The Hepatitis Foundation runs a Ministry of Health-funded national monitoring programme for people living with chronic hepatitis B.
How common is hepatitis B?
Hepatitis B is the most common serious liver infection in the world. It is the leading cause of liver cancer. About 100,000 people in New Zealand are chronically infected with the virus. Every year over one million people die from hepatitis B-related liver disease. This includes 200-300 people in New Zealand.
Hepatitis B risk factors
• New Zealanders of Maori, Pacific or Asian ethnicity, unless they are known to have been fully vaccinated as an infant
• People born in an area of high hepatitis B endemicity, including Asia, the Pacific Islands, Africa, the Middle East, southern Europe or the northern or eastern parts of New Zealand’s North Island
• Living with someone who has hepatitis B
• Being born to a woman with hepatitis B or having a close family member with the virus
• Unprotected sexual contact with someone who has hepatitis B
• Having a tattoo performed with unsterile equipment.
Natural history of chronic hepatitis B infection
Most people acquire hepatitis B in infancy or early childhood. The natural history of such infection follows a typical pattern.
During the first stage the virus is present at very high titres (>10^8) and the immune system is not active against the virus. As the virus itself is not hepatotoxic there is no damage occurring to the liver. This is the immune-tolerant HBeAg positive phase. This is often followed in later childhood or early adulthood by a period of active hepatitis when the immune system tries to destroy the virus by killing infected liver cells (immune active chronic HBV). A person may then become HBeAg negative and, with a much lower viral load, move into a prolonged phase of normal liver function (inactive CHB or immune control).
Subsequent viral mutation in some individuals can lead to partial escape of immune control and fluctuating or persistent chronic active hepatitis (HBeAg negative chronic hepatitis or immune active chronic hepatitis B). It is during periods of active hepatitis that progressive liver damage and fibrosis can occur, leading ultimately to cirrhosis.
Hepatocellular carcinoma (HCC) can develop in any person with CHB but predominantly arises in those with established liver cirrhosis. The primary aim of antiviral treatment is to prevent progressive fibrosis and the subsequent complications of cirrhosis, liver failure and HCC.
|Hepatitis B surface antigen (HBsAg)||Shows whether the person has current hepatitis B virus infection. In chronic HBV infection, HBsAg is always detected.|
|Hepatitis B surface antibody
(HBsAb or anti-HBs)
|Shows whether the person is developing immunity to HBV. It can be present while the person still has the virus (HBsAg positive). If HBsAg is negative and HBsAb is positive it means the person is immune either from vaccination or past infection.|
|Hepatitis B e antigen
|Usually detected in the absence of anti-HBe. Shows the hepatitis virus is multiplying at a high rate and is therefore very infectious. The HbeAg-positive phase is the earliest stage of HBV infection and the most common one in children and young adults.|
|Hepatitis B e antibody
(HBeAb or anti HBe)
|Usually detected in the absence of HBeAg. This later phase of HBV infection follows the development of the patient’s immune response against HBeAg and is the most common phase of HBV infection found in middle-aged and elderly patients. This phase is usually associated with suppression of the virus and reduction in level of viral replication. However, HbeAg-negative patients are still infectious. They may still have active liver disease and could progress to cirrhosis.|
|Hepatitis B core antibody
(HBcAb or anti-HBc)
|Shows whether a person has ever been exposed to the hepatitis B virus. Is detected in patients with current infection and people with previous acute infection that has resolved. Is not detected in individuals who have immunity through vaccination.|
|Anti Hbc IgM+||Always detected during acute infection and may be the only marker of acute infection in the ‘window phase’, when HBsAg has disappeared and anti-HBs levels are not yet high enough to be detected.|
|Hepatitis B virus DNA
|Measures the amount of hepatitis B virus present in the blood (viral load). High HBV DNA levels are one of the criteria for commencing anti-viral therapy (along with high ALT or advanced fibrosis stage). The HBV DNA level is one of the most important prognostic factors for the development of complications of hepatitis B.|
Our medical director Dr Chris Moyes and clinical director Dr Alex Lampen-Smith have co-authored a document outlining the situations in which anti-viral therapy could be considered.
The goal of therapy for patients with chronic hepatitis B infection is to improve survival and quality of life by preventing disease progression and consequently HCC development. Additional goals of antiviral therapy are to prevent mother to child transmission, hepatitis B reactivation and the prevention and treatment of HBV-associated extra-hepatic manifestations.
The rationale for pegylated interferon is to induce long-term immunological control with a finite duration of therapy. Pre-treatment predictors of response include HBeAg positive, HBV DNA < x10^8, elevated ALT and genotype A (more likely to be present in Asians). In patients with favourable pre-treatment characteristics approximately 30% will experience HBeAg seroconversion and 3-7% HBsAg seroconversion. Treatment is via once weekly subcutaneous injection for 48 weeks.
Entecavir sandoz (0.5mg) and tenofovir disoproxil (245mg) are once-daily oral tablets for chronic hepatitis B. They are potent antiviral agents with a high barrier to resistance leading to long-term undetectable HBV DNA levels (viral load) in the vast majority of adherent patients.
Apart from requiring dose adjustments in renal impairment there are no contra-indications to therapy. Entecavir and tenofovir have been used internationally for >10 years and have very good safety profiles. Minimal rates of renal function decline have been reported during long-term therapy with entecavir and slightly more so with tenofovir. It is recommended to monitor creatinine and phosphate annually.
Both these agents are only effective in suppressing viral replication while a patient is adherent to their use. Upon discontinuation the viral load rises within days to weeks. Viral reactivation can lead to severe hepatitis and subsequent hepatic decompensation, which can be fatal (especially in those with advanced liver disease at the time of treatment initiation). Close clinical and laboratory monitoring should be undertaken for several months after discontinuation and resumption of antiviral medication may be required.
Entecavir should be taken on an empty stomach, at least two hours after a meal and at least two hours before the next meal.
Tenofovir can be taken with or without food. It is also used in combination with other antiviral agents, for the long-term management of HIV. If a person has HIV/HBV co-infection, tenofovir should not be used as a single agent and their care should be supervised by a specialist.
Studies assessing sensitive markers of bone turnover have reported a decline in bone mineral density in patients treated with tenofovir.
Lamivudine, adefovir and telbivudine are also licensed for the treatment of CHB. Due to their low barrier to resistance these are no longer preferred first line agents. Small numbers of patients may remain on these agents and, while they are achieving effective viral suppression, they do not need to be switched. If a person has been on any prior nucleos(t)ide analogue therapy and develop resistance they should be switched to tenofovir.
Below are links to useful education tools.
Information about ordering Fibroscans for immigration purposes.