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Treatment of chronic hepatitis. Chronic viral hepatitis

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Symptoms of hepatitis C

Hepatitis C is one of the most common types of hepatitis, most severely affecting the liver, disrupting its functioning. Moreover, for a long time the disease can be completely asymptomatic, which is why the disease is detected too late. As a result, the infected person can become a hidden carrier and distributor of the virus.

Hepatitis C virus (HCV) has two forms: acute and chronic. Immediately after infection, an incubation period begins, sometimes lasting from 6 - 7 weeks to six months. Acute form Symptoms of the disease appear after completion incubation period and are expressed elevated temperature, headache, muscle and joint pain, general malaise and weakness. This period is also called anicteric, it lasts 2 ÷ 4 weeks. This is followed by the icteric phase, during which the patient may develop a icteric coloration of the skin, accompanied by pain in the right hypochondrium, vomiting, diarrhea, and lack of appetite. But the first thing that worries you is the color of the urine, which turns brown. Sometimes an anicteric form of the disease can be observed. During the acute phase, the level of bilirubin in the blood increases. It lasts for about a month, after which it begins recovery period lasting for several months. After it, in 15–25% of cases, self-healing can occur or the disease becomes chronic.

Symptoms of chronic hepatitis C

The transition of HCV from the acute to the chronic phase occurs in approximately 80% of cases. Moreover, in women the chronic form occurs less frequently than in men, and their symptoms of the disease are less pronounced. Although sometimes signs of the disease are not noticeable in men, this does not interfere with the inflammatory process that is actively occurring in the liver. As a result, the disease first takes a chronic form, and then develops into cirrhosis or liver cancer.

At asymptomatic Chronic hepatitis C (CHC) disease can be expressed in the following symptoms:

weaknesses;
decreased performance;
loss of appetite.

Periodically during the course of the disease, wave-like exacerbations occur, followed by remissions. But such exacerbations are rarely accepted severe form. Symptoms of HCV in adult patients are most often mild, while children suffer more severely. In them, the disease takes a more aggressive form, accompanied by exacerbation and the occurrence of complications in the form of cirrhosis. Signs of chronic hepatitis C virus (CHC) are worsened by exposure unfavorable factors, which include:

heavy physical or neuropsychic stress;
poor nutrition;
alcohol abuse.

Moreover, the last factor most strongly has a negative effect on the liver of patients with chronic hepatitis C. This happens due to the fact that patients may develop toxic alcoholic hepatitis, which increases the manifestations of chronic hepatitis C and contributes to the occurrence of complications in the form of cirrhosis. Wave-like changes are characteristic not only of the course of the disease, they are also directly reflected in laboratory parameters. Because of this, patients periodically notice increased levels of bilirubin and liver enzymes in their blood.

Moreover, a long period of time is recorded normal values laboratory parameters even in the presence of changes in the liver. This forces laboratory monitoring to be carried out more often - at least once or twice a year. Since HCV symptoms do not always manifest themselves clearly expressed form, you should pay attention to cases of weakness and decreased performance. Having noticed such signs, it makes sense to be examined for the presence of HCV infection.

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Chronic hepatitis is a diffuse polyetiological inflammatory process in the liver that develops over more than six months. In chronic hepatitis, unlike cirrhosis of the liver, there is no disturbance in the architecture of the liver.

Causes

Chronic hepatitis occurs as a result of the development of previous diseases:

HCV infection transforms into a chronic stage in 75% of cases, and HBV infection in 5–10%. Hepatitis A and E do not become chronic. The mechanism of occurrence of the chronic process is not fully understood; it is known that liver damage is caused by the immune system’s response to infection.

With idiopathic origin of hepatitis, the following are observed:

severe symptoms of hepatocellular immune damage, including serological immune markers;
association with haplotypes of histocompatibility antigens that are inherent in autoimmune diseases (HLA-DR4, HLA-B8, HLA-B1, HLA-DR3);
dominance of plasma cells and T-lymphocytes in histological preparations of pathological areas of the liver;
disorders of the immune regulatory function and cellular immunity during in vitro studies;
relationship with other autoimmune diseases (rheumatoid arthritis, hemolytic anemia, proliferative glomerulonephritis, etc.) and a positive reaction to treatment with immunosuppressants and corticosteroids.

Sometimes it's bad. hepatitis occurs with signs of other liver diseases (autoimmune hepatitis, primary biliary cirrhosis, etc.). Such conditions are referred to as overlap syndromes.

Chronic hepatitis can be caused by drugs (Paracetamol, Isoniazid, Nitrofurans, Methyldop, etc.). Mechanism of occurrence drug-induced hepatitis depends on the drug and may contain:

change in immune response;
the occurrence of intermediate cytotoxic metabolites;
genetically determined metabolic pathologies.

In the past hepatitis was classified according to histological characteristics:

chronic active hepatitis;
chronic persistent hepatitis;
chronic lobular hepatitis.

Modern classification takes into account the etiology, the severity of the inflammatory process and necrosis, the degree of fibrosis, examined during histological examination. Infiltration and inflammation are potentially reversible; necrosis is usually irreversible.

Symptoms

Chronic hepatitis often occurs after acute hepatitis (about every third case), but the disease usually develops gradually. In many cases, the disease occurs without symptoms, especially with HCV. Symptoms such as:

anorexia;
malaise;
fatigue;
discomfort in upper area belly;

Rarely, the disease is accompanied by low-grade fever. Jaundice is most often absent.

The initial clinical manifestations, especially with HCV, are symptoms of chronic liver disease:

splenomegaly;
palmar erythema;
spider veins or spiders;
pain in the hypochondrium on the right.

In some cases, signs of cholestasis appear. With the autoimmune nature of the disease, especially in women, the disease can involve almost any organ in the disease process and be expressed in amenorrhea, ulcerative colitis, thyroiditis, hemolytic anemia, pulmonary fibrosis, nephritis, arthralgia. Chronic HCV infection may be accompanied by Wilson's lichen, glomerulonephritis, mucocutaneous vasculitis, and cutaneous porphyria.

Chronic active hepatitis is characterized by striking symptoms: jaundice, splenomegaly, thrombocytopenia, hypergammaglobulinemia, enzyme activity, high titers of immunoglobulins.

