lacrimal glands), the nervous system, eyes, skin, joints, muscles has been established.

To confirm the diagnosis of chronic hepatitis C, methods of interrogation and examination are used, determination of blood and urine biochemistry parameters in dynamics, the presence of anti-HCV and HCV RNA in the blood serum. The standard for diagnosing chronic viral hepatitis C is a puncture liver biopsy, shown to all patients who have diagnostic criteria for a chronic inflammatory process in this organ. The objectives of the biopsy are to determine the degree of activity of pathological changes in the liver tissue, to clarify the staging of the disease by the strength of fibrotic changes (determination of the fibrosis index). A biopsy is used to assess the effectiveness of treatment.

Based on the data of liver histology, the patient's treatment plan, indications for antiviral therapy, and the outcome of the disease are predicted.

There is a clear standard for examining a patient who was suspected of having viral hepatitis C. The examination plan includes laboratory tests and instrumental diagnostics.

Obligatory laboratory diagnostic tests:

general blood analysis;
biochemical blood test (bilirubin, ALT, AST, thymol test);
immunological analysis: Anti-HCV; HBS Ag;
general urine analysis.

Additional laboratory diagnostic tests:

blood biochemistry;
coagulogram;
blood group, Rh factor;
additional immunological research;
analysis of feces for occult blood.

Ultrasound of the abdominal organs;
chest x-ray;
percutaneous puncture liver biopsy;
esophagogastroduodenoscopy.

Treatment for hepatitis C virus infection should be comprehensive. This implies basic and antiviral therapy.

Basic therapy includes adherence to a diet (table No. 5), course use of drugs that support the activity of the gastrointestinal tract (enzymes, hepatoprotectors, choleretic drugs, bifidobacteria).

It is necessary to reduce physical activity, observe psycho-emotional balance, do not forget about the treatment of concomitant diseases.

The purpose of the etiotropic therapy of chronic hepatitis C is to suppress viral activity, completely remove the virus from the body and stop the pathological infectious process. Antiviral therapy is the basis for slowing down the progression of the disease, it stabilizes and regresses pathological changes in the liver, prevents the formation of liver cirrhosis and primary hepatic carcinoma, and improves the quality of life.

Currently, the best option for etiotropic therapy for chronic viral hepatitis C is the use of a combination of pegylated interferon alfa-2 and ribavirin for a period from 6 months to 1 year (depending on the genotype of the virus that caused the disease).

Krasnoyarsk medical portal Krasgmu.net

Once infected with the hepatitis C virus, most people who are infected develop chronic hepatitis C. The probability is about 70%.

Please note that this article contains only general current understanding of chronic hepatitis C.

CHRONIC HEPATITIS C

Chronic hepatitis C is an inflammatory liver disease caused by the hepatitis C virus that has been present without improvement for 6 months or more. Synonyms: Chronic viral Hepatitis C (HCV), Chronic HCV infection (from the English hepatitis C virus), chronic hepatitis C.

Depending on the degree of activity of the infectious process, chronic viral hepatitis with minimal, mild, moderate, pronounced activity, fulminant hepatitis with hepatic encephalopathy are isolated.

Chronic viral hepatitis C with minimal activity (chronic persistent viral hepatitis) occurs in conditions of a genetically determined weak immune response.

ICD-10 CODE B18.2 Chronic viral hepatitis C.

Epidemiology of hepatitis C

The prevalence of chronic HCV infection in the world is 0.5-2%. Areas with a high prevalence of viral hepatitis C are distinguished: isolated settlements in Japan (16%), Zaire and Saudi Arabia (\u003e 6%), etc. In Russia, the incidence of acute HCV infection is 9.9 nanopopulations (2005).

Chronic viral hepatitis C over the past 5 years has come out on top in terms of morbidity and severity of complications.

There are 6 main genotypes of the hepatitis C virus and over 40 subtypes. This is the reason for the high incidence of chronic viral hepatitis C.

PREVENTION OF HEPATITIS C

Non-specific prophylaxis - see "Chronic hepatitis B".

Research results indicate a low probability of sexual transmission of HCV infection. A vaccine to prevent hepatitis C is under development.

Chronic hepatitis C is one of the main causes of liver transplants.

SCREENING

Determine the total antibodies to the hepatitis C virus (anti-HCV). Confirmation of a positive ELISA result by recombinant immunoblotting is recommended.

ROUTES OF HEPATITIS C INFECTION, ETIOLOGY

Transmission of infection occurs by hematogenous route, less often through sexual contact or from an infected mother to the fetus (3-5% of cases).

The hepatitis C virus is transmitted through blood. Sexual transmission is not relevant and sexual transmission of the hepatitis C virus is rare. Transmission of the virus from the mother during pregnancy is also extremely rare. Breastfeeding is not prohibited for hepatitis C, but caution should be exercised when blood appears on the nipples.

You can get infected with the virus when getting tattoos, piercing, visiting a manicure room, medical manipulations with blood, including blood transfusion, administration of blood products, operations, at the dentist. It is also possible to get infected by the general use of toothbrushes, razors, and manicure supplies.

It is impossible to become infected with the hepatitis C virus through household contacts. The virus is not transmitted by airborne droplets, shaking hands, hugging and sharing utensils.

After the virus enters the human blood, it enters the liver with the blood stream, infects the liver cells and multiplies there.

SYMPTOMS OF HEPATITIS C - CLINICAL PICTURE

Chronic viral hepatitis C proceeds, as a rule, with a poor clinical picture and transient levels of transaminases.

