There is a common view that once you start hepatitis B treatment, you will be on it for life. This is changing. In recent years, numerous studies have been done looking into the notion of functional cure for hepatitis B which, when achieved, means therapy can be stopped.Continue reading “Hepatitis B Treatment—not necessarily a life-long commitment”
An Australian expert panel of medical specialists have recommended that all people receiving immunosuppression cancer therapy be screened for hepatitis B.
If you have ever been infected by hepatitis B, cancer treatment which suppresses your immune system can allow the virus to reactivate – even if your body had dealt with it successfully before. Reactivation can lead to liver failure, death or sub-optimal cancer treatment.
Close to 234,000 Australians live with chronic hepatitis B—one of the leading causes of liver cancer—and almost four out of ten don’t know they have the condition. It is even more alarming in South Australia, where six out of ten are not diagnosed1.
Hepatitis B diagnosis rate in Australia remains stagnant at around 63 per cent from 2015 to 2017, and our treatment rate of 8.3 per cent falls far short of the recommended 20 per cent of people with chronic hepatitis B estimated to need treatment. In this respect too, South Australia lags with a treatment uptake of only 5.7 per cent—and only 16 per cent of those with chronic hepatitis B being monitored, well below the national average of 20.2 per cent2.
Australian researchers have found a way to predict the risk of liver cancer in people with chronic hepatitis B, promising earlier diagnosis, better management and potentially better prevention of hepatitis B- related liver cancer.
For some time now scientists have known that when the hepatitis B virus (HBV) replicates it leaves behind bits of its DNA in string form, different to its original circular shape. They refer to this as “splicing”. They also noticed that higher viral load results in more splicing; and retrospective examination of blood samples showed that splicing increased each year prior to the development of liver cancer.