The lupoid variant is characterized by arthralgia, allergic symptoms, lymphadenopathy, and cardiovascular changes.

Diagnostics

Chronic hepatitis is assumed in patients with characteristic symptoms, if an increase in the level of aminotransferases is accidentally detected, as well as if there is a history of acute hepatitis. Functional tests for the liver are analyzed, including determining the level of AST and ALT, serum bilirubin, and alkaline phosphatase.

Elevated aminotransferase levels are distinctive laboratory markers of the disease. Enzyme levels can fluctuate but average 100–500 IU/L. Aminotransferase levels may not be outside the normal range if the disease is stable, this is especially true with HCV infection. AST is usually lower than ALT.

Alkaline phosphatase is most often either normal or slightly elevated, and in in rare cases markedly high. Bilirubin in mild cases is usually within the normal range. When clinical signs of hepatitis are not confirmed by laboratory tests, serological tests are performed to exclude HCV and HBV. If serology does not reveal viral etiology, further analyzes are needed.

Research consists of determining the levels of immunoglobulins, autoantibodies and α1-antitrypsin. Children undergo a screening test for Wilson's disease to determine the ceruloplasmin level. Detection elevated levels Serum immunoglobulins are one of the markers of autoimmune chronic hepatitis. Autoimmune hepatitis is diagnosed by antinuclear body levels: over 1:80 in adults, over 1:20 in children. Also, to confirm the autoimmune nature of hepatitis, studies are carried out on kidney and liver microsomes (anti-LKMI) and anti-smooth muscle antibodies.

To confirm chronic hepatitis, a liver biopsy is needed. Sometimes chronic hepatitis manifests only with slight hepatocellular necrosis and inflammatory cell infiltration in the area of portal venules, with acinar architecture within normal limits, as well as little or no fibrosis.

IN severe cases According to the results of the biopsy, periportal necrosis with cellular mononuclear infiltration is revealed against the background of proliferation of the bile ducts and periportal fibrosis. Deformations due to foci of damage and fibrosis of the acinar architecture are possible. A biopsy is also necessary to analyze the severity and determine the stage of the disease.

The specific cause of chronic hepatitis is usually not possible to determine using a biopsy. However, cases of the disease caused by HBV infection are differentiated by the presence of frosted-vitreous hepatocytes and the special coloring of HBV components.

In autoimmune hepatitis, pronounced plasma cell and lymphocytic infiltration. In the presence of histological and absence of serological symptoms of chronic hepatitis of an autoimmune nature, its variants need to be diagnosed - some of them may meet the criteria for overlap syndrome.

If symptoms of cryoglobulinemia appear in the chronic form of the disease, it is necessary to analyze rheumatoid factor and cryoglobulin levels. High rheumatoid factor levels and low complement levels indicate cryoglobulinemia.

Liver failure is characterized by low albumin levels and prolonged prothrombin time.

To exclude hepatocellular carcinoma, annual ultrasound and serum a-fetoprotein testing are required. Patients suffering from chronic hepatitis C are screened for HCC only if liver cirrhosis is detected.

Forecast

Chronic drug-induced hepatitis often resolves when the drugs are discontinued. If chronic hepatitis B is not treated, the disease progresses and can transform into cirrhosis of the liver. Hepatitis B becomes most severe in its chronic form when combined with HDV infection. Untreated chronic hepatitis C leads to liver cirrhosis in 20–30% of cases, and the process can last for decades. Autoimmune hepatitis in its chronic form is usually treatable, but can lead to progressive fibrosis and often cirrhosis.

Hepatitis B in the chronic stage increases the risk of hepatocellular carcinoma. The same risk increases with chronic hepatitis C, but only in the presence of liver cirrhosis.

Treatment

The goals of therapy are to prevent complications (for example, encephalopathy and ascites) and smooth out the manifestations of the disease. If hepatitis is caused by taking medicines, it is necessary to discontinue the corresponding medications. Prevention of contact infection is useful. For HCV infection, preventative measures are not necessary.

Autoimmune hepatitis

The simultaneous use of glucocorticoids and azathioprine is a subject of controversy among specialists. Some believe that the combination of glucocorticoids and Azathioprine helps to increase the life expectancy of patients with autoimmune hepatitis. Azathioprine is prescribed to be taken orally at a dose of 1–1.5 mg per day in one dose. Other doctors prescribe Azathioprine only when low-dose Prednisolone does not provide suppression.

Prednisolone is taken orally at 30–40 mg per day in one dose. Later, the dose is reduced to a level that keeps aminotransferases within normal limits.

A liver transplant is necessary only in the final stage of the disease.

HBV

Therapy is needed for HBeAg-positive patients who have high levels of aminotransferases. Treatment goals: conversion of the patient from HBeAg to anti-HBe and elimination of HBV DNA. HBsAg disappears from the serum in approximately 10% of cases. Interferon or Lamivudine are used as medications.

The interferon drug is administered subcutaneously at 5 million IU per day or 10 million IU per day three times a week for 4 months. In approximately 40% of cases, this treatment regimen clears HBV DNA and promotes seroconversion to anti-HBe. Evidence of the effectiveness of treatment is a transient increase in aminotransferase levels.

The initiation of treatment with Interferon may occur against the background of a flu-like syndrome caused by it.

Other negative effects of Interferon:

malaise;
depression;
fatigue;
bone marrow suppression;
autoimmune pathologies and bacterial infections(occasionally).

Interferon contributes to the development of liver failure in people with cirrhosis. Therefore, in case of liver cirrhosis, Interferon is contraindicated. Also, the drug is not prescribed for immunosuppression, renal failure, cytopenia, substance abuse, or after organ transplantation. Patients with a combination of hepatitis D virus and HBV infections are difficult to treat. The effect of using pegylated Interferon in chronic hepatitis B, in contrast to chronic hepatitis C, remains incompletely studied.

An alternative drug for the treatment of HBV is Lamivudine - 150 mg orally daily. Compared to Interferon, Lamivudine has fewer side effects, but its use is designed for a long period. The drug reduces HBV DNA levels and aminotransferase levels in most cases, however, at the end of therapy, a relapse is observed until seroconversion from HBeAg to anti-HBeg. The onset of seroconversion is recorded in 15–20% of cases after a year of treatment and in approximately 40% of patients over a three-year period. With long-term therapy, resistance to lamivudine develops.