Extrahepatic clinical manifestations of viral hepatitis C:

often mixed cryoglobulinemia - manifested by purpura, arthralgia.
damage to the kidneys and rarely the nervous system;
membranous glomerulonephritis;
sjogren's syndrome;
lichen planus;
autoimmune thrombocytopenia;
late cutaneous porphyria.

DIAGNOSTICS OF HEPATITIS C

Anamnesis allows you to get information about the possible route of infection and sometimes about the previous acute hepatitis C.

Physical examination for hepatitis C

Laboratory tests for hepatitis C

Biochemical blood test for hepatitis C: Cytolytic syndrome reflects the activity of transaminases (ALT and AST). However, their normal values \u200b\u200bdo not exclude the cytological activity of hepatitis. In chronic hepatitis C, ALT activity rarely reaches high values \u200b\u200band is subject to spontaneous fluctuations. Constantly normal activity of transaminases and 20% of cases does not correlate with the severity of histological changes. Only with increased ALT activity 10 times or more is it possible (with a high degree of probability to assume the presence of bridging liver necrosis)

According to prospective studies, in about 30% of patients with chronic viral hepatitis C (CVHC), aminotransferase activity remains within the normal range.

Serological studies in hepatitis C: the main marker of the presence of the hepatitis C virus in the body is HCV-RNA. Aichi-HCV may not be detected in people with congenital or acquired immunodeficiency, in newborns from carrier mothers, or when using insufficiently sensitive diagnostic methods.

Chronic Hepatitis C Treatment

Hepatitis C Treatment Goals

Normalization of serum transaminase activity.
Elimination of serum HCV-RNA.
Normalization or improvement of the histological structure of the liver.
Prevention of complications (cirrhosis, liver cancer).
Reduced mortality.

Medication for chronic hepatitis C

Antiviral therapy for chronic hematitis C involves the use of interferons alfa (simple or pegylated) in combination with ribavirin.

The pharmacotherapy regimen for hepatitis C depends on the HCV genotype and the patient's body weight.

The drugs are used in combination.

Ribavirin inside 2 times a day with meals in the following dose: with a body weight of up to 65 kgmg / day, kgmg / day, kg 1200 mg / day. above 105 kg - 1400 mg / day.

For HCV infection with genotype 1 or 4, the duration of the combined treatment course is 48 weeks; for HCV infection with a different genotype, this treatment regimen is used for 24 weeks.

Prognosis for chronic hepatitis C

Even with decompensated cirrhosis, it reduces the risk of developing gelatocellular carcinoma to 0.9-1.4% per year, and the need for liver transplantation - from 100 to 70%.

Viral hepatitis c

ICD-10 code

Associated diseases

Ezervoir and the source of infection - patients with chronic and acute forms of the disease, proceeding both with clinical manifestations and asymptomatic. The serum and plasma of an infected person are infectious for a period beginning one or several weeks before clinical signs of illness appear, and may contain the virus indefinitely.

Transfer mechanism. It is similar to viral hepatitis B, but the structure of the infection routes has its own characteristics. This is due to the relatively low resistance of the virus in the external environment and a rather large infectious dose required for infection. The viral hepatitis C virus is transmitted primarily through contaminated blood and, to a lesser extent, through other biological fluids of a person. RNA of the virus is found in saliva, urine, seminal and ascitic fluids.

High-risk groups include people who have received multiple transfusions of blood and blood products, as well as people with a history of massive medical interventions, organ transplants from HCV-positive donors, and multiple parenteral manipulations, especially when reusing non-sterile syringes and needles. The prevalence of viral hepatitis C among drug addicts is very high (70-90%); this route of transmission represents the greatest danger in the spread of the disease.

Symptoms

Acute infection is mostly not clinically diagnosed, proceeds predominantly in a subclinical anicteric form, which makes up 95% of all cases of acute viral hepatitis C. Late laboratory diagnosis of acute infection is due to the existence of the so-called "antibody window": in the study of test systems of the first and second generations of antibodies to viral hepatitis C in 61% of patients appear in the period up to 6 months from the initial clinical manifestations, and in many cases, much later.

In the clinically manifest form of acute viral hepatitis C, the classic signs of the disease are insignificant or absent. Patients note weakness, lethargy, rapid fatigability, impaired appetite, decreased tolerance to food loads. Sometimes in the pre-icterus period, there is severity in the right hypochondrium, fever, arthralgia, polyneuropathy, dyspeptic manifestations. In a general blood test, leuko- and thrombocytopenia can be detected. Jaundice occurs in 25% of patients, mainly in persons with post-transfusion infection. The course of the icteric period is most often mild, icterus quickly disappears. The disease is prone to exacerbations, in which icteric syndrome reappears and the activity of aminotransferases increases.

At the same time, rare (no more than 1% of cases) fulminant forms of viral hepatitis C have been described.

In some cases, the manifestation of acute infection is accompanied by severe autoimmune reactions - aplastic anemia, agranulocytosis, peripheral neuropathy. These processes are associated with extrahepatic replication of the virus and can result in the death of patients before the appearance of significant antibody titers.

A distinctive feature of viral hepatitis C is a long-term latent or low-symptom course of the so-called slow viral infection. In such cases, the disease for the most part remains unrecognized for a long time and is diagnosed at advanced clinical stages, including against the background of the development of liver cirrhosis and primary hepatocellular carcinoma.

Chronic viral hepatitis

RCHD (Republican Center for Healthcare Development of the Ministry of Health of the Republic of Kazakhstan)

Version: Archive - Clinical protocols of the Ministry of Health of the Republic of Kazakhstan (Order No. 764)

general information

Short description

Protocol code: Н-T-026 "Chronic viral hepatitis"

For therapeutic hospitals

Other unspecified chronic viral hepatitis B18.9

Classification

Factors and risk groups

Persons with promiscuous sexual intercourse;

Patients in hemodialysis units;

Patients in need of repeated transfusions of blood or its components;

Family members of the virus carrier.

