Hepatitis B infection Kenneth Kabagambe Executive Director The National Organization for People Living with Hepatitis B (NOPLHB Uganda
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