Lamivudine can be used in individuals with advanced liver cirrhosis as it does not contribute to liver failure. Combining Lamivudine with Interferon did not reveal any advantages of this treatment tactic.

Adefovir, taken orally, may in the future become a popular drug of choice in the treatment of chronic hepatitis B. Adefovir is safe, and resistance to it is rare. Liver transplantation is relevant only in the final stage of liver disease caused by HBV. However, infection exposes the graft to intense attacks, so the prognosis for transplant success is worse than for transplantation for other indications. Long-term use of Lamivudine improves the prognosis for transplant success.

HCV

Treatment for chronic hepatitis C is necessary if the aminotransferase level is increased, and the biopsy shows the active development of the inflammatory process and fibrosis. Therapy is required to eliminate HCV RNA, as a result of which the aminotransferase level is normalized and the histological process stops.

Reliable results are achieved by simultaneous therapy with pegylated Interferon and Ribavirin. A comparable effect is achieved by injections of pegylated Interferon-alpha 2b (subcutaneous 1.5 mcg/kg per week in one dose) and pegylated Interferon-alpha 2a (subcutaneous 180 mcg/kg per week in one dose). Ribavirin is taken orally at a dose of 500–600 mg twice daily. For virus genotypes 2 and 3, a sufficient dose is two doses of 400 mg per day.

The viral load and genotype of HCV are established before treatment, since its regimen depends on this. Genotype 1 is observed more often and is quite resistant to treatment. Combination therapy lasts for a year and gives positive effect in 45–50% of cases. The favorable results depend on the stage of the disease at which treatment is started. 3 months after the start of therapy, the viral load is determined. If the RNA level has not decreased by at least 2 units, treatment is stopped.

Genotypes 2 and 3 are not as common, but are more treatable. The combination therapy period is 6 months, and a sustained response is observed in three quarters of patients. Extending the treatment period does not improve results. Regulated Interferon gives almost the same side effects, as standard Interferon, but they are more pronounced. The drug is used with caution or is not prescribed at all to drug-dependent patients and persons with mental disorders.

Ribavirin is well accepted, but can cause hemolytic anemia. Doses of the drug should be reduced if hemoglobin decreases to less than 10 g/dl. Since Ribavirin has a teratogenic effect, patients should use contraceptives throughout the entire period of treatment and for six months after its completion.

Patients who are intolerant to Ribavirin are prescribed monotherapy with pegylated Interferon. However, such treatment tactics are not as effective as a combination of drugs. The use of Ribavirin as the only drug of treatment is not effective.

For HCV, the most common indication for transplantation is the progressive nature of liver cirrhosis. Although the infection recurs in the transplanted organ, the long-term results of transplantation are favorable.

Hepatitis C – inflammatory disease liver, it develops under the influence of the hepatitis C virus. An effective vaccine that could protect against this virus simply does not exist in nature, and it will not appear soon.

It comes in two types – acute and chronic. In 20% of cases, people with acute hepatitis have a good chance of recovery, and in 80%, the patient’s body is not able to overcome the virus itself and the disease becomes chronic.

Transmission of the virus occurs through infection through blood. Today, there are 150 million people in the world who are carriers of chronic hepatitis C, and every year hepatitis ends in death in 350 thousand patients.

Basically, the first symptoms of hepatitis C appear 30-90 days after infection. That is why if you feel unwell, apathy, fatigue and other phenomena that are unusual for your body, then it is better for you to consult a doctor. This is necessary for the doctor to make an accurate diagnosis and, based on it, choose the most effective treatment.

How is hepatitis C transmitted?

What it is? Infection occurs mainly through contact with the blood of an infected person. Hepatitis C is also transmitted during medical procedures: blood collection and transfusion, surgical operations, manipulations at the dentist.

The source of infection can be manicure instruments, tattoo devices, needles, scissors, razors, etc. If the skin or mucous membranes are broken, contact with the blood of an infected person can cause infection.

In rare cases, hepatitis C is transmitted through sexual contact. Infected pregnant women have a risk that their baby will also become infected with the virus at birth.

The most severe cases of the virus are:

persons who abuse alcohol.
persons suffering from other chronic liver diseases, including others.
older people and children.

Hepatitis C disease is not transmitted through household contacts through hugs or handshakes; with this disease, you can share dishes and towels, but you cannot share personal hygiene items (razors, nail scissors, toothbrushes). The mechanism of transmission of the disease is only hematogenous.

Symptoms of hepatitis C

In most situations, viral hepatitis C proceeds slowly, without pronounced symptoms, remaining undiagnosed for years and manifesting itself after significant destruction of liver tissue. Often, patients are first diagnosed with hepatitis C when they already have hepatocellular liver cancer.

The incubation period of hepatitis lasts from 1 to 3 months. Even after this period ends, the virus may not manifest itself until liver damage becomes too obvious.

After infection, 10-15% of patients undergo self-healing, the remaining 85-90% develop primary chronic hepatitis C without any specific symptoms (such as pain, jaundice, etc.). And only in rare cases do patients develop an acute form with jaundice and severe clinical manifestations, which, with adequate therapy, leads to a complete cure of the patient from hepatitis C.

The first signs of hepatitis C in women and men

For a long time, symptoms practically do not bother patients. In the acute period, the disease manifests itself only as weakness, fatigue, and sometimes occurs under the guise of a respiratory viral infection with pain in the muscles and joints. These may be the first signs of hepatitis C in women or men.

Jaundice and any clinical manifestations of hepatitis develop in a very small percentage of infected people (the so-called icteric form of the disease). And this is actually great - patients immediately turn to specialists, and the disease is cured.

However, the majority of infected people suffer from hepatitis C on their feet: in the anicteric form, they either do not notice anything at all, or attribute the malaise to a cold.

Chronic hepatitis

The peculiarity of chronic hepatitis C is a latent or asymptomatic course for many years, usually without jaundice. , detection of anti-HCV and HCV RNA in the blood serum for at least 6 months are the main signs of chronic hepatitis C. Most often, this category of patients is discovered by chance, during examination before surgical intervention, when undergoing medical examination, etc.

