Hepatitis B & C - the Basics for Primary Care
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This presentation covers the basics in Hepatitis B & C, and is aimed at primary care physicians who may encounter such patients. It focuses mainly on the natural history, how to diagnose and monitor the disease, and when to refer to a specialist.
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Hepatitis B & C - the Basics for Primary Care
- 1. Hepatitis B & C The Basics for Primary Care Dr Jarrod Lee Mt Elizabeth Novena Hospital 1
- 5. Serological Markers • HBsAg: active infection • HBsAg + > 6months: chronic infection • HBeAg: high viral load, high infectivity • Anti HBe: low viral load, low infectivity • Anti HBc IgM: recent infection • Anti HBs: immunity • Anti HBc Total + HBsAg: chronic infection • Anti HBc Total + Anti HBs: resolved infection 5
- 7. Chronic HBV Infection HBV DNA HBeAg Anti-HBe HBsAg Anti-HBc Anti-HBc IgM Months Years
- 8. Immune tolerance < Immune clearance HBeAg + (wild) Immune control >< Immune escape HBeAg - / anti-HBe + > >105 cp/ml HBV-DNA <105 cp/ml 109-1010 cp/ml 107-108 cp/ml ALT Normal / mild CH Moderate/severe CH Cirrhosis HBeAg + Chronic hepatitis Normal/mild CH Moderate/severe CH Inactive cirrhosis Cirrhosis Inactive-carrier state HBeAg – Chronic hepatitis
- 9. Immuno Tolerance Phase • First 10-30 years of perinatally acquired infection • High DNA levels; normal ALT • Very low rates of spontaneous or treatment induced HBeAg seroconversion 9
- 10. Immune Clearance Phase • • • • HBeAg Anti HBe Seroconversion Annual rate: 5-15% High DNA levels High ALT • Hepatitis B Flares – ⅔ HBeAg seroconversion preceded by flares – ¼ flares followed by HBeAg seroconversion – Increased risk of cirrhosis 10
- 11. Inactive HBs Carrier State Immune Control Phase • HBeAg -, Anti HBe + • Low DNA levels; normal ALT • Subsequent outcome dependent on: – Damage accrued prior to entering inactive carrier state – Subsequent reactivation 11
- 12. HBeAg - Chronic Hepatitis B Immune Escape Phase • HBeAg -, Anti HBe + • High DNA levels; high ALT • Associated with pre core or core promoter mutations that prevent or decrease HBeAg production 12
- 13. Treatment • Goals – Suppress viral replication – Decrease hepatic inflammation and fibrosis – Prevent progression to cirrhosis and liver cancer • Who should be treated? – Not a question of who to treat but when to treat – All carriers are potential treatment candidates – Consider for patients in immune active phase • Need to identify patients in immune active phase! 13
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- 16. Hepatitis C 16
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- 19. Lab Tests 19
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- 22. Role of Primary Care Physician • Screening for Hepatitis B & C – At risk persons – Family members and sexual contacts of patients – Patients who require chronic steroid treatment • Initial evaluation and lab tests • Lifestyle advice – – – – Avoid transmission Avoid alcohol, herbal medications Balanced diet, exercise, healthy BMI Coffee 22
- 23. Role of Primary Care Physician • Vaccinate at risk persons for Hepatitis B • Hepatitis A vaccine if Anti HAV Total negative • Refer to specialist: – Immune active phase for treatment – Abnormal US liver or AFP for possible HCC – Evaluation of early fibrosis & cancer risk if > 40 years • Follow up of patients in immune tolerant and inactive carrier phases – HCC surveillance: 6 monthly AFP + US liver – LFT + HBV DNA every 3 – 6 months 23