Hepatitis d B18.0

Acute or chronic infectious disease of the liver caused by a simultaneous or additional (superinfection) infection of a person infected with hepatitis B with the hepatitis D virus The hepatitis D virus is an envelopeless RNA virus, which requires the envelope (HBsAg) of a helper virus (hepatitis B virus) for its replication. Thus, the infection in humans occurs exclusively as a co-infection or as a superinfection of a hepatitis B infection. From this it can be concluded that a vaccination against hepatitis B also protects against a hepatitis D infection.

The hepatitis D virus (HDV) is an incomplete, envelopeless RNA virus, a so-called virusoid, which consists of only one RNA ring without envelope proteins. The hepatitis D virus requires these envelope proteins for its replication. It obtains them from the hepatitis B virus as "envelope donors". The hepatitis D virus therefore has the property of binding envelope proteins (HBsAg) of the hepatitis B virus. From this it can be deduced that infection with the hepatitis D virus can only occur if the hepatitis B virus is also present at the same time. Only people infected with HBV can become infected with the hepatitis D virus at the same time.

About 5% of HB virus carriers worldwide are coinfected with the HD virus. The number of coinfected persons in Germany is low: 2015: 20 cases, 2016: 12 cases, 2017: 31 cases (number of cases reported to the RKI)

HDV is endemic in the Mediterranean region (in southern Italy 50% of HBsAg carriers are HDV-coinfected), in Romania, on the Arabian Peninsula, in the Middle East, in parts of Africa and Central and South America.

Incubation period: 4-7 weeks

Like hepatitis B, hepatitis D is transmitted mainly through sexual intercourse and the use of infected needles. Other ways of getting infected include the use of contaminated blood, syringes, tattoo or acupuncture needles. A vertical perinatal infection is also possible.

The clinical symptoms correspond to those of HBV infection.

Serology: 1-2ml serum

Serological antibody detection:

Acute hepatitis (HDV/HBV co-infection): Anti-HDV IgM: positive; HDV RNA: positive.

Acute hepatitis (HDV/HBV superinfection): HBsA: positive; HDV RNA: positive; Anti HD IgM: positive

Chronic Hepatitis (HDV/HBV): HBsA: positive; HDV-RNA: positive; Anti HD-IgM: +/-; Anti HD-IgG: positive

General Laboratory:

BSG↑; CRP↑; Liver function tests: Bilirubin mostly elevated: 2-3mg/dl; increase of transaminases (500-3.000U/l); GPT>GOT; cholestasis parameters ↑. Possibly only slight increase of gamma-GT. Furthermore: determination of prothrombin time or INR; increase in serum iron, possibly increase in gamma globulin fraction in electrophoresis. Blood count: possibly lymphocytosis. Virus serology to determine virus type and antigen/antibody status.

Liver values increase early during the prodromal phase, reach their peak before the icterus is maximal and then slowly decrease during the convalescence phase. Bilirubin excretion in urine usually precedes the icterus. Hyperbilirubinemia is differently pronounced in acute viral hepatitis. However, their differentiation has no clinical benefit. Alkaline phosphatase is usually only moderately elevated, strong elevations suggest the suspicion of extrahepatic cholestasis and trigger imaging procedures (e.g. sonography).

medical history, clinic, microbiological results

So far only limited therapeutic options due to the double infection. A 24-month treatment with pegylated interferon alfa-2a leads to virus elimination in 25% of cases. However, the amount of virus often increases again after the end of therapy. Overall, however, the course of hepatitis D disease seems to be protracted under this therapy.

The nucleoside and nucleotide analogues effective against hepatitis B are not effective against the hepatitis D virus. In advanced liver disease, hepatitis B and D co-infected patients can be transplanted.

For the prognosis of the patient it is important whether the infection with hepatitis D virus occurred simultaneously with the infection by the hepatitis B virus (simultaneous infection) or whether it occurred subsequently (superinfection).

Simultaneous infection (HBV/HBD) leads in the majority of cases to complete elimination of both types of virus. In 5-20% fulminant course.

The superinfection of an HBsAg carrier as a "second hit" is significantly more aggressive (direct cytotoxicity of the HD virus) than the "simple" HBV infection or the simultaneous HB/HD infection. It is usually chronic with transition to cirrhosis; increased risk of hepatocellular carcinoma.

Chronic hepatitis B/D co-infection has a significantly higher risk of cirrhosis and a higher mortality rate than chronic hepatitis B alone.

Hepatitis B vaccination. Those who are vaccinated against hepatitis B also have protection against hepatitis D infection.