Acute viral hepatitis: causes, symptoms, diagnosis, treatment

Acute viral hepatitis is a diffuse inflammation of the liver caused by specific hepatotropic viruses characterized by different transmission routes and epidemiology. Nonspecific prodromal period with viral infection is accompanied by anorexia, nausea, often with fever and pain in the right upper quadrant of the abdomen. Jaundice often develops, usually after other symptoms begin to disappear. In most cases, the infection is resolved spontaneously, but sometimes progresses to chronic hepatitis. In rare cases, acute viral hepatitis progresses with the development of acute hepatic insufficiency (fulminant hepatitis). Compliance with hygiene can prevent infection with acute viral hepatitis. Depending on the specificity of the virus, prophylaxis before and after the disease can be carried out by vaccination or the use of serum globulins. Treatment of acute hepatitis hepatitis, usually symptomatic.

Acute viral hepatitis is a widespread and important disease worldwide with a different etiology; each type of hepatitis has its own clinical, biochemical and morphological features. Liver infections caused by other viruses (eg, Epstein-Barr virus, yellow fever virus, cytomegalovirus) are not generally called acute viral hepatitis.

[1],

What causes acute viral hepatitis?

At least five specific viruses cause acute viral hepatitis. The causes of acute viral hepatitis may be other, unknown, viruses.

Certain diseases or pathogens that cause inflammation of the liver

Diseases or pathogens	Manifestations
Viruses
Cytomegalovirus	In newborns: hepatomegaly, jaundice, birth defects. In adults: mononucleosis-like disease with hepatitis; possibly after a blood transfusion
Epstein-Barr	Infectious mononucleosis. Clinical hepatitis with jaundice in 5-10%; subclinical liver damage in 90-95%. Acute hepatitis in young (important)
Yellow fever	Jaundice with general intoxication, bleeding. Necrosis of the liver with a slight inflammatory reaction
Other	Rarely, hepatitis caused by herpes simplex viruses , ECHO, Coxsackie, measles, rubella or chicken pox
Bacteria
Actinomycosis	Granulomatous liver reaction with progressive necrotic abscesses
Pyogenic abscess	Severe infectious complication of portal pyemia and cholangitis; a hematogenous pathway or direct distribution is also possible. Various microorganisms, especially gram-negative and anaerobic bacteria. Disease and intoxication, only mild liver dysfunction. Differentiate from amoebiasis
Tuberculosis	The liver is often involved. Granulomatous infiltration. Usually subclinical manifestations; rarely jaundice. Disproportionate increase in alkaline phosphatase
Other	Minor focal hepatitis with various systemic infections (often, usually subclinical)
Mushrooms
Histoplasmosis (Darling's disease)	Granulomas in the liver and spleen (usually subclinical), followed by calcification
Other	Granulomatous infiltration in cryptococcosis, coccidiomycosis, blastomycosis and other
Protozoa
Amebiasis	Has an important epidemiological significance, often without a marked disorder of stool. Usually a single large abscess with melting. An enlarged, painful liver with mild dysfunction. Differentiate from pyogenic abscess
Malaria	Hepatosplenomegaly in endemic areas (main cause). Jaundice is absent or mild, if there is no pronounced hemolysis
Toxoplasmosis	Transplacental infection. In newborns: jaundice, CNS damage and other systemic manifestations
Visceral leishmaniasis	Infiltration of the reticuloendothelial system with a parasite. Hepatosplenomegaly
Helminths
Ascaridosis	Biliary obstruction by adults, granulomas in the parenchyma caused by larvae
Clonorchosis	Invasion of the biliary tract; Cholangitis, concrements, cholangiocarcinoma
Echinococcosis	One or more hydatid cysts, usually with peripheral calcification. Often occurs asymptomatically; the function of the liver is preserved. Can be complicated by a breakthrough in the abdominal cavity or biliary tract
Fasciolus	Acute: suggests hepatomegaly, fever, eosinophilia. Chronic: biliary fibrosis, cholangitis
Schistosomiasis	Periportal granulomatous reaction to eggs with progressive hepatosplenomegaly, pipestem fibrosis (fibrosis of Simmers), portal hypertension, varicose veins of the esophagus. Hepatocellular function preserved; is not a true cirrhosis of the liver
Toxocariasis	Syndrome of visceral migration of the larva. Hepatosplenomegaly with granulomas, eosinophilia
Spirochetes
Leptospirosis	Acute fever, prostration, jaundice, bleeding, kidney damage. Necrosis of the liver (often mild, despite severe jaundice)
Syphilis	Congenital: neonatal hepatosplenomegaly, fibrosis. Acquired: variable course of hepatitis in the secondary stage, gums with uneven scarring in the tertiary stage
Recurrent fever	Borreliosis. Common signs, hepatomegaly, sometimes jaundice
Unknown
Idiopathic granulomatous hepatitis	Active chronic granulomatous inflammation of unknown etiology (potyparusaridosis). Common signs (may dominate), fever, malaise
Sarcoidosis	Granulomatous infiltration (common signs, usually subclinical course); rarely jaundice. Sometimes progressive inflammation with fibrosis, portal hypertension
Ulcerative colitis, Crohn's disease	It is combined with liver diseases, especially with ulcerative colitis. Includes periportal inflammation (pericholangitis), sclerosing cholangitis, cholangiocarcinoma, autoimmune hepatitis. Slight correlation with intestinal activity or treatment

