Unfortunately, only very few patients with chronic hepatitis B infection can completely eradicate the virus with the medication currently available. Treatment can therefore only be aimed at suppressing viral replication. Because the hepatitis B virus cannot be eliminated from the body, treatment to prevent the virus from replicating often has to be lifelong. If the virus multiplies, this usually leads to increased inflammation of the liver. The immune system kills the infected liver cells, which again leads to liver damage. This should be prevented by the treatment. If liver cells were to die again and again, scars would form, which is initially referred to as liver fibrosis. If the liver is completely scarred and there are fewer and fewer liver cells, this is known as liver cirrhosis.
Patients with liver cirrhosis or permanently increased inflammatory activity have an increased risk of developing liver carcinoma (“liver cancer” or hepatocellular carcinoma): they should therefore be examined with an ultrasound of the liver at six-monthly intervals as part of a monitoring program in addition to drug-based antiviral therapy.
The hepatitis B vaccination induces anti-HBs antibodies, which provide almost 100% protection. It is recommended for all risk groups and is now also recommended together with the standard childhood vaccinations. A titer of > 100 IU is considered to be reliably protective.
Before immunosuppressive (immune inhibitor) therapy and chemotherapy, the presence (HBsAg) or history (anti-HBc IgG) of hepatitis B should be investigated due to the risk of a severe flare-up of hepatitis B (a “fulminant HBV reactivation”) and even liver failure.
In principle, treatment is indicated for all patients with chronic HCV infection who wish to be treated and have no contraindications. The treatment of chronic hepatitis C has undergone a dramatic change in recent years. Fixed combinations of directly antiviral drugs (DAA) are now available, which lead to a cure rate of over 98%. These substance combinations, which are also generally very well tolerated, achieve freedom from the virus after a treatment period of 8 or 12 weeks; in rare cases, 24 weeks of treatment is necessary.
As mentioned, there are very specific drugs: The combination medication velpatasvir (NS5A inhibitor) and sofosbuvir (polymerase inhibitor) or glecaprevir (protease inhibitor) and pibrentasvir (NS5A inhibitor) is used to treat all subtypes (genotypes) (“pangenotypic therapy”). The combination of grazoprevir (protease inhibitor) and elbasvir (NS5A inhibitor) can be used to treat patients with genotype 1b infection. In the very rare cases of treatment failure after DAA therapy, a triple combination of voxilaprevir, velpatasvir and sofosbuvir can be used after recommended resistance testing.
Even after successful viral eradication, patients who had indications of advanced liver fibrosis or cirrhosis before treatment should continue to receive regular follow-up care, including ultrasound.
The hepatitis D virus (HDV) is a so-called satellite virus, as it does not have its own envelope protein but relies on the envelope of the hepatitis B virus as packaging. It is estimated that around 5% of all patients infected with hepatitis B worldwide are also infected with the hepatitis D virus. If HDV is transmitted simultaneously with HBV, the course of the acute infection is similar to that of a single HBV infection, with a spontaneous recovery rate of > 95% for both viruses.
In the case of an HDV superinfection following a longstanding hepatitis B infection, the HBV envelopes already present in large numbers lead to a strong multiplication of hepatitis D viruses and thus to a highly replicative hepatitis D infection, which can lead to severe hepatitis attacks with partial failure of liver function (hepatic decompensation). In this situation, hepatitis D is chronic in 70-90% of cases, often with progressive liver fibrosis and cirrhosis.
Bulevirtide has been available since September 2024 as the first approved medication for the treatment of hepatitis D virus infection. It is applied subcutaneously daily in a dosage of 2 mg. Bulevirtide blocks the sodium taurocholate co-transporting polypeptide (NTCP) on hepatocytes and thereby inhibits the uptake of HBV/HDV virus particles. In 40-60% of patients, long-term use of this therapy leads to a reduction or loss of HDV RNA and normalization of transaminases.
Hepatitis E is an RNA virus that infects humans as well as wild animals, livestock, pigs, rats, mice and dogs. In epidemics, transmission usually occurs via smear infections or via contaminated water or the consumption of raw game or pork. Neurological symptoms are not uncommon. In special cases (immunosuppression), the hepatitis E infection can take a chronic course.
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University Hospital Zurich
Department of Gastroenterology and Hepatology
Raemistrasse 100
8091 Zurich