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Hepatitis B & C
The Basics for Primary Care
Dr Jarrod Lee
Mt Elizabeth Novena Hospital
1
Hepatitis B

2
Natural History

3
Disease Progression

4
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
Acute HBV Infection
HBV
DNA
HBeAg

Anti-HBe
Anti-HBe
Anti-HBs
AntiHBc

HBsAg

0

Anti-HBc
IgM

2
Months

4

6
Years
Chronic HBV Infection
HBV DNA
HBeAg

Anti-HBe

HBsAg
Anti-HBc

Anti-HBc IgM

Months

Years
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
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
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
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
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
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
14
15
Hepatitis C

16
17
18
Lab Tests

19
20
21
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
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
Thank You
Questions?

24

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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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  • 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