Viral hepatitis A (HAV)

Viral hepatitis A is a picornavirus containing single-stranded RNA. HAV infection is the most common cause of acute viral hepatitis, especially among children and adolescents. In some countries, more than 75% of adults undergo exposure to HAV, primarily through the fecal-oral route of transmission, so this type of hepatitis occurs in areas with low hygiene. The transmission of infection through water and food and epidemics are most common in underdeveloped countries. Sometimes the source of infection can be an edible infected raw clam. There are also sporadic cases, usually as a result of human-to-human contact. The virus is excreted from the body with feces before the symptoms of acute viral hepatitis A develop , and usually this process ends a few days after the onset of symptoms; Thus, when hepatitis manifests itself clinically, the virus no longer has infectiousness. Chronic carriage of HAV is not described, hepatitis does not take chronic course and does not progress to cirrhosis.

Viral hepatitis B (HBV)

Viral hepatitis B is a complex and most fully characterized hepatitis virus. An infectious particle consists of a viral core and an outer surface shell. The nucleus contains a circular double helix of DNA and DNA polymerase, replication occurs in the nucleus of the infected hepatocyte. The superficial shell is formed in the cytoplasm, for unknown reasons in a large excess.

HBV is the second most frequent cause of acute viral hepatitis. Undiagnosed infections occur frequently, but are much less common than HAV infections. Viral hepatitis B is most often transmitted parenterally, usually through infected blood or blood products. A standard blood test for hepatitis B (determination of the surface antigen of HBsAg) virtually eliminated the possibility of transmission of the virus through blood transfusions, but there is a risk of infection through a common needle when injecting drugs. The risk of HBV infection is elevated among patients in hemodialysis and oncology departments, as well as in hospital staff in contact with blood. The non-parenteral route of infection is characteristic of sexual contacts (heterosexual and homosexual), as well as in closed institutions such as psychiatric hospitals and prisons, but the infectivity of this virus is much lower than the infectivity of HAV, and the transmission route often remains unknown. The role of insect bites in the transmission is not clear. In many cases, acute hepatitis B occurs sporadically in an unexplained source.

For unknown reasons, HBV is sometimes associated primarily with certain extrahepatic manifestations, including nodular polyarteritis and other connective tissue diseases, membranous glomerulonephritis and idiopathic mixed cryoglobulinemia. The pathogenetic role of HBV in these diseases is unclear, but autoimmune mechanisms are assumed.

Chronic carriers of HBV create a global reservoir of infection. Prevalence varies widely and depends on a number of factors, including geographical areas (for example, less than 0.5% in North America and Northern Europe, more than 10% in some regions of the Far East). Often there is a direct transmission of the virus from mother to child.

Viral hepatitis C (HCV)

Hepatitis C virus (HCV) contains single-stranded RNA and belongs to the family of flaviviruses. There are six main subtypes of HCV that differ in the sequence of amino acids (genotypes); These subtypes differ depending on the geographic area, their virulence and response to therapy. HCV can also alter the amino acid structure over time in the infected patient's body (quasi-species).

Infection is usually transmitted through the blood, especially when using drug addicts a common needle for the administration of intravenous drugs, but also with tattooing and body-piercing. Transmission of the virus during sexual intercourse and direct transmission from mother to child are relatively rare. Transmission of the virus with blood transfusion has become very rare after the introduction of a screening test of donor blood. Some sporadic cases occur in patients without obvious risk factors. The prevalence of HCV varies with geography and other risk factors.

