Hepatitis ( Greek ἡπατῖτις from ἥπαρ - liver) - inflammatory diseases of the liver , usually of viral origin.
Micrograph of liver cells affected by alcoholic hepatitis
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WHO recognizes hepatitis as a dangerous disease  .
In 2016, a large international study showed that mortality from hepatitis is comparable to tuberculosis , malaria and HIV  . World Hepatitis Day is celebrated on July 28th.
Jaundice is the best known symptom. It occurs when bilirubin , not processed in the liver, enters the bloodstream and gives the skin a characteristic yellowish tint. However, there are often anicteric forms of hepatitis. Sometimes the onset of hepatitis resembles the flu : fever, headache, general malaise, body aches. As a rule, this is the so-called “mask” of incipient viral hepatitis , characterized by weakness.
Pain in the right hypochondrium, as a rule, occurs due to stretching of the membrane of the liver (enlargement of the liver) or may be associated with the gallbladder and pancreas . The pains can be either dull, prolonged, aching, or paroxysmal, intense, can give to the right shoulder and right shoulder blade.
Clinical Aspects of Hepatitis
Two main forms of the clinical course of hepatitis are distinguished: acute and chronic .
The acute form of the course is most characteristic of hepatitis of a viral nature, as well as for hepatitis caused by poisoning, including strong poisons . In the acute form of hepatitis, there is a noticeable deterioration in the general condition of the patient, the development of signs of general intoxication of the body and impaired liver function (fever, in some cases the development of jaundice, etc.), as well as an increase in the level of transaminases and total blood bilirubin . Acute hepatitis, as a rule, ends with the full recovery of the patient, however, in some cases, the acute course of the disease becomes chronic.
The chronic form can develop independently (for example, with chronic poisoning with ethyl alcohol), or continue the development of acute hepatitis (viral hepatitis B, D). The clinical picture in chronic hepatitis is poor, the disease is asymptomatic for a long time. A characteristic persistent increase in liver size, dull pain in the right hypochondrium, intolerance to fatty foods, etc. In chronic hepatitis, liver cells are gradually replaced by connective tissue, so that in most cases, untreated chronic hepatitis leads to the development of liver cirrhosis . Patients with chronic hepatitis are at high risk for developing primary liver cancer . Chronic viral hepatitis B, C, D in some cases respond to antiviral therapy. Treatment is carried out by an experienced infectious disease specialist-hepatologist.
Etiology of hepatitis
Inflammation of the liver (hepatitis) can be caused by various factors ( hepatotropic factors ) that can damage the liver parenchyma . Etiotropic classification of hepatitis includes
1. Infectious (viral) hepatitis :
- Hepatitis A
- Hepatitis B
- Hepatitis C
- Hepatitis D
- Hepatitis E
- Hepatitis F
- Hepatitis G
- Hepatitis as a component: yellow fever , cytomegalovirus infection, rubella , mumps , Epstein-Barr virus infection, a variety of herpes infections, Lassa fever , AIDS .
- Bacterial hepatitis: with leptospirosis , syphilis .
- Parasitic hepatitis: with amoebiasis , toxoplasmosis , fascioliasis , opisthorchiasis , schistosomiasis
2. Toxic hepatitis:
- Alcoholic hepatitis
- Drug hepatitis
- Hepatitis due to poisoning with various chemicals
3. Radiation hepatitis (component of radiation sickness )
4. Autoimmune hepatitis
Hepatitis A (Botkin's disease) causes an RNA- containing hepatitis A virus from the Picornaviridae family. The disease is transmitted alimentarily . The virus enters the human body with contaminated food, water, household items. The main source of infection are patients with anicteric forms of the disease (proceed without jaundice ). The virus is excreted with the feces of the patient during the incubation period and at the beginning of the disease.
When it enters the gastrointestinal tract, the virus penetrates through the intestinal mucosa and is introduced into the liver with a blood stream, where it penetrates the liver cells and begins to multiply actively. The incubation period is on average 15-30 days with variations from 7 to 50 days. Damage to the liver is associated with a direct destructive effect of the virus on hepatocytes (liver cells). Hepatitis A virus has an acid-resistant membrane. This helps viruses caught in contaminated foods and water to pass the acidic protective barrier of the stomach.
The severity of clinical manifestations varies depending on the degree of liver damage.
- acute (icteric) form,
- subacute (anicteric) and
- subclinical form of the disease (clinical manifestations are almost absent).