The course of chronic hepatitis C can be accompanied by such immune-mediated extrahepatic manifestations as mixed cryoglobulinemia, mesangiocapillary glomerulonephritis, porphyria cutanea tarda, etc.

Photo

The photo shows liver damage due to long-term hepatitis.

Forms

According to the presence of jaundice in the acute phase of the disease:

Icteric.
Anicteric.

According to the duration of the flow.

Acute (up to 3 months).
Protracted (more than 3 months).
Chronic (more than 6 months).

By severity.

Easy.
Medium-heavy.
Heavy.
Fulminant.

Complications.

Hepatic coma.

Recovery.
Chronic hepatitis C.
Cirrhosis of the liver.
Hepatocellular carcinoma.

The nature clinical manifestations In the acute phase of the disease, a distinction is made between typical and atypical hepatitis C. Typical include all cases of the disease accompanied by clinically visible jaundice, and atypical include anicteric and subclinical forms.

Stages

The disease is divided into several stages, depending on which treatment is prescribed.

Acute – it is characterized by an asymptomatic course. A person often does not even suspect that he is a carrier of the virus and a source of infection.
Chronic - in the vast majority of cases (about 85%) following acute stage the chronic course of the disease begins.
Liver cirrhosis develops with further progression of the pathology. This is a serious disease that threatens the patient’s life both in itself and because its presence significantly increases the risk of developing other complications - in particular, liver cancer.

A distinctive feature of the virus is its ability to undergo genetic mutations, due to which human body Approximately 40 subtypes of HCV (within one genotype) can be detected simultaneously.

Virus genotypes

The severity and course of the disease depend on the genotype of hepatitis C infecting the body. Currently, six genotypes with several subtypes are known. Most often, viruses of genotypes 1, 2 and 3 are found in the blood of patients. They are the ones that cause the most pronounced manifestations diseases.

In Russia, the most common genotype is 1b. Less often – 3, 2 and 1a. Hepatitis C, caused by genotype 1b virus, is characterized by a more severe course.

Diagnosis of hepatitis

The main method for diagnosing hepatitis is to determine the presence of antibodies to the hepatitis C virus (anti-HCV) and HCV RNA. Positive results Both tests confirm the presence of infection. The presence of IgM class antibodies (anti-HCV IgM) makes it possible to distinguish active hepatitis from carriage (when there are no IgM antibodies and ALT is normal).

A PCR test for hepatitis C (polymerase chain reaction) allows you to determine the presence of hepatitis C RNA in the patient’s blood. PCR testing is mandatory for all patients with suspected viral hepatitis. This method is effective from the first days of infection and plays an important role in early diagnosis.

When is hepatitis C more difficult to treat?

According to statistics, hepatitis C is more difficult to treat in men, people over 40 years of age, in patients with normal transaminase activity, with a high viral load, and in those with genotype 1 b of the virus. Of course, the presence of liver cirrhosis at the time of treatment worsens the prognosis.

The effectiveness of antiviral treatment depends on many factors. With a long course of hepatitis C, it is not easy to achieve complete eradication of the virus. The main task is to slow down the process of active reproduction of viruses.

This is possible in most cases using modern antiviral therapy regimens. In the absence of active reproduction of viruses in the liver, the severity of inflammation significantly decreases and fibrosis does not progress.

Treatment of hepatitis C

In the case of hepatitis C, combination therapy with interferon-alpha and ribavirin is considered the standard of treatment. The first drug is available as a solution for subcutaneous injection under trademarks Pegasys®, PegIntron®. Peginterferons are taken once a week. Ribavirin is available under different brand names and is taken as tablets twice daily.

Interferon-alpha is a protein that the body synthesizes independently in response to a viral infection, i.e. it is actually a component of natural antiviral defense. In addition, interferon-alpha has antitumor activity.
Ribavirin as self-treatment has low efficiency, but when combined with interferon it significantly increases its effectiveness.

The duration of therapy can range from 16 to 72 weeks, depending on the genotype of the hepatitis C virus and the response to treatment, which is largely associated with the individual characteristics of the patient, which are determined by his genome.

A course of antiviral therapy using the “gold standard” can cost a patient from $5,000 to $30,000, depending on the choice of drugs and treatment regimen. The main costs are for interferon drugs. Foreign-made pegylated interferons are more expensive than conventional interferons from any manufacturer.

In most regions of Russia, treatment is not covered by compulsory medical insurance and is provided at the expense of regional programs. For example, in Moscow alone, up to 2,000,000,000 rubles are spent annually on treating people with hepatitis C, treating up to 1,500 patients per year. At the same time, 70,000 patients are officially registered in Moscow alone. It turns out that it will take 50 years to cure them all.

In addition to standard therapy, interferon-free therapy is recommended in 2018 for patients with chronic hepatitis C who are not at high risk of death from other causes. antiviral drugs direct acting (DAA), for a period of 8 to 24 weeks. Patients at high risk of complications (assessed by the degree of liver damage) should be considered first. Currently, interferon-free AVT regimens use inhibitors of the replication of three non-structural HCV proteins: NS3/4A protease, NS5A interferon-resistant protein, and NS5B polymerase.

The effectiveness of hepatitis C treatment is assessed by biochemical blood parameters (decreased transaminase activity) and the presence of HCV-RNA, and a decrease in the level of viral load.

New in hepatitis treatment

Although AbbVie Inc.'s second-generation NS3 and NS5A viral protein inhibitors glezaprevir/pibrentasvir received FDA registration on August 3, 2017, final phase 3 clinical trials of individual Maviret-based regimens are still ongoing and will continue until 2019. In particular, the optimal duration of therapy with glezaprevir/pibrentasvir for acute hepatitis C is being established, and the combination of glezaprevir/pibrentasvir and sofosbuvir is being studied as a “last resort” therapy for people with multidrug resistance.

The first pangenotypic representatives of the class of non-nucleoside NS5B polymerase inhibitors GSK2878175 and CC-31244 are undergoing phase I-II clinical trials. Both inhibitors can potentially be used in combination therapy with both other classes of DAAs and indirect-acting antiviral drugs.