Viral hepatitis C is sometimes observed simultaneously with specific systemic diseases, including idiopathic mixed cryoglobulinemia, late cutaneous porphyria (approximately 60-80% of patients with porphyria have HCV, but only in some patients viral hepatitis C develops porphyria) and glomerulonephritis; mechanisms are not clear. In addition, viral hepatitis C is detected in 20% of patients with alcoholic liver disease. The reasons for such a high association are unclear, since only in a number of cases drug addiction is combined with alcoholism. In these patients, viral hepatitis C and alcohol act synergistically, enhancing liver damage.

Viral hepatitis D (HDV)

Viral hepatitis D, or delta-factor, is a defective RNA-containing virus, the replication of which can occur only in the presence of HBV. In rare cases, it is observed in the form of co-infection with acute hepatitis B or as a superinfection with chronic hepatitis B. The affected hepatocyte contains delta particles coated with HBsAg. The prevalence of HDV varies over a wide range depending on the geographic region, in some countries there are localized endemic foci. A relatively high risk group includes those who use intravenous drugs, but, unlike HBV, HDV is not common among homosexuals.

Viral hepatitis E (HEV)

Viral hepatitis E is an RNA-containing virus with an enteral transmission route. Outbreaks of acute hepatitis E are registered in China, India, Mexico, Pakistan, Peru, Russia, central and northern Africa and are caused by the entry of water into the water along with sewage. These outbreaks have epidemiological features similar to HAV epidemics. Sporadic cases are also observed. There were no outbreaks in the USA or in Western Europe. Like hepatitis A, HEV does not cause chronic hepatitis or cirrhosis, chronic carrier is absent.

Symptoms of acute viral hepatitis

Acute infection has predictable phases of development. Acute viral hepatitis begins with an incubation period during which the virus multiplies and spreads asymptomatically. The prodromal, or pre-jaundiced, phase has nonspecific symptoms of acute viral hepatitis, such as severe anorexia, malaise, nausea and vomiting, often have fever and pain in the upper right quadrant of the abdomen, sometimes hives and arthralgia, especially with HBV infection. After 3-10 days urine darkens, jaundice (icteric phase) occurs. The common symptoms of acute viral hepatitis often regress, the patient's well-being improves despite progressive jaundice. During the icteric phase, the liver is usually enlarged and painful, but the edge of the liver remains soft and smooth. Moderate splenomegaly is observed in 15-20% of patients. Jaundice usually reaches a maximum between the first and second weeks and then disappears within 2 to 4 weeks (recovery phase). Appetite is restored after the first week. Acute viral hepatitis, as a rule, is resolved spontaneously after 4-8 weeks.

Sometimes acute viral hepatitis proceeds according to the type of influenza-like disease without jaundice, which is the only manifestation of infection. This is more common than hepatitis with jaundice, with HCV infection and in children with HAV infection.

Some patients may experience recurrent hepatitis, characterized by a relapse of symptoms during the recovery phase. Manifestations of cholestasis can develop during the icteric phase (cholestatic hepatitis), but they are usually resolved. In the case of persistent flow, despite general regress of inflammation, jaundice can persist for a long time, leading to an increase in the level of alkaline phosphatase and the appearance of skin itching.

HAV often does not cause jaundice and does not show any signs. It is almost invariably resolved after an acute infection, although there may be an early relapse.

HBV causes a wide range of liver diseases, from subclinical carrier to severe or fulminant acute hepatitis, especially in the elderly, whose mortality may be as high as 10-15%. In chronic infection with HBV, hepatocellular carcinoma may eventually develop, even without previous cirrhosis of the liver.

Viral hepatitis C can be asymptomatic during the acute phase of infection. The degree of severity often changes, with exacerbations of hepatitis and wave-like increases in the level of aminotransferases for several years or even decades. HCV has the highest risk of developing a chronic process (approximately 75%). Chronic hepatitis is usually asymptomatic or with minor manifestations, but always progresses to cirrhosis in 20-30% of patients; Cirrhosis of the liver before its manifestation often develops for decades. Hepatocellular carcinoma can be a consequence of HCV-induced liver cirrhosis and is very rarely a result of a chronic infection without cirrhosis (as opposed to HBV infection).