Diagnostics

CVHB often occurs with symptoms of asthenovegetative syndrome, patients are worried about weakness, fatigue, insomnia or flu-like syndrome, muscle and joint pain, nausea. Less common are epigastric pain, diarrhea, skin rash, jaundice.

General urine analysis;

Liver biochemical tests (ALT, AST, alkaline phosphatase, GGTP or GGT, bilirubin, serum proteins, coagulogram or prothrombin time, creatinine or urea);

Serological markers (HBsAg, HBeAg, anti-HBc, HBe IgG, anti-HBc IgM, anti HBe IgG, DNA HBV, anti-HCV total, RNA HCV, anti-HDV, RNA HDV);

List of additional diagnostic measures:

Hepatitis C (C)

Hepatitis C (hepatitis C) is a severe anthroponous viral disease that belongs to the conditional group of transfusion hepatitis (transmitted mainly by parenteral and instrumental routes). It is characterized by liver damage, anicteric course of the disease and a tendency to become chronic. Hepatitis C ICD 10, depending on the form of the disease, classifies as B17.1 and B18.2

General information

Hepatitis is an inflammation of the liver that occurs when viruses, toxic substances, and autoimmune diseases occur. Ordinary people often call hepatitis "jaundice", because yellowing of the skin and sclera in many cases accompanies various types of hepatitis.

Although still Hippocrates in the 5th century. BC e. noted that jaundice has contagious forms, and Europeans from the 17th century paid attention to the epidemic nature of the disease, its nature remained unclear until the end of the 19th century.

The first attempts to explain the nature and pathogenesis of epidemic jaundice date back to the 19th century. During the 19th century, three theories of the pathogenesis of this disease appeared:

Humoral or dyscratic, according to which the disease developed as a result of increased blood breakdown (the Austrian pathologist Rokitansky (1846) was a supporter of this theory).
Choledochogenic, according to which the development of the disease occurs as a result of inflammation of the biliary tract, their subsequent edema and blockage, i.e. as a result of a disturbed outflow of bile. The author of this theory is the French clinician Broussais (1829), who considers the appearance of jaundice as a consequence of the spread of the inflammatory process of the duodenum to the biliary tract. The famous German pathologist Virchow in 1849 put forward on the basis of the ideas of Broussais and the pathological observation of the concept of the mechanical nature of jaundice, linking it with catarrh of the common bile duct.
Hepathogenic, according to which the disease develops as a result of liver damage (hepatitis). In 1839, the Englishman Stokes suggested that the liver was involved in the pathological process associated with gastrointestinal catarrh. The hepatic nature of jaundice was suggested by K.K.Seidlitz, H.E. Florentinsky, A.I. Ignatovsky, and others, but the first scientifically substantiated concept of the etiology of the disease belongs to the outstanding Russian clinician S.P. Botkin, who in 1888 formulated the main provisions teachings about viral hepatitis. Even before the discovery of S.P. Botkin in his clinical lectures attributed viral hepatitis to acute infectious diseases, so for a long time this disease was called Botkin's disease (nowadays, this is sometimes called viral hepatitis A).

The viral nature of this type of hepatitis was discovered by chance through clinical and epidemiological observations. For the first time such studies were carried out by Findlay, McCallum (1937) in the USA and P.S. Sergiev, Ε. M. Tareev and A. A. Gontaeva et al. (1940) in the USSR. The researchers tracked an epidemic of "viral jaundice" that developed in individuals immunized against yellow fever in the United States, and pappatachi fever in Crimea (human serum was used for vaccination). Although it was not possible to identify the causative agent of the disease at this stage, extensive experimental studies have significantly enriched the understanding of the main biological properties of the virus.

In 1970, D. Dein discovered a virus in a patient with jaundice in the blood and liver tissue - spherical and polygonal formations, called "Dane particles" and possessing infectiousness and various antigenicity.

In 1973, WHO divided viral hepatitis into hepatitis A and hepatitis B, and hepatitis viruses other than these forms were separated into a separate group of "non-A, no B".

In 1989, American scientists under the leadership of M. Houghton isolated the hepatitis C virus, which is transmitted by the parenteral route.

Hepatitis C is common throughout the world. It is most often found in the regions of Africa, Central and East Asia. In some countries, the virus can mainly affect certain groups of the population (people who use drugs), but it can also affect the entire population of the country.

The hepatitis C virus has many strains (genotypes), the distribution of which depends on the region - genotypes 1-3 are found around the world, and its subtype 1a is more common in the Americas, Europe, Australia and parts of Asia. Genotype 2 is found in many developed countries, but it is less common than genotype 1.

According to some studies, the types of hepatitis may depend on different routes of transmission of the virus (for example, subtype 3a is detected mainly in drug addicts).

Every year 3-4 million people are registered who are infected with the hepatitis C virus. At the same time, about 350 thousand patients die from liver diseases associated with hepatitis C.

Due to the peculiarities of the clinical picture of the disease, the disease is often called the “affectionate killer” - acute hepatitis C in most cases is asymptomatic and rarely causes the patient to see a doctor.