Maviret was officially registered with the Ministry of Health of the Russian Federation on April 13, 2018, after which it appeared in pharmacies. average cost Mavyret packages exceed 350 thousand rubles, and the price of a standard 8-week course of treatment reaches 600-700 thousand rubles or more.

It is worth noting that treatment standards for people with hepatitis C are changing rapidly. Sofosbuvir, daclatasvir and combination drug sofosbuvir/ledipasvir are part of the preferred treatment regimens in WHO guidelines and can achieve cure rates of 95%.

Side effects of antiviral therapy

If treatment with interferons is indicated, side effects cannot be avoided, but they are predictable.

After the first interferon injections, most people experience the syndrome. After 2-3 hours, the temperature increases to 38-39 0 C, there may be chills, pain in muscles and joints, and noticeable weakness. The duration of this condition can be from several hours to 2-3 days. Within 30 days, the body is able to get used to the administration of interferon, so by this time the flu-like syndrome disappears. Weakness and fatigue persist, but we have to put up with it.

As for Ribavirin, it is usually well tolerated. But quite often, a general blood test reveals mild hemolytic anemia. Mild dyspepsia, rarely headache, increased levels of uric acid in the blood may occur, and very rarely intolerance to the drug is observed.

How long can people live with hepatitis C if left untreated?

It is very difficult to say unambiguously how many people live with hepatitis C, just like with HIV infection. In the average number of patients, cirrhosis can develop in approximately 20 to 30 years.

In percentage, depending on the age of the person, cirrhosis develops:

in 2% of patients infected before 20 years of age;
6% of those who received the virus aged 21–30 years;
in 10% of those infected at 31–40 years of age;
in 37% of cases aged 41–50 years;
63% of those infected are over 50 years of age.

Also, most studies have proven that the development of fibrosis also depends on gender. In men this pathology develops much faster and in a more severe form, even if treated.

An accurate distinction between chronic hepatitis into parenchymal (or epithelial) and interstitial (mesenchymal) is impossible, as is the case with acute forms. Chronic hepatitis often occurs in an anicteric form or only periodically gives exacerbations in the form of jaundice, when it is usually more certain to speak about the predominance of parenchymal lesions.

Often, along with the stroma of the organ, reticuloendothelial tissue is predominantly affected, as, for example, in chronic malarial, brucellosis hepatitis, hepatitis in subacute septic endocarditis, etc. Among chronic hepatitis, as well as among acute ones, focal hepatitis is also distinguished , for example, with gummous syphilis with a predominant perivascular location of specific infiltrates, healing with partial scarring (organ fibrosis).

The term “chronic hepatitis” refers to the presence of inflammation, necrosis and fibrosis of liver tissue. The causes of chronic hepatitis are varied. The course of the disease and the effectiveness of treatment depend on the etiology of hepatitis, age and condition of the patient. However, the final stage of any form of chronic hepatitis is cirrhosis of the liver, and its complications are the same regardless of the cause of hepatitis.

Hepatitis B is a serious occupational risk for healthcare workers.

Frequency. Chronic hepatitis occurs with a frequency of 50-60 cases per 100,000 population, predominantly affecting men. The prevalence of HBV in Russia reaches 7%. The prevalence of CHC is 0.5-2%.

Classification. According to etiology, chronic hepatitis is distinguished: viral B; viral D; viral C; viral, unspecified; autoimmune; alcoholic; drug; due to primary biliary cirrhosis; due to primary sclerosing cholangitis; due to Wilson's disease; due to α-antitrypsin deficiency; rective.

Forms of chronic hepatitis

There are three histological forms of chronic hepatitis:

Chronic hepatitis with minimal activity is a mild disease in which the inflammatory process is limited to the portal tracts. Serum aminotransferase activity may be close to normal or moderately increased.
Chronic active hepatitis is a disease that occurs with extensive clinical picture, in which liver function indicators and histological patterns correspond to active inflammation, necrosis and fibrosis. Histological examination reveals active inflammation of the parenchyma outside the portal tracts, stepwise necrosis and fibrosis.
In chronic lobular hepatitis, inflammatory infiltration of the hepatic lobules with isolated foci of necrosis is detected.

Histological classification emphasizes the importance of liver biopsy for diagnosis, treatment and prognosis. For each cause of hepatitis, any of the described histological forms of the disease is possible, so histological examination alone is not enough to make a diagnosis and select the appropriate treatment.

Causes of chronic hepatitis

The causes of chronic hepatitis can be divided into several main groups: viral hepatitis, metabolic disorders, autoimmune and drug-induced hepatitis.

Various infections, collagen diseases, transition of acute to chronic hepatitis, excess and malnutrition, exposure to hepatotropic poisons, hepatotropic medications.

Chronic hepatitis, leading to significant changes in the structure of the organ, can be considered as precirrhotic diseases; however, it should be emphasized that in a normal liver there are significant amounts of parenchyma reserve, the great ability of liver tissue to regenerate and the significant reversibility of even long-term hepatitis, which does not allow identifying chronic hepatitis with the irreversible final stage of their liver cirrhosis. Indeed, in the clinic one can often observe how, even with many years of liver enlargement during a protracted course of brucellosis or with repeated diseases of malaria, subsequently, with the cure of the main suffering, a complete clinical recovery occurs with the return of the size and function of the liver to normal.

Hepatitis A and E viruses are not able to persist and lead to chronic forms hepatitis A. For other viruses, there is not enough information about the possibility of chronic inflammation.

The incubation period of HCV is 15-150 days.

Pathogenesis

The development of hepatitis B begins with the introduction of the pathogen into the body or infection. Lymphocytes produce antibodies. As a result, immune complex damage often occurs various organs and systems. With the development of pronounced immunity, the virus is suppressed and recovery occurs.

The development of autoimmune hepatitis is often preceded by bacterial or viral infection. A T-cell immune response occurs with the formation of antibodies to self-antigens and tissue damage as a result of inflammation. The second mechanism of autoimmune damage is associated with molecular mimicry caused by the similarity of cell antigens with the virus antigen herpes simplex. Antinuclear (ANA), anti-smooth muscle (SMA/AAA) and other antibodies that damage tissue are formed.

