Hepatitis B

A viral hepatitis can be caused by different agents, but the most common is the hepatitis B virus. The disease is of particular importance for the high number of chronic carriers around the world.
The virus is most common within people using intravenous drugs and men who have relations with the same sex. Nevertheless the most transmisions happen in sexual relations between men and women. Medical staff also has a higher risk than the average population.
The Virus can not only be detected in blood, but also in saliva, sperm and vaginal secretion.

The hepatitis B virus (HBV) is a DNA-Virus, belonging to the family of hepadnaviridae. 8 different serotypes exist. The virus consists of various elements, of which the following have special importance in diagnostics:

Surface antigen (HBsAg)
Core antigen (HBcAg)
Envelope antigen (HBeAg)
DNA in the nucleus

Hepatitis-B-specific antigens and antibodies

In the course of the disease at first the HBs antigen and nearly at the same time the HBe antigen can be detected. The HBs antigen already apears prior to the elevation of liver enzymes and presists during the whole course of clinical symptoms. In cases, in which no chronification develops, the HBs antigen disapears shortly after the emergence of anti HBs antibodies. The latter normally persist a whole life and provide protection against recurrent infections. The detection of the HBe antigen is a sign for active replication of the virus. The same can be shown by detection of DNA using polymerase chain reaction (PCR), which also generates positive findings from the onset of the infection.
The first antibody appearing in the course of the disease is anti HBc. It presents itself 1 to 2 weeks after the appearance of the HBs antigen and thus before the presentation of anti HBs antibodies. The HBc antigen itself can never be detected, due to its localization inside the virus. Primarily antibodies of the IgM group prevail, wich later are displaced by antibodies of the IgG group.
Anti HBe-antibodies appear between the presentation of anti HBc and anti HBs antibodies.

Overview of the oder of presentation of antigens and antibodies

HBs antigen
Hbe antigen
anti HBc antibodies
anti HBe antibodies
anti HBs antibodies

It has to be considered that this order only aplies in cases of complete recuperation. The risk of chronification is about 10%. In those cases, no anti HBs antibodies appear and the HBs antigen remains. The HBe antigen also presists primarily, but often disappears within a few years. Patients, who do not presents this disappearence, thus suffering an active course of the disease, have a risk of 20% on developing cirrhosis or hepatocelular carzinoma within the next 30 years.

Clinical findings

The incubation period lasts an average of 12 to 14 weeks, but also can take until half a year. The disease begins insidious and in most cases is not noticed by the patient. Of 90% that experience full recuperation, 2/3 stay asymptomatic during the whole course of the infection.
Those who develop symptoms, begin with unspecific complaints such as nausea and vomiting, athralgias and pain of the upper belly. Later more classic symptoms as pain in the liver region due to hepatomegalia, jaundice, pruritus and decoloration of heces appear. On the other hand, many viral hepatitis take an anicteric course.
Only about 1% of all patients develop fulminant hepatitis with a high mortality rate of up to 60%.

Extrahepatic manifestations

In contrast to other viral hepatitis, extrahepatic manifestations occur more often in hepatitis B.
Cutaneous manifestations are maculopapulous exanthema, as well as in childreen unfrequently the Gianotti-Crosti-Syndrome. In the latter, there is papular rash, which is accompanied by lymphadenopathia and splenomegalia.
Rheumatic complications inlcude athralgias, polymyalgia rheumatica, polyarteritis nodosa, vascular lesions and cryoglobulinemia.
The kidneys sometimes develop glomerulonephritis, especially in chronic courses of hepatitis B.
Neurologic manifestations are multiple neuropathy and the Guillain-Barré syndrome.

While the complications mentioned so far primarily are caused by the effects of immune complexes, complications directly caused by the virus itself are very rare. They include aplastic anemia, pancreatitis and pericarditis.

Diagnostics

To prove an acute infection, dectection of anti HBc antibodies of the IgM group is essential. Tests on the HBs antigen are also performed, but can be negative in some cases in spite of acute infection. To estimate the infectiousness and monitor medical therapy, the polymerase chain reaction can be used to detect hepatitis B DNA.

Therapy

The first line therapy can be accomplished with interferon α and lamivudin, but is only indicated in cases of chronic course.
Much more important are prophylactic measures through active immunization, which sould be performed on all infants and toddlers. An indication for active immunization is also given in all persons with negative anti HBc antibodies and persons with positive anti HBc antibodies, but low titers of anti HBs antibodies.
After contact, as through needlestick injury, a passive immunization with hepatitis B hyperimmunglobulin should be enforced.

Hepatitis B and pregnancy

The risk for infection of the child strongly depends on the antigen status. In mothers with positiv HBs and HBe antigen, the risk is with about 90% very high, while the exclusive presence HBs antigen is associated with a risk of only 10%. Birth by cesarean does not reduce the risk for infection in contrast to vaginal birth. All pregnant women with positiv HBs antigens should be treated with hepatitis B hyperimmunglobulin. Because of the very high risk of chronification in infected newborns, the child is given the first active immunization within the first 12 hours and is also treated with hyperimmunglobulin. Further active immunizations follow after 1 to 2 and 6 month, respectively. After completion of the immunization, another serologic test should be performed.