Forms

Based on the clinical picture of the disease, hepatitis C is divided into:

Acute form (acute hepatitis C, ICD code 10 - B17.1). In most cases, this form in adults is asymptomatic, there is no yellowing of the skin and eyes (a characteristic sign of hepatitis). There is no exact statistics on the number of patients - hepatitis C, the symptoms of which are not expressed, is rarely associated with a life-threatening disease. In addition, in% of cases, within 6 months from the moment of infection, infected individuals spontaneously and without any treatment get rid of the virus. This form often becomes chronic (55-85% of cases).
Chronic viral hepatitis C (ICD code 10 B18.2). Refers to diffuse liver diseases that develop with the hepatitis C virus and last 6 months or more. The chronic form is characterized by a poor clinical picture with transient levels of transaminases. A certain sequence of phases is observed - the acute phase is replaced by a latent one, followed by a reactivation phase, liver cirrhosis and the formation of hepatocellular carcinoma (in the acute phase, periods of exacerbation alternate with phases of remission). Chronic viral hepatitis C affects approximately 150 million people. The risk of developing cirrhosis in these patients is 15% –30% within 20 years.

It is also possible to carry a chronic virus (a hepatitis C virus carrier is a self-cured patient with an acute form of the disease or a patient with chronic hepatitis C in remission).

Also, hepatitis C, depending on the genetic variant or strain (genotype), is divided into:

6 main groups (from 1 to 6, although many scientists assume that there are at least 11 genotypes of hepatitis C);
subgroups (subtypes denoted by Latin letters);
quasispecies (polymorphic populations of one species).

Genetic differences between genotypes are approximately 1/3.

Since the hepatitis C virus daily reproduces more than 1 trillion virions (full-fledged viral particles) and, in the process of replication, makes mistakes in the genetic structure of newly-forming viruses, one patient can be diagnosed with millions of quasispecies of this type of hepatitis.

The genotypes of the hepatitis C virus according to the most common classification are subdivided into:

Hepatitis C genotype 1 (subtypes 1a, 1b, 1c). Genotype 1a is found primarily in the Americas and Australia, while genotype 1b of hepatitis C is found in Europe and Asia.
Hepatitis C genotype 2 (2a, 2b, 2c). Subtype 2a is most often found in Japan and China, 2b - in the United States and northern Europe, 2c - in western and southern Europe.
Hepatitis C genotype 3 (3a, 3b). Subtype 3a is most common in Australia, Europe and South Asia.
Hepatitis C genotype 4 (4a, 4b, 4c, 4d, 4e). Subtype 4a is most often found in Egypt, and 4c - in Central Africa.
Hepatitis C genotype 5 (5a). Subtype 5a is mostly found in South Africa.
Hepatitis C genotype 6 (6a). Subtype 6a is common in Hong Kong, Macau and Vietnam.
Genotype 7 (7a, 7b). These subtypes are most commonly found in Thailand.
Genotype 8 (8a, 8b). These subtypes have been identified in Vietnam.
Genotype 9 (9a). Distributed in Vietnam.

Genotype 10a and genotype 11a are common in Indonesia.

In Europe and Russia, genotypes 1b, 3a, 2a, 2b are most often detected.

In Russia, more than 50% of patients have hepatitis C genotype 1c. Subtype 3a is observed in 20% of patients, and the remaining percentages are for hepatitis C virus genotype 2, 3b and 1a. At the same time, the prevalence of hepatitis 1b is gradually decreasing,

genotype 3 of hepatitis C virus remains at the same level, and the prevalence of genotype 2 is slowly increasing.

Among the countries of the Middle East, the largest number of infected people was registered in Egypt - about 20% of the population.

In European countries with a high standard of living, in the USA, Japan and Australia, the number of cases ranges from 1.5% to 2%.

In Northern Europe, the number of people infected with hepatitis C does not exceed 0.1-0.8%, and in Eastern Europe, North Africa and Asia, the number of patients is 5-6.5%.

In general, there is an increase in the number of hepatitis C infections due to the identification of patients with chronic form.

Causative agent

For the first time, information about the causative agent of hepatitis C was obtained as a result of experiments on chimpanzees - a virus-containing material passed through a filter made it possible to determine the size of the virus, and the treatment of this material with various chemical preparations - to establish sensitivity to fat-soluble agents. Thanks to these data, the virus was assigned to the Flaviviridae family.

Using the plasma of infected chimpanzees and new molecular biological methods, in 1988 the genome of the hepatitis C virus (HCV), an RNA-containing virus from the Flaviviridae family, was cloned and sequestered.

The genome of this virus is a single-stranded linear RNA with positive polarity (approximately 9600 nucleotides). The virus is spherical in diameter and has a lipid membrane. On average, the diameter of the virus is 50. It contains two zones that encode:

structural proteins (locus El and E2 / NS1);
non-structural proteins (locus NS2, NS3, NS4A, NS4B, NS5A and NS5B).

Structural proteins are part of the virion, and non-structural (functional) proteins have the enzymatic activity necessary for viral replication (protease, helicase, RNA-dependent RNA polymerase).

Virus mutation occurs continuously - significant changes in nucleotide sequences occur in the hypervariable and variable regions (E1 and E2). It is thanks to these parts of the genome that the virus evades the body's immune response and remains in a functionally active state for a long time.

Changes in hypervariable regions lead to changes in antigenic determinants (parts of antigen macromolecules that the immune system recognizes) so rapidly that the immune response is delayed.

Reproduction of the virus occurs mainly in the hepatocytes of the liver. The virus can also multiply in peripheral blood mononuclear cells, which negatively affects the patient's immune system.

When the virus reproduces:

At the initial stage, it is adsorbed on the cell membrane, after which viral RNA is released into the cytoplasm.
At the second stage, RNA is translated (protein is synthesized from amino acids on messenger RNA) and the viral polyprotein is processed, after which a reactive complex is formed, which is associated with the intracellular membrane.
In the future, for the synthesis of intermediate minus-chains of the RNA of the virus, the plus-chains of its RNA are used, new plus-chains and viral proteins are synthesized, which are necessary for collecting new particles of the virus.
The final stage is the release of the virus from the infected cell.