The main symptoms are: general malaise, fever , muscle pain, vomiting , diarrhea , dull pain in the right hypochondrium, enlarged liver, dark urine . There may be icteric coloration of the skin and mucous membranes, but this is not always the case.
Acute hepatitis is verified by serum IgM antibodies. After the disease develops, lifelong immunity due to IgG develops.
Hepatitis B causes DNA-containing hepatitis B virus from the Hepadnaviridae family, and provokes both acute and chronic forms of hepatitis. Chronic hepatitis develops in 10% of adult patients who have had hepatitis B. There is an effective vaccine against hepatitis B virus.
Sources of infection are patients with acute and chronic forms of hepatitis, as well as virus carriers . Transmission of the virus is carried out parenterally by natural and artificial routes. Of the natural ways, the most common sexual transmission of infection. It is also possible the transmission of infection during childbirth from a sick mother to a child or transplacental infection of the fetus during pregnancy . An artificial route of transmission is carried out by transfusion of infected blood or its components, using unsterilized surgical or dental instruments, syringes , etc. For such infection, 0.0001 ml of blood is enough.
Having penetrated into the bloodstream, the virus with blood flow is introduced into the liver, where it is introduced into hepatocytes. Due to the intracellular propagation of the virus, viral proteins are inserted into the hepatocyte membrane, which, when recognized by the cells by the immune system , cause the development of an immune response . Further destruction of the liver cells occurs under the influence of T-lymphocytes (killers).
The incubation period can last from 50 to 180 days. The clinical manifestations of hepatitis B are largely similar to those of hepatitis A. Most often, the icteric form develops. Patients complain of indigestion , joint pain , weakness. In some cases, itchy rashes appear on the skin. Jaundice increases in parallel with the deterioration of the patient's well-being. Most severe and moderate forms of the disease are recorded. Compared with hepatitis A, with hepatitis B more often, liver dysfunction is more pronounced. More often cholestatic syndrome , exacerbation, a protracted course, as well as relapses of the disease and the development of hepatic coma develop. The acute form of hepatitis B in about 10% of patients passes into a chronic active or chronic persistent form , which eventually leads to the development of cirrhosis . After the disease, a long-term immunity develops. In order to prevent the planned vaccination of the population.
There are rapid tests that allow testing for hepatitis B in the laboratory or at home using test strips. An immunochromatographic rapid test that detects antibodies to hepatitis B is a reliable and safe tool that can diagnose the presence or absence of a disease in 10-15 minutes. The material for the study is blood from the finger. If a disease is detected, 2 purple bars appear on the test indicator. A negative result is one strip in the control zone. One strip in the test zone or their complete absence indicates that the analysis must be repeated and with a new indicator.
With the use of modern antiviral drugs, there is little chance of a complete cure for hepatitis B. Pegylated interferon may be considered the first choice for the treatment of patients with chronic hepatitis B.
In view of the danger of side effects during interferon therapy of chronic viral hepatitis, in particular hepatitis B, such as depression, dermatological problems, etc., treatment should be carried out under the supervision of an experienced infectious disease specialist-hepatologist.
Hepatitis C causes an RNA- containing hepatitis C virus (HCV) of the Flaviviridae family. At the moment, 11 major genotypes of hepatitis C virus are distinguished: 1a, 1b, 1c; 2a, 2b, 2c; 3a, 3b; 4a, 4b, 4c, 4d, 4e; 5a; 6a; 7a, 7b; 8a, 8b; 9a; 10a; 11a.
Hepatitis C (formerly called “hepatitis neither A nor B”, and is now described as systemic HCV infection) is transmitted through contact with infected blood. Hepatitis C can lead to the development of chronic hepatitis resulting in cirrhosis and liver cancer.
A hepatitis C vaccine does not exist.
Patients with hepatitis C are predisposed to develop severe hepatitis if they come into contact with hepatitis A or B, therefore all patients with hepatitis C should be vaccinated against hepatitis A and B. As a rule, 3-5 out of 100 infected people die. Risk groups are primarily associated with transfusion of blood and its preparations, surgical operations, drug injections using common syringes, promiscuous sexual contacts. It is assumed (though unlikely) that infection is possible with the general use in everyday life of epilators, manicure, razor accessories, etc.
It is believed that 15-20% of hepatitis C virus infected people can be cured on their own using their own immune system. In other patients, the disease becomes chronic. About 20% of chronic patients are at risk for cirrhosis or liver cancer.
