|Prof Bob Batey
Robert Batey, Trained as a Hepatologist and Addiction Medicine specialist and has worked in Sydney, Newcastle and the UK over the 44 years of his career. In the last 11 years he has also regularly visited Alice Springs Hospital where he has been providing services for patients with hepatitis C and B. For 5 years he has also covered one of the medical teams on the wards of the hospital for 3-4 months of each year. He continues a research interest in drug dependence, alcohol related organ damage and alternative medicines in liver pathophysiology.
Hepatitis B and C Update.
Staff Specialist Physician, Hepatologist and Addiction Medicine Specialist; Alice Springs (NT) and John Hunter (NSW) Hospitals.
Hepatitis B (identified in 1964) and hepatitis C (identified in 1989) are now viruses under threat of eradication! Greatly improved understanding of viral biology, the introduction of a vaccine for HBV and drug therapy for both viruses is changing both epidemics but more than 500 million people are still infected with one or other virus
A DNA virus, 8 genotypes with genotype C4 being unique to our Australian Indigenous people. Genotypes do influence disease progression, HCC risk and treatment responsiveness.
Increased educational input to health care workers has ensured better diagnosis and classification of HBV infection in recent years but many patients are still ill- or under- informed about their disease status. Effective vaccination programs have reduced mother to child (MTC) transmission >90% and protected millions from infection. Protection may not be life-long for a small minority.
Treatment for HBV.
Cost and clinical concerns mean the vast majority of people who could benefit from the current drugs, tenofovir and entecavir, do not receive them. Current oral drugs lead to HBs Ag clearance in only 5% or so of the treated population and most need lifelong therapy at this stage. Peg interferon remains an approved agent and recent work combining it with an oral agent suggest HBsAg clearance is achievable in up to 10% but most patients refuse interferon.
New agents providing much higher HBsAg clearance will mean finite treatment courses allowing attention to be focussed on achieving effective treatment uptake and adherence as has been the case in HCV.
HBV and pregnancy
Tenofovir has changed the outlook for pregnant mothers with high HBV loads and thus higher risk of MTC transmission. The use of tenofovir in the third trimester in mothers with HBV viral load > 107 IU/ml reduces this risk significantly and this is now accepted best practice. Cessation of maternal tenofovir is controversial.
On 1/3/2016 new, more effective and safer antiviral agents for our HCV infected patients became available in Australia. In the 4 months to writing this summary approx. 20,000 people have commenced these new treatments (annualised to 60,000 minimum) compared to an average of 3000 per annum nationally for the last several years. Treatment courses range from 8 to 24 weeks and treatment is moving away from specialised liver units for many patients and into primary care.
Viral genotype (1-6) still directs treatment choice but soon pan-genotypic, highly efficacious agents will be available.
HCV and pregnancy.
MTC transmission is far less a risk with HCV compared to HBV. Approx. 3-5% of babies will be infected at delivery or as neonates. There are no strategies such as we have for HBV in the case of HCV. All babies will have HCV Ab for up to 18 months, presumed representing maternal Ab. HCV RNA can be tested for at 3-6 months and if positive indicates transmission.