As a result of continuous mutations, all hepatitis C genotypes have millions of different quasispecies (differing in nucleotide sequence) that are unique to a particular person. According to the assumptions of scientists, quasi-species have an impact on the development of the disease and on the response to treatment.

The level of homology (similarity) between subtypes of one group of the hepatitis C virus does not exceed 70%, and the difference in the nucleotide sequence in quasispecies does not exceed 1-14%.

It has not yet been possible to cultivate the hepatitis C virus, so its properties have not been sufficiently studied. Like all members of the flavivirus family, the hepatitis C virus is not stable in the external environment - it is inactivated with the help of fat-soluble disinfectants, is sensitive to ultraviolet irradiation, at 100 ° C it dies in 1-2 minutes, at 60 ° C in 30 minutes, but withstands heating up to 50 ° C.

Transmission routes

Infection with hepatitis C occurs parenterally - the transmission of hepatitis C from an infected person to a healthy person occurs in most cases through blood and blood components, and in 3% of cases through semen and vaginal discharge.

The main modes of transmission of hepatitis C:

Transfusion of blood and its components. Before the isolation of the virus and the appearance of laboratory diagnostics, this route of infection was the main one for hepatitis C, however, the obligatory examination of donors and laboratory blood tests significantly reduced the possibility of infection in this way (in 1-2% of donors a virus is detected that patients do not even suspect).
Piercing and tattooing procedures. This method of infection is currently the most common, since there is poor-quality sterilization of the instruments used or its complete absence.
A visit to the hairdresser, manicure or dental office, acupuncture procedure.
Use of razors and other personal care products for a sick person.
Injection addiction (using shared syringes). In this way, about 40% of patients are most often infected, genotype 3a is mainly transmitted.
Provision of medical care (when treating wounds, working with blood and blood products in the presence of skin lesions).

There are other ways of transmission of hepatitis C:

Vertical, that is, from mother to child during childbirth. The risk of infection increases if there is acute hepatitis C in pregnant women, or an acute form of the disease was observed in the last months of pregnancy.
Sexual. The probability of infection with constant sexual intercourse of heterosexual couples is quite low in the northern hemisphere - in the northern European countries 0 - 0.5%, in North America - 2 - 4.8%. In South America, sexual transmission is observed in 5.6 - 20, 7%, and in Southeast Asia from 8.8 to 27%.

The routes of transmission of viral hepatitis C during unprotected sexual intercourse and during childbirth are not often observed in comparison with the total number of patients (3-5%).

For hepatitis C, methods of infection through breast milk, food, water and safe contact (hugs, etc.) are not typical. The virus does not spread when using common utensils.

Risk factors

Risk factors include:

the need for blood transfusion and organ transplantation;
injecting drug use;
the need for extrarenal blood purification (hemodialysis);
professional contact with blood and blood products;
sexual contact with the patient.

The high-risk group includes people who inject drugs, patients in need of hemodialysis or systematic blood transfusion procedures, patients with hematopoietic cancer, donors and medical personnel.

Because it is possible to acquire hepatitis C through sexual contact, the risk group includes:

people of non-traditional sexual orientation;
persons with multiple sex partners;
persons who do not use protective equipment during sexual intercourse.

Pathogenesis

The incubation period for hepatitis C is 14 days to 6 months. Most often, clinical manifestations begin to appear after 1.5 - 2 months.

The pathogenesis of hepatitis C is not fully understood, however, it is known that the virus enters the body with blood particles of previously infected people, and, once it enters the bloodstream, it enters the hepatocytes with the blood stream, where replication (copying) of the virus mainly occurs. The process of introducing the virus can be seen below.

Liver cells are affected by:

Direct cytopathic action on cell membranes and hepatocyte structures. Degenerative changes in cells are caused by components of the virus or specific products of its vital activity.
Immunologically mediated (including autoimmune) damage that targets intracellular antigens of the virus.

In the affected cell, about 50 viruses are formed per day.

The course and outcome of hepatitis C (the death of the virus or its preservation in an active state) depends on the effectiveness of the body's immune response.

The acute phase is accompanied by a high concentration of hepatitis C virus RNA in the blood serum during the first week after infection. The specific cellular immune response in acute hepatitis C is delayed by a month, humoral immunity - by 2 months.

A decrease in hepatitis C RNA titer is observed with a maximum increase in the level of ALT (a marker enzyme for the liver) in the blood 8-12 weeks after infection.

Jaundice due to T-cell liver damage is rare in acute hepatitis C.

Antibodies to hepatitis C are detected somewhat later, but they may not be present.

In most cases, the acute form of the disease becomes chronic. Upon recovery, Rirus RNA (HCV) is not detected by standard diagnostic tests. The virus disappears from the liver and other organs later than from the blood, since in some cases the return of the virus to the blood is observed even 4-5 months after the RNA of the virus has ceased to be detected in the blood.

Until now, it has not been established whether the virus completely disappears from the body, or whether a person, even after recovery, is a carrier of hepatitis C.

The viral load in chronic hepatitis C is stable and 2-3 orders of magnitude lower than in the acute form of the disease.

Almost all spontaneously recovered patients from acute hepatitis C have a strong polyclonal specific T-cell response, and in patients with chronic HCV infection, the immune response is weak, short-lived, or narrowly focused. This confirms the dependence of the outcome of the disease on the duration and strength of the specific cellular immune response.