In the clinical picture of chronic hepatitis C, asthenic syndrome is most characteristic: weakness, fatigue, progressive decline in working capacity, sleep disturbance.
The cost of treatment for hepatitis C in the United States can reach up to $ 70 thousand per course. Generics of modern drugs are sold in India, Egypt and are intended for sale only in some countries with low incomes. The cost of the course there is about 500 - 1000 dollars. In the treatment, both imported drugs and their Russian counterparts are used.
The cost of treatment, the duration of treatment, as well as the likelihood of cure, depends on the genotype of the virus, the age and sex of the patient, the duration of the disease, and other factors. Currently, antiviral therapy is a combination therapy with sofosbuvir in combination with daclatasvir , ledipasvir or veltapasvir . The encouraging results of such treatment are observed in 95-98% of people. With old treatment regimens, the third genotype responded best to treatment. At the moment, the picture has changed. There are practically no side effects from modern drugs.
First of all, you need to think about prevention and timely detection of the virus. The main method currently used to diagnose HCV infection is ELISA and PCR ( polymerase chain reaction ). To clarify the condition of the liver, fibroscanning and / or liver biopsy is performed.
Hepatitis D (hepatitis delta) is provoked by the hepatitis D virus and is characterized by acute development with massive liver damage. The delta virus is able to multiply in the liver cells only in the presence of hepatitis B virus, since the particles of the delta virus use hepatitis B virus proteins to exit the cell. Hepatitis D is ubiquitous. The source of the virus is a sick person or a virus carrier. D virus infection occurs when the virus enters directly into the blood. Routes of transmission are similar to those for hepatitis B or C. The incubation period lasts from 3 to 7 weeks. The clinical picture resembles a clinic of viral hepatitis B, however, the course of the disease is usually more severe. Acute forms of the disease can result in a complete recovery of the patient. However, in some cases (3% with co-infection with hepatitis B and 90% in HBsAg carriers), chronic hepatitis develops, leading to cirrhosis. Hepatitis B vaccine protects against hepatitis D infection.
Hepatitis E provokes symptoms similar to those of hepatitis A, although it can sometimes take on fulminant development, especially in pregnant women. According to the transmission methods, hepatitis E is close to hepatitis A. It can be transmitted through virus-infected water, food, and also through the blood.
Severe outcomes in the form of fulminant hepatitis, leading to death, are much more common with hepatitis E than with hepatitis A and acute hepatitis B.
Hepatitis E is most common in Central Asia and Africa .
The virus was discovered and described in the early 80s of the 20th century at the Institute of Poliomyelitis and Viral Encephalitis (Moscow) by a group of scientists led by Nikita Balayants.
Another type of human viral hepatitis, the existence of which is assumed on the basis of epidemiological data and preliminary studies in experiments on monkeys of individual virus isolates from patients with post-transfusion hepatitis. There is evidence that a certain proportion of patients who underwent clearly post-transfusion hepatitis remains seronegative for all markers of known human viral hepatitis; in various Western countries, this proportion reaches 15–20%. Moreover, long-term monitoring of individual patients - persons with a high risk of infection with post-transfusion hepatitis - such as drug addicts or patients with hemophilia, showed that they have repeated jaundice diseases, including etiologically not related to hepatitis A, B, C viruses, D, E and G.
The term “hepatitis F” obviously refers to two different viruses of post-transfusion hepatitis, which in some respects differ from hepatitis B, hepatitis C and hepatitis G. One of them was present in samples of donated blood; it was resistant to fat solvents and did not cause the formation of ultrastructural changes in hepatocytes characteristic of hepatitis C (the so-called tubular structures); infection of chimpanzees immune to hepatitis C led to the development of a hepatitis-like disease, and infection of non-immune chimpanzees was not accompanied by the appearance of antibodies to hepatitis C virus. Another was isolated from the feces of a patient with post-transfusion hepatitis; when infected with rhesus monkeys, he caused hepatitis; was able to multiply in monolayer cell cultures and in its morphological properties resembled adenovirus.
Hepatitis G virus (HGV, GBV-C) was isolated in 1995 by a scientific group of the company " Abbott " under the direction of I. Mushahvar from a patient with chronic hepatitis C, and subsequently from patients with hepatitis "no-A-no-E". It is suggested that there are at least 3 genotypes and several subtypes of the virus. Routes of transmission through blood and through sexual contact are possible, but it is not yet clear whether it causes hepatitis itself or is associated with hepatitis of another etiology. Its primary reproduction in the liver is not yet proven. Hepatitis G virus is classified as pegyvirus , single-stranded RNA-containing. Unstable in the environment, instantly dies when boiled.