When consuming more than 20-40 g of alcohol per day for men and up to 20 g for women, which is considered the maximum permissible dose, the alcohol entering the liver interacts with the enzyme alcohol dehydrogenase to form toxic acetaldehyde and other aldehydes. Another operating mechanism - microsomal oxidation of ethanol - leads to the formation of reactive oxygen species, which also damage the liver. Macrophages entering the liver during inflammation produce cytokines, including TNF-a, which aggravate damage to the organ. Many chemical reactions in the liver are disrupted, including fat metabolism, methionine metabolism with a decrease in the activity of methionine adenosyltransferase, and the release of homocysteine, which stimulates liver fibrosis.

At non-alcoholic steatohepatitis apoptosis of hepatocytes accelerates, the level of circulating TNF- increases; There is an increase in lysosome permeability and the release of cathepsins, dysfunction of cell mitochondria, which induce β-oxidation in mitochondria with activation of oxidative stress.

Symptoms and signs of chronic hepatitis

Dyspeptic complaints after eating, sometimes mild jaundice with a moderate increase direct bilirubin in blood. The course is slow (long-term, persistent chronic hepatitis) or rapidly progressive (active chronic hepatitis). Moderate impairment of liver function. Shifts in the protein spectrum of the blood (increase in α 2 - and γ- globulins in the blood). Often relapsing. Hypersplenism and intrahepatic cholestasis may occur. According to radioisotope scanning data, paint absorption appears to be moderately diffusely reduced (normally there is dense, uniform shading, indicating a high degree of absorption of labeled compounds).

Clinically, chronic hepatitis is manifested mainly by liver enlargement varying degrees, usually uniform or with a predominance of one, usually the left, lobe. The liver is dense to the touch, can be sensitive and even painful in the presence of pericholecystitis; At the same time, there may be independent pain. Jaundice is usually observed only periodically, with exacerbations of the process, and less often it can take a protracted course. With severe jaundice, skin itching and other phenomena characteristic of severe parenchymal jaundice develop. More often, in chronic hepatitis, only subictericity of the sclera and skin is found. Liver function outside of exacerbations of jaundice is usually slightly impaired, or this disorder is detected only by deviations from the norm in one or two more sensitive liver tests. The spleen is often enlarged.

With mesenchymal hepatitis, symptoms of the underlying disease are usually observed (brucellosis, subacute septic endocarditis, collagen diseases, malaria, etc.). Hepatomegaly or hepatolenal syndrome is possible. The function of the organ is not significantly impaired.

Manifestations of liver damage are more typical for hepatocellular, especially active (recurrent or aggressive) forms of chronic hepatitis. They are accompanied by pain in the right hypochondrium, dyspepsia, enlargement of the liver and sometimes the spleen, “spider veins” may occur, and during exacerbations - yellowness of the sclera and skin, and are characterized by a greater or lesser degree of dysfunction.

Chronic hepatitis can progress (continuously or in waves) - with the transition to liver cirrhosis, take a stationary (persistent) course, or regress.

Given the importance of the liver in performing many metabolic functions, clinical syndromes Liver damage in chronic hepatitis is very diverse.

Asthenovegetative syndrome, or “liver laziness syndrome.”
Dyspeptic syndrome.
Pain syndrome with hepatitis.
Hepatomegaly. A common sign of hCG.
Jaundice. An increase in conjugated bilirubin indicates a high activity of the process, this is a sign of disease progression (necrosis of hepatocytes).
Hemorrhagic syndrome in chronic hepatitis is associated with hepatic cellular failure (clotting factors are not synthesized) or the development of vasculitis, indicating the systemic nature of the lesion, the inclusion immune reactions antigen-antibody.
Skin itching. If it is the leading syndrome, then this indicates cholestasis. The screening test is alkaline phosphatase (ALP).
Lymphadenopathy in chronic hepatitis.
Fever.
Edema-ascitic syndrome. This is a complication of portal hypertension.
Endocrine disorders in chronic hepatitis.

Superinfection with the hepatitis D virus, even against the background of a sluggish HBV process, causes progression of the disease. Rarely, this causes fulminant hepatitis.

Diagnosis of chronic hepatitis

A carefully collected anamnesis and examination allow us to diagnose correct diagnosis. Difficulties arise in cases of prolonged acute hepatitis. Timely diagnosis of transition acute course diseases into chronic ones are facilitated by polarographic analysis of blood serum. To establish the morphological direction, activity of the process, solve differential diagnostic problems (fatty liver, early cirrhosis, amyloid, congenital hyperbilirubinemia, etc.), especially great importance has a needle biopsy of the liver.

The diagnosis of chronic hepatitis should be made taking into account the possibility of other causes of enlargement or changes in the borders of the liver. At differential diagnosis The following forms must be excluded in particular:

Liver prolapse is found in women with careful examination in 4-5% and much less often in men (Kernig).

Laboratory diagnosis of hepatitis is based on the detection of cytolysis syndrome, accompanied by damage to hepatocytes and the release of ALT, AST, GGTP, ALP enzymes into the blood, the activity of which increases, and an increase in bilirubin levels.

An ultrasound scan of the liver, pancreas, spleen, and portal vein is performed. The ultrasound picture of chronic hepatitis is characterized by signs of diffuse liver damage, especially increased echo density.

If virus markers are detected, a confirmatory qualitative study is carried out for the presence of viral DNA: HV-B DNA (qualitative) and/or HV-C RNA (qualitative).

When the presence of chronic viral hepatitis is confirmed, tests are performed to identify replication markers in order to clarify the severity of the process.

At each stage of viral hepatitis, it is possible to study a number of other antigens, antibodies and other sources, but this is rarely necessary.

Autoimmune hepatitis can be diagnosed when, in addition to increased ALAT and AST, hypergammaglobulinemia and autoantibodies are noted in the blood serum. The most common (85% of all cases) is the 1st subtype - classic autoimmune hepatitis, in which antibodies ANA - antinuclear, AMA - antimitochondrial, LMA - antiliposomal are detected. In the 3rd subtype, SMA antibodies are detected - anti-smooth muscle.