The virus escapes from the control of the host's immune response due to the high mutational variability of the hepatitis C genome, as a result of which the virus is able to remain active for a long time (possibly lifelong) in the human body.

The factors that affect immunity and cause its inability to control the hepatitis C virus are not well understood.

In the presence of HCV infection, a variety of extrahepatic lesions may appear, which arise as a result of immunopathological reactions of immunocompetent cells. These reactions can be realized as immunocellular (granulomatosis, lymphomacrophage infiltrates) or immunocomplex reactions (vasculitis of various localization).

Morphological changes in the liver in this disease do not differ in specificity. They mainly reveal:

lymphoid infiltration of the portal tracts, which is accompanied by the formation of lymphoid follicles;
lymphoid infiltration of the lobules;
stepwise necrosis;
steatosis;
damage to small bile ducts;
liver fibrosis.

These changes in the liver, which determine the stage of hepatitis and the degree of histological activity, are observed in various combinations.

In the chronic form of the disease:

inflammatory infiltration is characterized by the predominance of lymphocytes around the foci of death and damage of hepatocytes, as well as in the portal tracts (thus, the participation of the immune system in the pathogenesis of liver damage is confirmed);
fatty degeneration of hepatocytes (steatosis) is observed, which is more pronounced with a lesion with genotype 3a than with a lesion with genotype 1.

Even with low histological activity in the chronic form of the disease, liver fibrosis can be observed (it can affect both the portal and periportal zones of the lobules, and their central part (perivenular fibrosis)).

Grade 3 liver fibrosis in hepatitis C leads to the development of cirrhosis, against which hepatocellular carcinoma can develop.

Grade 4 fibrosis in hepatitis C is essentially cirrhosis (diffuse fibrosis with the formation of false lobules).

Liver cirrhosis occurs in 15-20% of patients and is accompanied by significant inflammatory changes in the liver tissue.

Symptoms

After an incubation period, approximately 80% of those infected will develop an asymptomatic form of the disease (inactive hepatitis C).

Clinic for acute hepatitis C includes:

The temperature, which usually does not exceed 37.2-37.5 ° C, and only in rare cases reaches high numbers. The temperature in hepatitis C rises smoothly and can last for a long period, but it may not be at all.
Feeling tired.
Decreased appetite.
Nausea, vomiting, which is episodic.
Feeling of heaviness and pain in the right hypochondrium (area of \u200b\u200bthe liver projection).
Discoloration of urine and stool. As a result of liver tissue damage, an excess amount of bilirubin pigment is present in the urine, so the urine becomes dark brown. Normally light foam becomes yellow and does not spread evenly over the surface, but forms small, rapidly disappearing bubbles. The feces acquire a gray tint (discolored) as a result of the loss of the ability of hepatocytes to excrete bilirubin (it is bilirubin that turns into stercobilin in the intestine, which gives the feces a brown tint).
Joint pain, often mistaken for arthritis.
Yellowing of the skin and whites of the eyes (jaundice). This symptom manifests itself in the same way as with other types of hepatitis.

Yellowing of the skin and whites of the eyes with hepatitis C

If a person develops acute hepatitis C, symptoms develop gradually until jaundice and changes in the color of urine and stool resemble the flu.

In some cases, liver dysfunctions cause a rash in hepatitis C. In the acute form, rashes appear extremely rarely (may be accompanied by itching), more often this symptom accompanies cirrhosis.

The symptoms of hepatitis C in men are the same as those in women.

The chronic form of the disease is characterized by:

weakness, fatigue after minor exertion, feeling weak after sleep;
joint pain;
prolonged subfibrillation for no apparent reason;
bloating, decreased appetite;
unstable stools;
decreased immunity.

Possible yellow coating on the tongue. There is also a violation of the biological rhythm of sleep (daytime sleepiness, nighttime insomnia) and mood changes up to depression (such symptoms are more often observed in women with hepatitis C).

The first signs of hepatitis C in men and women appear after a serious liver injury, if the disease was not detected earlier by tests.

Clearly noticeable signs are:

jaundice;
an increase in the volume of the abdomen (ascites);
severe weakness and fatigue;
varicose asterisks in the abdomen.

Hepatitis C in children is characterized by an increased tendency to chronicity (about 41% of all chronic hepatitis in this age group) and progression to cirrhosis. Perhaps the development of liver failure and the appearance of malignant neoplasms.

The acute form of hepatitis C begins with the development of asthenovegetative syndrome (a functional disorder of the autonomic nervous system, which is manifested by dyspeptic disorders).

stomach ache;
pain in large joints (not always observed);
body temperature increased to subfebrile values;
darkening of urine and discoloration of feces;
intoxication, in which there is nausea, vomiting, headache.

A yellow tint of the skin and sclera is observed in 15-40% of cases (the icteric period is easier than with other types of hepatitis, and lasts for weeks).

The chronic form can proceed for many years without clinical symptoms (it is detected by chance during examinations). The relatively satisfactory condition of children is accompanied by hepatomegaly, and in 60% of patients and splenomegaly. A third of children suffer from asthenia, increased fatigue, and extrahepatic symptoms (telangiectasia, capillaritis) are also present.

Even with a minimal and low degree of activity of chronic hepatitis C, there is a persistent tendency to develop fibrosis (in 50% of cases one year after infection and in 87% of cases after 5 years).

Hepatitis C in newborns is manifested by:

lack of appetite;
constant low-grade fever;
stool disorders;
enlarged liver;
dark urine;
discoloration of feces;
skin rashes;
low immunity.

Developmental delay and jaundice are possible.

