Hepatitis B infection

Kenneth Kabagambe

Executive Director

The National Organization for People

Living with Hepatitis B (NOPLHB Uganda

General introduction: Viral

hepatitis in Uganda

• Viruses that affect the liver

• Commonly hepatitis A, B, C, D and E

• Rarely other viruses

Hepatitis A• Transmitted through eating or

drinking food contaminated by stool.

• Hepatitis A common in developing

countries

• 2/3 of children infected by 5 years of

age

• Mainly does not make them ill

• They become protected for life

Hepatitis A

• In developed countries, HAV occurs in outbreaks– Contaminated salads, raw seafoods

– Travels to developing countries

• Causes sickness like sore throat, fever, fatigue

• Rarely may cause severe liver disease (liver failure)

• Prevention– Good hygiene and sanitation practices

– vaccine

Hepatitis E

• Acquired through contaminated food & drinks

• In developing countries it occurs in outbreaks– e.g Kitgum (2007), outbreak in Napak 2013-2014

• Mainly causes mild disease

• More deaths among pregnant women

• Prevention– Hygiene

– No readily available vaccine

Hepatitis C• Transmitted through

IV drug use,

Sexual transmission

Tattooing and body piercing

blood transfusion before 1990

• In Uganda – at 3% across studies

• Causes liver scarring and its

complications

• No vaccine

Hepatitis D

• Only infects in the presence of

hepatitis B.

• The two viruses together cause more

severe disease

• Vaccination against HBV protects

against HDV

Hepatitis B virus

• DNA virus in the hepadnaviridae

family

• Partially double stranded DNA

• Affects Humans

Hepatitis B infection:

epidemiology

• Global health problem

• 2 billion persons with evidence of past or current infection

• 400 million have chronic HBV infection worldwide

• Major cause of morbidity and mortality

World Health Organization, 2002. 2. Lok AS et al. Gastroenterology. 2001;120:1828-53. 3. Lee W. N Engl J Med. 1997;337:1733-45.

4. Poterucha JJ. Ann Intern Med. 1997;126:805-07. 5. Moyer LA, Mast EE. Am J Prev Med. 1994;10(suppl):45-55. 6. Stevens

CE et al. J Med Virol. 1979;3:237-41.

1. WHO. Hepatitis B. 2002. 2. Custer B, et al. J Clin Gastroenterol. 2004;38(10 suppl):S158. 3. WHO/WPRO data.

HBsAg Prevalence (%)1

>8: High

2–8: Intermediate <2: Low

Geographic Distribution of Chronic HBV Infection

Uganda

Bwogi et al. Afri Health Sci. 2005

Transmission of HBV

• Contact with infected blood

• Sexual contact with an infected person

• Sharing contaminated sharps including

tattooing

• Mother to child

• Blood transfusion (contaminated)

Transmission of HBV

• HBV NOT TRANSMITTED THROUGH:

Hugging

Sharing clothes, cups, plates, basins, or

toilets

Sitting close to an infected person

• Therefore NO NEED FOR ISOLATION

of infected persons

Who should be screened?

• Blood donors

• All persons with abnormal liver tests

• All HIV positive persons

• All most at risk persons- IVDU, MSM, sex workers

• Persons planning to take immunosuppressingtherapy

• All persons from endemic areas–Uganda 10%

Natural Progression of CHB

Adapted from: Fattovich, et al. Gastroenterology. 2004;127:S35-S50. Torresi, et al. Gastroenterology. 2000;118:S83-

S103. Fattovich, et al. Hepatology. 1995;21:77-82. Perrillo, et al. Hepatology. 2001;33:424-432.

Chronic Infection Cirrhosis

Liver Failure

Liver

Cancer (HCC)

Death30%

23% in 5 yr

Liver Transplantation

Acute flare

10%–15% in 5 yr

5%–10%

15%–40% of CHB patients may experience disease progression

Clinical features

• Majority asymptomatic

• Usually vague constitutional

symptoms

• Acute hepatitis- Jaundice, fever,

abdominal pain, encephalopathy

NAs: Potency versus resistance

Likelihood of resistance development

Po

ten

cy o

f HB

V D

NA

su

pp

ressio

n

LAM

LdTETVTDF

ADV

Nucleoside analogue

Nucleotide analogue

Primary Goal of Hepatitis B Therapy:

Preventing Cirrhosis, HCC, and Death

Durable Suppression of HBV Replication

Goals of HBV Therapy

• The clinical goal of HBV treatment Reduction in decompensation and HCC Reduction in mortality

Normalization of liver enzymes

If HBeAg positive - HBeAg loss and HBeAb

seroconversion

Suppression of HBV replication to

undetectable levels (<10-15 IU/mL)

Goal of cure (i.e negative HBsAg still very

difficult with current therapy)

Monitoring• Patients not on antiviral treatment

Monitor Disease progression every 3-6 months

• Patients on treatment

Adherence

Treatment response- ALT, viral load, HBeAg

loss, HBeAb seroconversion, ultimately HBsAg

loss

Drug toxicity

Decompensation in patients with advanced

fibrosis

Monitoring

• HCC screening

In patients with cirrhosis or advanced

fibrosis

Family history of HCC

Persons >30 years with high viral load

• Annual HIV screening if previously negative

Can Antiviral treatment be

stopped?

• Lifelong treatment in patients with cirrhosis or APRI

score >2

• May be discontinued in patients who start treatment

when HBeAg positive without cirrhosis

And HBeAg loss/HBeAb gain

And persistently normal ALT

And Who can be monitored closely

• When HBsAg becomes negative

• Treatment should be continued for at least one

additional year after attaining these endpoints

Prevention

• HBV is vaccine preventable disease

• HBV vaccine prevents development

of HCC

24

Hepatitis B Vaccines

Available since 1981

Composed of HBsAg

Elicits development of neutralizing antibodies

to HBsAg

Confers protection from infection

Plasma-derived and recombinant

formulations

Vaccination• Prevention of mother to child transmission

Exposed infants should get birth dose within 24

hours after birth

HBV immunoglobulin + HBV recombinant

vaccine at different sites

Followed by regular vaccination

Shown to reduce prevalence of HBV

• Antiviral therapy

Not recommended for routine mother to child

prevention

Childhood vaccination

• All children in areas of high endemicity

• In Uganda vaccine introduced in 2002

• Pentavalent with DPT

Schedule 6 weeks, 10 weeks, 14 weeks

Dose schedules

• Generally, 3 doses recommended

First Injection - At any given time

• Time 0

Second Injection - At least one month after the first dose

• 4 weeks

Third Injection - Six months after the first dose

• 6 months

28

Long-Term Protection with

Hepatitis B Vaccine

Vaccine provides long-term protection

Immunity persists despite loss of anti-HBs

Booster doses of hepatitis B vaccine NOT

currently recommended

Prevention• Vaccination of High risk groups

Health care workers

PWID

Sex workers

Close contacts of infected persons

• Standard infection prevention strategies for

HBV

Safe sex

Safe injection practices, etc

Way forward

• Increase awareness

• Update epidemiological data

• Scale up screening

• Avail facilities for further testing

• Access to vaccine

• Access to treatment

Summary• High prevalence of HBV in Uganda

• Chronicity of HBV depends on age of

acquisition

• Liver damage in HBV is largely due to

immune interaction than directly

• Early diagnosis through screening

• Treatment criteria should be used to select

treatment candidates

• HBV is a vaccine preventable disease