There is no complete cure for chronic hepatitis B. However, some effective treatment options can reduce the risk of liver damage and slow or stop the spread of the virus.
Chronic hepatitis B infection can be treated with antiviral medications such as pegylated interferon, tenofovir, entecavir and elaprol tenofovir. Antiviral drugs help remove the virus from the bloodstream and also reduce the risk of developing liver cancer and cirrhosis.
The treatment of patients with chronic hepatitis B has changed dramatically in the last two decades. Currently, oral nucleotide analogues with potent viral suppression and high genetic barriers to resistance, namely entecavir, tenofovir disoproxil and tenofovir elaprednisolone, are recommended as first-line antiviral agents.
Long-term treatment with antiviral drugs can inhibit hepatitis B virus replication, reverse liver fibrosis, and reduce the risk of hepatocellular carcinoma.
In the era of oral antiviral therapy, functional cure and limited treatment are among the few unmet needs that clinicians need to address.
Researchers found that in 33 HBeAg-negative, genotype D-infected patients with chronic hepatitis B who had not received antiviral drugs, treatment discontinuation may have led to the disappearance of up to 40% of HBsAg during up to 6 years of post-treatment follow-up after discontinuation of adefovir monotherapy.
4-5 years of successful treatment. Higher ALT levels at non-retreatment and end of treatment (EOT) were associated with a higher incidence of HBsAg disappearance.
Since then, a growing number of studies have shown that HBsAg can be cleared after cessation of antiviral therapy treatment due to activation of the host immune response and post-treatment relapse in Asian and Caucasian HBeAg-negative patients.
In a European randomized controlled trial (RCT) (FINITE study), 42 HBeAg-negative, predominantly Caucasian patients discontinued or continued antiviral therapy treatment; 19% of patients in the discontinuation group achieved HBsAg disappearance at week 144 of discontinuation, while no patients in the continuation group cleared HBsAg.
Despite growing evidence of increased HBsAg disappearance rates after treatment cessation, the effectiveness of treatment cessation remains controversial, primarily related to concerns about the harms of cessation.
There are two types of HBsAg clearance after treatment cessation: one is a smooth transition from complete viral suppression during treatment to complete viral clearance after treatment without any viral rebound, while the other is an initial viral and clinical flare followed by immune control. The second is more frequent than the first and is not what doctors and patients want to encounter.
This can help clear HBsAg to achieve a functional cure; however, necrosis, inflammation, and liver regeneration associated with clinical episodes are well-known risk factors for hepatitis B virus-associated hepatocellular carcinoma.
Theoretically, patients with cured clinical episodes are still at risk of developing hepatocellular carcinoma.
Consideration should also be given to the physical, financial and psychological harm that may result from discontinuing treatment. Physical harm may result from closely monitored testing and is not limited to medical complications.
Current studies on treatment discontinuation are not sufficient or comprehensive enough to lead to a broad paradigm shift that would recommend discontinuation of oral therapy in HBeAg-negative hepatitis B patients with sustained viral suppression.
Until novel anti-hepatitis B virus drugs with new targets and mechanisms are available, our main goal is to reduce liver-related mortality caused mainly by hepatocellular carcinoma, which is also the goal of the World Health Organization.