Acute HDV infection usually occurs as an unusually severe acute HBV infection (coinfection), as an exacerbation in chronic carriage of HBV (superinfection) or as a relatively aggressive chronic infection of HBV.

HEV can have a severe course, especially in pregnant women.

Diagnosis of acute viral hepatitis

In the prodromal period, acute viral hepatitis resembles various nonspecific viral diseases, and therefore the diagnosis of acute viral hepatitis is difficult. In patients without jaundice and suspected hepatitis in the presence of risk factors, nonspecific functional liver tests, including aminotransferases, bilirubin and alkaline phosphatase, are first examined. Usually suspicion of acute hepatitis occurs only in icteric period. Therefore, differential diagnosis of acute viral hepatitis from other diseases that cause jaundice is needed.

As a rule, acute viral hepatitis differentiates from other causes of jaundice in increasing ACT and ALT (usually> 400 IU / L). The level of ALT is usually higher than the ACT level, but there is almost no absolute correlation of enzyme levels with the severity of the clinical course. Enzyme levels rise early in the prodromal phase, the peak of the rise precedes the maximum manifestation of jaundice, and the decrease occurs slowly during the recovery period. Bilirubin in the urine usually precedes jaundice. Hyperbilirubinemia in acute viral hepatitis can be expressed to varying degrees, the determination of bilirubin fractions has no clinical value. Alkaline phosphatase usually rises moderately; a significant increase may indicate extrahepatic cholestasis and require an instrumental examination (for example, ultrasound). A liver biopsy is generally not required if the diagnosis is beyond doubt. If the results of laboratory tests suggest acute hepatitis, especially if ALT and ACT> 1000 IU / L, MHO is being investigated. Manifestation of portosystemic encephalopathy, hemorrhagic diathesis and prolongation of MHO indicate fulminant hepatitis.

If there is a suspicion of acute viral hepatitis, it is necessary to verify its etiology. Anamnesis can be the only way to diagnose a drug or toxic hepatitis. Anamnesis should also reveal risk factors for viral hepatitis. Prodromal pain in the throat and diffuse adenopathy can indicate infectious mononucleosis, rather than viral hepatitis. Alcoholic hepatitis presupposes alcohol abuse in history, gradual development of symptoms, the presence of vascular asterisks or signs of chronic alcohol abuse or chronic liver disease. Aminotransferase levels rarely exceed 300 IU / L, even in severe cases. In addition, unlike alcoholic liver damage, with viral hepatitis, ALT is usually higher than ACT, although this is not a reliable differential diagnostic feature. In doubtful cases, liver biopsy helps to distinguish between alcoholic hepatitis and viral hepatitis.

In patients with suspected viral hepatitis, the following studies should be performed to identify the hepatitis A, B or C virus: anti-HAV IgM, HBsAg, IgM to the hepatitis B virus antigen (anti-HBc IgM) and anti-HCV. If some of them are positive, further serological testing may be required for the differential diagnosis of acute hepatitis from a previous or chronic infection. If serology presupposes hepatitis B, an analysis is usually performed for hepatitis B e-antigens (HBeAg) and anti-HBe for more accurate prognosis of the course of the disease and for antiviral therapy. In severe serologically confirmed HBV, an anti-HDV assay is performed. If the patient has recently been in an endemic focus, an assay for anti-HEV IgM should be performed.

HAV is present in the serum only during an acute infection and is not detected by known clinical tests. IgM antibodies usually appear early in the course of infection, and their titer reaches a maximum about 1-2 weeks after the development of jaundice, gradually decreasing within a few weeks; this is accompanied by the emergence of protective IgG antibodies (anti-HAV), which persist, as a rule, throughout life. Thus, IgM is a marker of acute infection, whereas anti-HAV IgG simply indicates the transferred HAV and the presence of immunity to the infection.

[2], [3], [4], [5], [6],

Serological diagnosis of hepatitis A

	HAV	Transferred HAV
Anti-HAV IgM	+	-
Anti-HAV IgG	-	+

HAV is the hepatitis A virus. Postponed infectious HAV.