Diagnostics

Diagnosis of hepatitis C according to ICD10 is based on:

Epidemic anamnesis data for a month before the first detected signs of the disease.
The presence of antibodies to hepatitis C. Total antibodies to hepatitis C (the simultaneous presence of antibodies of the IgG and IgM class, which are formed against the proteins of the hepatitis C virus and are detected by ELISA) are normally absent in the blood. On average, antibodies are produced after infection. Antibodies of the IgM class are formed within a week, and after 1.5 - 2 months - antibodies of the IgG class. The maximum concentration is observed for the month of the disease. These antibodies can be present in serum for years.
The presence of hyperenzymemia. A 1.5 - 5-fold increase in ALT activity is considered moderate hyperenzymemia, at once - moderate hyperenzymemia, and more than 10 times - high. In the acute form of the disease, the ALT activity reaches a maximum at the 2nd - 3rd week of the disease and normalizes after a day with a favorable course (usually, in acute hepatitis C, the ALT activity level is 0 IU / L). In the chronic form of the disease, there is a moderate to medium degree of hyperenzymemia. AST levels also increase in acute hepatitis C.
The presence of a violation of pigment metabolism.

Diagnosis of the disease includes:

A general blood test, which allows you to identify an increase in the erythrocyte sedimentation rate (ESR), characteristic of viral hepatitis.
A biochemical blood test that detects increased activity of liver enzymes (transaminases that enter the bloodstream from damaged liver cells).
A serological test (ELISA) to detect antibodies to hepatitis C.
Ultrasonography. Ultrasound of the liver with hepatitis C allows you to determine changes in the structure of the liver.

Since HIV and hepatitis C can be combined (coinfection, which is more common with genotype 3a), if one of the diseases is detected, an analysis is made for the second disease.

If hepatitis C antibodies are found in the blood or hepatitis C is suspected, the patient is referred for:

PCR analysis for hepatitis C (blood test, which allows you to identify the genetic material of the virus).
Elastometry. It is performed on the Fibroscan apparatus, which allows the density of the liver tissue to be determined using ultrasound.

PCR for hepatitis C is:

Qualitative - confirms the presence of the virus in the blood. It has a certain sensitivity (IU / ml), therefore, it does not detect the virus at a very low concentration.
Quantitative - determines the concentration of the virus in the blood. Differs in higher sensitivity than a quality test.

A qualitative analysis for hepatitis C is performed in all patients who have antibodies to hepatitis C (the norm is “not detected”). When conducting high-quality PCR for hepatitis C, tests with a sensitivity of at least 50 IU / ml are usually used. Effective for monitoring therapy results.

A quantitative analysis for hepatitis C (viral load) allows you to determine the number of units of genetic material of viral RNA in a certain volume of blood (standard - 1 ml). The unit of measurement for the amount of genetic material is IU / ml (international units per milliliter). It is also possible to use a unit such as copies / ml.

The viral load affects infectivity (with a high concentration of the virus, the risk of vertical or sexual transmission of infection increases), as well as the effectiveness of interferon-based treatment (with a low viral load, such therapy will be effective, but with a high viral load, it will not).

There is currently no consensus among specialists on the borderline between high and low viral loads, but some foreign authors in their works note 400,000 IU / ml. Thus, the viral load in hepatitis C, the norm for interferon-based therapy, is values \u200b\u200bup to 400,000 IU / ml.

A quantitative test is done before the appointment of treatment and after 12 weeks from its start if the qualitative test still shows the presence of the virus in the blood. The result of this test can be a quantitative assessment of the virus concentration, "below the measuring range" and "not detected".

A PCR blood test for hepatitis C gives accurate results, with the exception of a false-positive test at the final stage of recovery.

The ELISA test can, in rare cases, give a false positive result for hepatitis C, which can occur as a consequence of:

Little researched cross-reactions.
Pregnancy. A false positive test for hepatitis C during pregnancy is associated with the gestation process, the formation of specific proteins and changes in the trace element composition of the blood and hormonal levels of the body.
Acute upper respiratory tract infections, including influenza.
Recent vaccination against influenza, tetanus, or hepatitis B.
Recently conducted alpha interferon therapy.
Pre-existing tuberculosis, herpes, malaria, hernia, multiple sclerosis, scleroderma, arthritis and kidney failure.
Increase in bilirubin in the blood, which is individual.
Autoimmune diseases.
The presence of malignant and benign neoplasms.

If a false-positive test for hepatitis C is suspected, more research is needed. If a positive test for hepatitis C is obtained by PCR, the patient is prescribed treatment.

Treatment

Treatment for hepatitis C includes:

adherence to a healthy lifestyle;
drug treatment.

Adequate rest, balanced nutrition and plenty of drink in combination with genetically inherited polymorphism of the interferon-λ IL28B C / C gene in 20% of cases leads to spontaneous cure of patients with an acute form of the disease.

Until 2011, the main drug for hepatitis C that was used all over the world was a combination of interferons and ribavirin. These drugs for the treatment of hepatitis C were prescribed for 12 to 72 weeks, depending on the type of virus genotype. This treatment for hepatitis C virus was effective in% of patients with genotypes 2 and 3, and in% of patients with genotypes 1 and 4.

Since many patients experienced adverse flu-like symptoms, and one third had emotional problems, patients with chronic hepatitis C and no high risk of death due to other diseases are now prescribed interferon-free therapy using direct-acting antiviral drugs.

Interferon-free therapy for hepatitis C is based on the use of replication inhibitors of 3 non-structural proteins of the hepatitis C virus (NS3 / 4a protease, NS5a interferon-resistant protein, NS5b polymerase). Sofosbuvir (a nucleotide inhibitor of NS5b polymerase) is distinguished by a high threshold of resistance, therefore antiviral therapy for hepatitis C with any treatment regimen is based on the use of this drug in the absence of individual contraindications.