Most often, hepatitis can be caused by the following drugs:
- Isoniazid , Rifampicin , Pyrazinamide (and other anti-TB drugs )
- Phenytoin , sodium valproate
- Antibiotics of the tetracycline group, clarithromycin
- Ibuprofen , indomethacin
- Hormonal contraceptives
Sensitivity to a particular drug varies from person to person. In general, almost any drug can cause liver damage and the development of hepatitis of varying severity. Particularly severe forms of hepatitis develop when poisoned by substances such as: amatoxins and fallotoxins — toxins of the fruiting bodies of some species of fungi of the genus Amanita or Amanita ( pale toadstool , white grebe, etc.), Galerin and Lepiot ; white phosphorus , paracetamol , carbon tetrachloride , industrial poisons, etc.
Like other autoimmune diseases , autoimmune hepatitis is more common in women, the total incidence is approximately 15-20 people per 100 thousand of the population. The pathogenetic mechanism of the development of autoimmune hepatitis is based on a congenital defect in HLA II membrane receptors .
Autoimmune hepatitis is an independent disease that develops due to a defect in the immune system. And first of all, the development of pathological immune responses against their own hepatocytes. Moreover, quite often not only the liver is involved in the process, but also large glands of external and internal secretion, including the pancreas, thyroid gland, and salivary glands.
The International Autoimmune Hepatitis Group has identified signs that make the diagnosis of autoimmune hepatitis “definite” or “probable.” In favor of autoimmune hepatitis indicate:
- elevated serum aminotransferases (AST and ALT);
- low levels of alkaline phosphatase (ALP);
- hypergammaglobulinemia with increased serum IgG;
- positive antinuclear antibodies (ANA);
- smooth muscle antibodies (AGM);
- hepato-renal microsomal antibodies of type 1 (LKM-1);
- lack of serum markers of viral infections;
- denial of alcohol abuse to patients;
- lack of evidence of a blood transfusion or history of hepatotoxic drugs.
For the diagnosis of autoimmune hepatitis, a high titer (at least 1:80 in adults and 1:20 in children) of antinuclear antibodies, antibodies to smooth muscles or antibodies to liver and kidney microsomes of type 1 is required  .
According to WHO, as of 2017, about 325 million people lived with chronic hepatitis, including 257 million people living with hepatitis B virus, and 71 million with hepatitis C virus  .
The most effective way to prevent hepatitis A and B is through vaccination. In the Russian Federation, immunization of the population against hepatitis B has been carried out as part of the national calendar of preventive vaccinations since 1996. Since 2000, about 100 million children, adolescents and adults have been vaccinated against hepatitis B in Russia. In 2017, about 3 million people were vaccinated, including 1.7 million children  .
In 2017, the incidence rates of acute hepatitis B and C in Russia reached the lowest levels for all years of observation - 0.9 and 1.22 cases per 100 thousand people  .
Diagnosis of hepatitis in animals
Take into account the history, the results of clinical and laboratory studies. It is necessary to exclude cirrhosis, hepatosis, cholecystitis and cholangitis. In all cases, a possible etiological factor is taken into account. Cirrhosis occurs chronically without fever. The liver is dense, the spleen is enlarged, cystitis is possible. Acute hepatitis is differentiated from hepatosis by etiology, severity, temperature reaction. Chronic hepatitis is difficult to differentiate from hepatosis. With fatty hepatosis, the spleen is not enlarged. 
Animal Hepatitis Treatment
Low-quality feeds are excluded from the diet, feeding fatty foods is limited, good vitamin hay, haylage, cereal concentrates, bran mash, root crops or potatoes are prescribed. In the pasture period, green feeds with a low content of nitrates and nitrites are used to the maximum. The feeding of sugary-rich foods should be limited, as this leads to increased liver lipogenesis. 
- Disease Ontology release 2019-05-13
- Monarch Disease Ontology release 2018-06-29sonu
- Hepatitis . World Health Organization. Date of treatment July 8, 2016.
- Imperial College article .
- Autoimmune hepatitis . Medicine of Altai. Archived on February 5, 2012.
- July 28 is World Hepatitis Day . www.rospotrebnadzor.ru. Date of treatment July 27, 2018.
- B.V. Usha et al. Internal diseases of animals. - M .: KolosS, 2010 .-- 311 p.
- Viral hepatitis
- Gilbert's syndrome