Serological diagnosis of hepatitis B

	HBV	Chronic	Postponed2
HBsAg	+	+	-
Anti-HBs	-	-	+
Anti-HBc IgM	+	-	-
Anti-HBc IgG	-	+	+
HBeAg	+	+	-
Anti-HBe	-	+	+
HBV DNA	+	+	-

HBV - hepatitis B virus; HBsAg is the surface antigen of the hepatitis B virus; HBcAg - nuclear antigen of the hepatitis B virus; HBeAg is the hepatitis B virus e-antigen.

Levels of anti-HBV antibodies should be determined when serologically confirming the presence of HBV in severe infection.

² Postponed HBV infection with convalescence.

Anti-HBs are also considered as the only serological marker after HBV vaccination.

Serological diagnosis of hepatitis C

	Acute	Chronic	Postponed HCV
Anti-HCV	+	+	+
HCV RNA	+	+	-

HCV - hepatitis C virus. Postponed HCV infection with spontaneous recovery or effective therapy.

Acute viral hepatitis B has at least three different antigen-antibody systems that can be tested: HBsAg, HBeAg, and HBeAg. Viral DNA (HBV DNA) can also be examined. In the serum, the surface antigen of HBV, i.e., HBsAg, can be detected. HBsAg usually appears during the incubation period, usually 1-6 weeks before the onset of clinical symptoms or changes in biochemical analyzes, and indicates the presence of viremia, which disappears in the process of recovery. However, the presence of HBsAg is sometimes transient. Appropriate protective antibodies (anti-HBs) appear weeks or months after clinical recovery and usually persist for life; thus, its detection indicates a transferred HBV infection and their immunity. In 5-10% of patients, HBsAg persists and antibodies are not produced: these patients become asymptomatic carriers of the virus or they develop chronic hepatitis in the future.

HBcAd is the nuclear antigen of the virus. Without the use of special methods is detected only in the affected cells of the liver, but not in the blood serum. Antibodies to HBcAd (anti-HBc) usually appear at the beginning of the clinical phase of the disease; subsequently, antibody titers gradually decrease over a period of several years or throughout life. Their presence along with anti-HBs indicates a recovery from a previous HBV infection. Anti-HBc antibodies are also present in chronic carriers of HBsAg, which do not give an anti-HBs response. In acute infection, anti-HBc is mainly represented by IgM immunoglobulins, whereas for chronic infection, anti-HBc IgG predominate. Anti-HBc IgM are sensitive markers of acute HBV infection, and in some cases are the only markers of a recent infection in the period between the disappearance of HBsAg and the appearance of anti-HBs.

HBeAg is a viral nucleus protein (not to be confused with the hepatitis E virus), which appears only in the presence of HBsAg in the serum, HBeAg suggests active replication and greater infectivity of the virus. In contrast, the presence of an appropriate antibody (anti-HBe) suggests a lower infectivity. Thus, the e-antigen is more informative as a prognostic marker than for diagnostics. Chronic liver disease develops more frequently among patients with HBeAg and less frequently among patients with anti-HBe.

In patients with active HBV infection, viral DNA (HBV-DNA) can be detected in the serum in a special study, but this test is not always available.

With HCV, serum antibodies (anti-HCV) almost always indicate an active infection; they are not protective. Anti-HCV usually appear within 2 weeks of an acute infection, but sometimes at a later date. In a small percentage of patients, anti-HCV simply reflects the previously transferred exposure of the virus with spontaneous clearance, and not the presence of an active infection. Levels of ALT and ACT are within normal limits. In unclear cases, HCV RNA is quantified.

When HDVaHTH-HDV indicates an active infection. They may not be detected within a few weeks after the onset of an acute illness.

In HEV, anti-HEV IgM is not detected by conventional methods. In patients with an endemic history in combination with clinical data, the presence of anti-HEV indicates an acute infection of HEV.

If a biopsy is performed, a similar histopathological pattern is usually seen, regardless of the specificity of the virus: acidophilic hepatocellular necrosis, mononuclear inflammatory infiltrates, histological signs of regeneration. HBV can sometimes be diagnosed by the presence of the symptom of "frosted glass" (due to the filling in the cytoplasm of HBsAg) and using special methods of immunological staining of the components of the virus. However, these signs are not characteristic of acute HBV and are much more typical of chronic HBV infection. Identification of HCV as an etiological factor is sometimes possible on the basis of little expressed morphological features. A liver biopsy helps in the prognosis of acute hepatitis, but is rarely performed exclusively for this purpose. Complete histological recovery occurs if there is no extensive necrosis that connects all the acini (bridge necrosis). Most patients with bridge necrosis recover completely. However, in some cases, the process progresses to chronic hepatitis.