Non-alcoholic steatohepatitis often develops in overweight and obese patients. Disorders of lipid metabolism, often hyperinsulinemia, are detected. These patients very often develop hepatic steatosis. Apply non-invasive methods diagnostics using FibroMax and Fibro-Meter tests to detect fibrosis and cirrhosis.

Drug-induced hepatitis accounts for 15-20% of fulminant hepatitis in Western Europe, and 5% in Russia. More often they occur in elderly women when combining several drugs due to their drug interactions (for example, during general metabolism through cytochrome P450), in diseases of the liver and kidneys. Toxic liver damage, depending on the dose of the drug, can be caused by paracetamol, aspirin, nimesulide, amiodarone, estrogens, semisynthetic penicillins, cytostatics, and very rarely statins. Idiosyncratic liver damage is caused by increased sensitivity, often genetically determined. Substances can act as haptens, causing the formation of antigens to hepatocytes.

Differential diagnosis. Differential diagnosis for liver lesions is most often carried out according to the syndromes of jaundice and hepatomegaly.

There are three types of jaundice: hemolytic (suprahepatic), parenchymal (hepatic) and mechanical (subhepatic).

With hemolytic jaundice, a triad of signs is identified: anemia, jaundice and splenomegaly. The number of reticulocytes in the blood is increased, indicating activation of the bone marrow. Hemolytic anemias are divided into congenital and acquired (autoimmune).

Hepatic jaundice is divided into a predominance of unconjugated and conjugated bilirubin.

An increase in unconjugated bilirubin in the blood can be observed with Gilbert's syndrome. Occurs in 1-5% of the population. Jaundice is caused by a violation of the transport of bilirubin into the hepatocyte, and therefore its conjugation with glucuronic acid is disrupted. Periodic episodes of jaundice may appear from childhood. Asthenia is characteristic. Liver functions are not impaired. Treatment with phenobarbital eliminates jaundice.

Mechanical, or obstructive, jaundice is most often caused by compression of the biliary tract by a stone or tumor. The skin color gradually changes from yellowish to greenish-yellow. Characterized by persistent itching of the skin and multiple scratches. The disease is confirmed by ultrasound and CT scanning, which reveal dilated bile ducts.

Hepatomegaly syndrome (liver enlargement) is observed in many diseases:

heart failure;
acute viral, drug-induced, alcoholic hepatitis;
chronic hepatitis;
cirrhosis of the liver;
liver tumors;
polycystic liver disease;
portal vein thrombosis;
infiltrative processes (amyloidosis, hemochromatosis), etc.

It should be noted the importance of assessing the duration of hepatitis: when the process lasts up to 6 months, it is considered acute, and more of this period- like chronic hepatitis.

Treatment of chronic hepatitis

Treatment of chronic hepatitis is carried out both through specific therapy and through pathogenetic, including dietary, treatment of liver damage as such according to the principles set out in the treatment of Botkin's disease.

A complete diet (during an exacerbation, it is carried out against the background of bed rest), rich in carbohydrates, proteins, vitamins, mineral salts and electrolytes - diet No. 5. Vitamin therapy: intramuscular vitamin B 1, 1 ml of 5% solution, vitamin B 6, 1 ml 5 % solution, vitamin B 12 100 mcg intramuscularly every other day, a total of 15 injections, 10-20-40% glucose solution 20-40 ml along with 5 ml of 5% ascorbic acid solution intravenously. During remission Spa treatment in Essentuki, Zheleznovodsk, Pyatigorsk, Borjomi, Morshyn, Truskavets, Druskininkai.

Outside of exacerbation - mainly a gentle regime, rational employment, a nutritious diet rich in proteins, carbohydrates and vitamins. During periods of exacerbation - bed rest, B vitamins, liver extracts (campolon, sirepar, vitohepat), with active (aggressive) chronic hepatitis - glucocorticoids. combination with anabolic hormones dianabol, nerobol) and immunosuppressants, especially if corticosteroids have no effect. Hormone therapy(for example, prednisolone 30-40 mg daily with a gradual dose reduction by an average of 5 mg per week) is carried out for a long time, sometimes for many months (on average 2-3 months), if necessary repeated courses. Patients are subject to dispensary observation. In case of stable remission, sanatorium-resort treatment is indicated (Essentuki, Pyatigorsk, Zheleznovodsk, etc.).

Diet therapy is an important component of the treatment of chronic hepatitis. Preferably 4-5 meals a day. They recommend a sufficient amount of protein contained in dairy products, fish, and meat; fruits and vegetables, rice, oatmeal, semolina and buckwheat porridge are sources of plant fiber; from fats - vegetable and dairy, which have a lipotropic effect, as well as products containing vitamins A, C, group B. Refractory fats and foods high in fat, rich broths, fried foods, spicy seasonings.

For autoimmune hepatitis, glucocorticosteroids (GCS) are used: prednisolone. As an alternative, the cytostatic drug azathioprine can be used.

For the treatment of chronic hepatitis and toxic liver damage, hepatoprotectors are used:

milk thistle preparations: legalon, karsil, silymar; including the combination drug hepabene;
preparations with flavonoids of other plants: Liv 52, artichoke (chophytol), pumpkin seed oil (tykvenol);
essential phospholipids: essentiale, essentiale, phosphogliv;
ornithine aspartate (hepamerz);
drugs with an indirect detoxifying effect: reducing the formation of toxins: lactulose (Duphalac); activating the formation of endogenous detoxicants: ademetionine (heptral); accelerating the metabolism of toxicants: metadoxyl, phenobarbital; excreting toxic bile acids: ursodeoxycholic acid (ursosan).

For alcoholic liver damage, adeomethionine (Heptral) is used; for encephalopathy - ornithine (Hepamerz) orally.

Ursodeoxycholic acid (ursosan, ursofalk, ursodez) showed high efficiency with toxic liver damage, non-alcoholic steatohepatitis, increased ALAT, AST while taking statins.

Chronic viral hepatitis D

Pathogenesis. The D virus has a cytopathogenic effect on hepatocytes.

Symptoms. The disease is characterized by a severe course with a pronounced symptom of hepatic cellular failure (weakness, drowsiness, bleeding, etc.). A significant proportion of patients develop jaundice and itchy skin. Physically, hepatomegaly, splenomegaly with hypersplenism, edematous-ascitic syndrome and early development of liver cirrhosis are detected.