For hepatitis C therapy to be effective, treatment must be comprehensive.

The treatment regimen depends on the form of the disease and the genotype of the virus, therefore genotyping of hepatitis C is important in the diagnosis.

If the person has acute hepatitis C, treatment is more effective during the first six months after infection. Medicines for hepatitis C:

sofosbuvir + daclatasvir or sofosbuvir + velpatasvir for 6 weeks;
sofosbuvir + daclatasvir or sofosbuvir + velpatasvir for 8 weeks in HIV infection.

Chronic hepatitis C, treatment:

In the absence of cirrhosis of the liver and with virus genotypes 1, 2, 4, 5, 6 - sofosbuvir + velpatasvir for 12 weeks.
In the absence of cirrhosis of the liver, hepatitis C 3 genotype, treatment - sofosbuvir or ombitasvir + paritaprevir (ombitasvir + ritonavir), or sofosbuvir + velpatasvir (possibly in combination with ribavirin) for 12 weeks.
In case of compensated cirrhosis of the liver with virus genotypes 1, 2, 4, 5, 6, sofosbuvir + velpatasvir is prescribed for 12 weeks.
With compensated cirrhosis of the liver and virus genotype 3, sofosbuvir and mudoprevir or elbasvir are prescribed for 12 weeks, it is possible to prescribe ombitasvir + paritaprevir + ritonavir or a less optimal option - sofosbuvir or velpatasvir and ribavirin.
With decompensated cirrhosis of the liver, sofosbuvir or velpatasvir and ribavirin are used for 12 weeks (mudoprevir and other protease replication inhibitors are not prescribed due to their high hepatotoxicity).

In the treatment of hepatitis C, the drugs with the best treatment results are sofosbuvir or velpatasvir + ribavirin (effective in% of cases), but there are other possible treatment regimens.

Sofosbuvir is an active chemical in the patented antiviral drug Sovaldi, which is produced by the American corporation Gilead Sciences Inc. Due to the drug's ability to inhibit hepatitis C NS5B polymerase, viral replication is significantly reduced or stopped. Sofosbuvir is more effective than all other drugs for hepatitis C currently available.

Treatment of hepatitis C, drugs with the best treatment results with the active ingredient sofosbuvir:

Cimivir, SoviHep, Resof, Hepcinat, Hepcvir, Virso of Indian manufacturer;
Gratisovir, Grateziano, Sofocivir, Sofolanork, MPI Viropack of Egyptian production.

Hepatoprotectors for hepatitis C do not reduce the activity of the virus, but only stimulate the regeneration of liver cells and reduce the symptoms of the disease.

Hepatitis C and pregnancy

Pregnancy and hepatitis C in the mother - the risk of transmitting the virus to the child during childbirth (in the absence of HIV infection in the mother, infection occurs only in 5% of cases, and in the presence of HIV infection - about 15.5% of cases).

Due to the potential for intrauterine transmission

prenatal diagnostic techniques are not recommended for such patients. Currently, antiviral therapy for pregnant women is not carried out, although the use of alpha-interferon in the treatment of chronic myelogenous leukemia in pregnant women gives good results and does not cause fetal damage.

If hepatitis C is diagnosed in pregnant women, maternal viral load should be measured in the first and third trimesters. Depending on the viral load, delivery with hepatitis C can be either natural or by caesarean section (with a viral load of more than 106-107 copies / ml, women are recommended to have a caesarean section).

Forecast

Currently, hepatitis C is completely cured in 40% of patients with hepatitis 1 genotype and in 70% of patients with genotypes 2 and 3.

Because acute hepatitis C infection is rarely detected early, treatment is usually not given. At the same time, from 10 to 30% of patients recover on their own, and in the rest of the infected, the disease becomes chronic.

Life with hepatitis C is qualitatively worsening (the condition of a particular patient depends on the characteristics of his body, the genotype of the virus and the presence / absence of treatment). In the course of treatment, side effects may develop (insomnia, irritability, decreased hemoglobin levels, lack of appetite and the appearance of skin rashes).

Complications of hepatitis C include:

liver fibrosis;
cirrhosis of the liver (in 20-30%);
hepatocarcinoma (3-5%);
diseases of the biliary tract;
hepatic coma.

These consequences of hepatitis C are more common in patients at risk.

Extrahepatic manifestations are also possible - glomerulonephritis, mixed cryoglobulinemia, late cutaneous porphyria, etc.

In severe hepatitis C, life expectancy is significantly reduced - with cirrhosis of the liver, the 10-year survival rate is 50%.

Disability for hepatitis C is granted if there are complications of the disease (severe cirrhosis or liver cancer).

Prevention

There are currently no approved vaccines for hepatitis C, but some of the vaccines in development are showing promising results.

Since hepatitis C is transmitted primarily through blood, the main preventive measures are:

screening of donated blood;
observance of precautionary measures in medical institutions;
using disposable needles for tattooing, preventing the use of personal hygiene items by different people;
substance abuse treatment and concurrent provision of new needles and syringes.

Since hepatitis C and sex are rarely, but nevertheless, interrelated, protected sex is a precaution (especially for people who have a partner with hepatitis C).

To prevent the development of complications of hepatitis C, people who are already sick are advised to lead a healthy lifestyle and follow a diet (table number 5). It is believed that alcohol and hepatitis C are incompatible concepts, although there is no evidence that alcohol in small doses affects the development of fibrosis.