Treatment of acute viral hepatitis

No treatment for acute viral hepatitis does not affect the course of this disease, with the exception of individual cases of effective immunization after exposure. Avoid alcohol that increases liver damage. Restrictions in diet or physical activity, including the usually prescribed bed rest, do not have any scientific justification. Most patients can safely return to work after resolving jaundice, even if the ACT or ALT levels are slightly elevated. With cholestatic hepatitis, the administration of cholestyramine 8 g orally 1 or 2 times a day can reduce itching. The case of viral hepatitis should be reported to the local or city health department.

Prevention of acute viral hepatitis

Since the effectiveness of treatment is limited, prevention of acute viral hepatitis is very important. Personal hygiene can prevent transmission, especially fecal-oral, which is observed with HAV and HEV. Blood and other physiological fluids (eg, saliva, semen) in patients with acute HBV and HCV and stool patients with HAV are considered infectious. Barrier protection measures against infection are recommended, but patient isolation is not important for preventing the spread of HAV and in general for HBV or HCV infections. The incidence of posttransfusion infections is minimized by eliminating unnecessary transfusions and examining all donors for HBsAg and anti-HCV. Screening of donors reduced the incidence of posttransfusion infections to 1 / 100,000 transfused units of blood components.

Immunoprophylaxis can include active immunization with vaccines and passive immunization.

Prevention of acute viral hepatitis A 

Pre-exposure prophylaxis for HAV infection should be provided to people traveling to highly endemic areas. It should also be conducted among the military, kindergarten workers and staff of diagnostic laboratories, as well as in patients with chronic liver disease due to the increased risk of fulminant hepatitis A. Several HAV vaccines have been developed with different doses and vaccination regimens; they are safe, provide protection for about 4 weeks and provide prolonged protection (perhaps more than 20 years).

Standard immunoglobulin, formerly called serum immunoglobulin, prevents or reduces the severity of HAV infection and is used for postexposure prophylaxis; It is usually recommended to inject 0.02 ml / kg intramuscularly, but some experts suggest increasing the dose to 0.06 ml / kg (from 3 ml to 5 ml for adults).

Prevention of acute viral hepatitis B

Vaccination in endemic areas dramatically reduced the prevalence of infection. People with high risk have long been recommended to carry out pre-exposure immunization. However, selective vaccination of high-risk groups in the US and other non-endemic areas did not lead to a significant reduction in the incidence of viral hepatitis B; Thus, vaccination is now recommended to all Americans under the age of 18, from birth. Universal vaccination is desirable in all countries, but it is too expensive and therefore unrealistic.

Two recombinant vaccines have been developed; they are safe, even during pregnancy. The vaccination regime provides for three intramuscular injections into the deltoid muscle - primary immunization and repeated administration at 1 month and 6 months. Children are given lower doses, and patients receiving immunosuppressive therapy or who are on hemodialysis, higher doses.

After vaccination, the protective level of anti-HBs persists to 5 years in 80-90% and up to 10 years in 60-80% of vaccinated. Patients on hemodialysis or receiving immunosuppressive drugs with an anti-HBs of less than 10 mIU / mL are recommended to perform booster immunizations.

Postcontact immunoprophylaxis of HBV infection combines vaccination with the introduction of immunoglobulin against hepatitis B (IHGV), a drug with a high titre of anti-HBs. Apparently, IHGV does not prevent the development of infection, but prevents or reduces clinical manifestations of the disease. Newborns from HBsAg-positive mothers are given an initial dose of vaccine and 0.5 ml of IHD intramuscularly in the thigh immediately after birth. Within a few days after sexual contact with the HBsAg-positive partner or contact of damaged skin or mucosa with HBsAg-positive blood, it is necessary to administer intramuscularly 0.06 ml / kg IHGV together with the vaccine. Previously, a vaccinated patient after a percutaneous exposure to HBsAg-positive blood should be tested for anti-HBs; if the titers are less than 10 mIU / ml, a booster vaccination is performed.

Prevention of acute viral hepatitis C, D, E

Currently, there are no drugs for immunoprophylaxis of HDV, HCV or HEV infections. However, the prevention of acute viral hepatitis B prevents acute viral hepatitis D. The creation of a vaccine against HCV infection is hampered by the pronounced variability of the viral genome.