Laboratory tests: severe dysproteinemia - hypoalbuminemia and hypergammaglobulinemia, increased ESR, 5-10-fold increase in ALT and bilirubin levels. Virus markers - HDV RNA and anti-HDV IgM class; integration markers - HBsAg and anti-HBe.

Chronic viral hepatitis C

Symptoms. There is a moderately pronounced asthenic syndrome and hepatomegaly. The course is undulating, with episodes of deterioration, with hemorrhagic manifestations and a prolonged increase in ALT levels. Liver cirrhosis develops after decades in 20-40% of patients. Markers - RNA virus and antibodies to it (anti-HCV).

Treatment. Outside the acute phase, treatment consists of following a diet. In the acute phase, bed rest (increases blood flow in the liver), detoxification measures (glucose, hemodez intravenously), vitamins B1, B2, B12, E, C, hepatoprotectors (heptral, hofitol, essentiale, karsil, etc.), lactulose (duphalac) are indicated ). In order to eliminate or stop the replication of the virus, antiviral therapy with interferon is carried out. However, there is no convincing evidence that interferon prevents disease progression, the development of cirrhosis, or reduces mortality. Currently, therapy with interferon alpha is being replaced by complex antiviral therapy consisting of long-acting pegylated interferon and ribavirin. Liver transplantation is usually contraindicated.

Autoimmune hepatitis

Traditionally, there are two types of autoimmune hepatitis. Type 1, the most common, is characterized by the presence of antinuclear antibodies and autoantibodies to the smooth muscle elements of the liver (70-100%).

A clear connection was revealed with HLA, alleles DR3 (the disease usually begins at a young age, the course is severe) and DR4 (hepatitis begins at an older age and is characterized by a more benign course).

Symptoms. Mostly women aged 10-30 years or older than 50 years are affected (the ratio of women to men is 8:1). The onset is gradual with asthenia, malaise, pain in the right hypochondrium. In 30% of patients, the disease begins suddenly with the development of jaundice and sharply increased aminotransferase activity. Signs of chronic liver damage appear: skin telangiectasias, palmar erythema, stretch marks on the thighs and abdominal wall. Physically: the liver is dense with a predominantly enlarged left lobe, splenomegaly, polyarthritis of large joints, erythema, purpura, pleurisy, lymphadenopathy.

In 48% of cases, other autoimmune processes make themselves felt: thyroid diseases, arthritis, vitiligo, ulcerative colitis, diabetes, lichen planus, alopecia, mixed disease connective tissue.

Laboratory tests: moderate pancytoenia, a noticeable increase in ESR and AST levels (2-20 times), which reflects the degree of inflammatory changes in the liver; hyperproteinemia (90-100 g/l or more), hypergammaglobulinemia. In 30-80% of cases, HLA-DR3, DR4 is detected; determination of autoantibodies (see above).

Treatment. It is carried out with prednisolone in an initial dose of 20-40 mg/day under the control of AST activity. A combination of glucocorticoids with azathioprine is useful (and azathioprine allows you to reduce the dose hormonal drug). Moreover, remission remains in more than 80% of patients for 1-10 years. If there is no effect from the therapy described above, it is possible to use new immunosuppressants - tacrolimus, cyclosporine, mycophenolate mofetil, but their true significance is not fully understood. If cirrhosis develops, liver transplantation is indicated.

Alcoholic hepatitis

Alcoholic hepatitis develops in persons who take more than 100 g of vodka per day for women and more than 200 g for men with frequent and long-term use.

Pathogenesis. When drinking alcohol, acetaldehyde (which is a direct liver poison) accumulates with the formation of hepatic lipoprotein and alcoholic hyaline, which attract leukocytes; inflammation forms.

Symptoms. Anicteric and cholestatic (more severe) variants are possible. Characteristic: hepatomegaly with a rounded edge of the liver, dyspeptic and abdominal syndromes, signs of myocardial dystrophy, skin changes, weight loss, Dupuytren's contracture.

Laboratory studies show an increase in the activity of both serum transaminases (mainly AST), gammaglutamyl transpeptidase, alkaline phosphatase, and IgA. The concentration of markers of the acute phase of inflammation (SRV, ferritin) increases. Liver biopsy shows macrovesicular fatty degeneration, diffuse inflammatory reaction to necrosis, and Mallory's alcoholic hyaline.

Treatment. A complete abstinence from drinking alcohol is required. Vitamins Bq, 512, riboflavin, fosic acid and ascorbic acid are shown). Thiamine is prescribed (to prevent Wernicke encephalopathy); prednisolone or methylprednisolone; if necessary, pulse therapy with prednisolone 1000 mg intravenously for 3 days; metadoxyl - 5 ml (300 mg) intravenously drip for 3-5 days or in tablets; pentoxifylline; membrane-stabilizing drugs (heptral, hofitol, essentiale, picamilon, etc.); carry out detoxification therapy (glucose, electrolytes, hemodez).

Chronic reactive hepatitis

Nonspecific reactive hepatitis is a secondary lesion of liver tissue in some extrahepatic diseases. In essence, this is secondary hepatitis, reflecting the reaction of the liver tissue to a large number of extrahepatic diseases.

Causes. The causes of reactive hepatitis can be gastrointestinal diseases (peptic ulcer, pancreatitis, cholecystitis, ulcerative colitis), systemic connective tissue diseases (SLE, RA, scleroderma, polymyositis, etc.), diseases endocrine glands(thyrotoxicosis, diabetes mellitus), more than 50 acute and chronic infections, tumors of various locations before they metastasize to the liver.

Pathomorphology. The histological picture of reactive hepatitis of different etiologies is identical and is characterized by polymorphism of hepatocytes, focal protein and fatty degeneration, and necrosis of single hepatocytes. Morphological changes are moderate, usually do not progress and are completely reversible when the underlying disease is eliminated.

Symptoms. Asymptomatic. Only observed moderate increase liver. In this case, liver function tests do not change significantly.

Diagnostics. The diagnosis is based on morphological data, moderate hepatomegaly, slight changes in liver function tests and consideration of the underlying disease.

Treatment. Consists of therapy and prevention of aggressive effects on the liver (alcohol, etc.).