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Hepatitis C


The epidemiologic data of hepatitis C in New Zealand is poor compared to that in Australia where chronic hepatitis C is a notifiable disease. However, in a Ministry of Health initiative in 2000, a complex model developed by the National Centre in HIV Epidemiology and Clinical Research in Australia was applied to New Zealand, using local data on prevalence of IDU and HCV and accepted assumptions on disease progression. Using this model, there are currently 40,000 New Zealanders with either past or active hepatitis C infection and this number will exceed 50,000 by 2010, of whom almost 2000 will have cirrhosis. Already, chronic hepatitis C has overtaken CHB as the leading indication for liver transplantation – currently 8/22 adults listed.

Unlike HBV, there is no vaccine and the only means of prevention will be avoidance of high-risk behaviour through education and needle exchange. This was addressed in the 2002 Ministry of Health Action Plan for Hepatitis C Prevention.

However, even if such strategies significantly reduced the incidence of new infections, almost 20% of those currently infected (i.e. 8000) will progress to cirrhosis and complications thereof. This can only be prevented by successful antiviral therapy. Unfortunately, less than 5% have been treated, of whom more than half were not cured. There is therefore a great need to increase both the accessibility and the effectiveness of therapy.

Drug Treatments

The last 10 years has seen dramatic improvements in antiviral therapy for this condition, from 6% cure with 24 weeks standard interferon to 62% cure with combination pegylated interferon plus ribavirin. This combination was initially funded by PHARMAC in March 2001 in People infected with HCV Genotype 1. In June same year, funding was extended to Genotype non-1 with cirrhosis. In 2005, funding was extended to all people with haemophilia and in 2006 to all with HIV co-infection. Later this year, PHARMAC will consider a proposal to removal the only group of patients not funded – the non-cirrhotic non-1 genotype infections.
Retrospective analyses of the registration studies of both PegasysTM and PegintronTM have identified early positive and negative predictors of response. Early virologic response (EVR), defined as reduction in HCV RNA after 12 weeks therapy to PCR nondetectability or at least 2-logs from baseline has a negative predictive value of 99%. Therefore, lack of EVR is an accepted early stopping rule after 12 weeks therapy, reducing the morbidity associated with a further 36 weeks therapy and increasing the cost-effectiveness of treatment. Lack of EVR is an accepted early stopping rule in the latest published AASLD and APASL guidelines for the management of chronic hepatitis C. The Hepatitis subcommittee have proposed that the 12 week stopping rule is made mandatory in patients who do not achieve EVR. PHARMAC are currently considering this proposal.

More recent studies have defined two other types of responses in HCV Genotype 1 patients: “rapid virologic response” (RVR) is defined as PCR nondetectability after only 4 weeks therapy and “slow (or partial) response” defined as 2 log reduction but still PCR positive after 12 weeks. RVR accurately identifies “super-responders” who need only 24 weeks of therapy rather than the standard 48 weeks (SVR=90% with both 24 and 48 weeks therapy). In contrast, “slow responders” may benefit from prolongation of antiviral therapy for an additional 24 weeks (i.e. 72 weeks total). Adoption of both new rules - treatment shortened to 24 weeks for rapid responders and extended to 72 weeks for slow responders - would increase overall SVR by almost 5% in HCV Genotype 1 patients, without any increase in cost. The Hepatitis subcommittee will propose that PHARMAC considers implementing this.

Current Treatment Trials:

Unfortunately, combination pegylated interferon plus ribavirin has limited efficacy in Genotype 1 and previous nonresponders. In addition, many patients will either not tolerate or decline therapy because of associated side-effects.  These limitations of current therapy together have encouraged research into direct molecular antiviral agents.  There are now more than 20 oral agents in the HCV pipeline, including nucleoside analogue polymerase inhibitors, non-nucleoside polymerase inhibitors and protease inhibitors. Phase I and II trials of several of these are being conducted in the new Auckland Clinical Studies unit (ACS) and it’s sister unit in Christchurch(CCST). Later this year, ACS is performing the first triple therapy study, combining polymerase inhibitor, pegylated interferon plus ribavirin. A similar study with a different agent is planned for early 2008. It is hoped that this strategy will significantly increase both RVR and SVR in Genotype 1 infection.

Patient Compensation

In December 2006, the Ministry of Health announced a $30 million dollar package, to compensate an estimated 550 patients who developed chronic hepatitis C infection following transfusion (see

Improved Treatment Access

The Ministry has also commissioned the Hepatitis C Treatment Advisory Group, which includes both clinicians who treat hepatitis C (a gastroenterologist, hepatologist and ID physician) and also patient advocates and general practitioners. Their brief is to identify and target the real and perceived barriers to antiviral treatment for New Zealanders with hepatitis C and to devise strategies to improve access to treatment. The stocktake completed by all DHBs earlier this year identified specific areas of concern, including the lack of resource to staff hepatitis clinics. Possible initiatives include nurse-led hospital assessment clinics and shared-care community-based treatment. Both initiatives are well established in most states of Australia.
The first pilot Shared Care programme has commenced at Auckland Hospital, involving 50 patients in 4 practices – 2 in central city and 2 on Waiheke Island.

Finally, the Medical Council is in the process of redrafting the Health Regulatory Authorities of New Zealand (HRANZ) policy on transmissible major viral infections (TMVI) – i.e. HBV, HCV, HIV. These changes will reflect advances in understanding of risks for infectivity, and availability of better virologic assays and also ability to suppress viruses to very low levels associated with reduced infectivity. A national expert panel will be appointed to include physicians experienced in management of HIV, HBV and HCV.

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