Hepatitis B is a viral infection that affects the liver and is transmitted through contact with infected blood or body fluids. It remains a major global health problem, with over 250 million chronic carriers worldwide. In Nigeria, the prevalence of hepatitis B is high, with an estimated 19 million people currently infected. Mother-to-child transmission during birth is the most common mode of infection in highly endemic areas like Nigeria. While most adults clear the virus, chronic infection develops in the majority of those infected as newborns or children. This puts them at risk of developing serious liver conditions like cirrhosis or liver cancer later in life. Vaccination and antiviral treatment can help prevent or manage the infection.

1. HEPATITIS B
Dr. Situ Oladele
South Atlantic Petroleum Medical
Centre, Nasarawa State University,
Keffi, Nasarawa State, Nigeria

2. WORLD HEPATITIS DAY
July 28

3. INTRODUCTION
• Viral hepatitis refers to a group of inflammatory
diseases of the liver caused by viruses that have
affinity for the liver.
• Clinically relevant ones are typed A, B, C, D and E.
Hepatitis B and C are the most clinically important
ones.
• DNA hepadnavirus (retrovirus). 3.2 kilobase pairs
virus discovered in 1965 however it was first seen
in 1970.
• HBV is 50 -100 times more infectious than HIV

4. EPIDEMIOLOGY: WORLD

5. EPIDEMIOLOGY
• HBV affects about 2 billion (about 1/3 world
population) worldwide (past or present infections)
and of those affected, 600,000 die annually.
• About 300-350 million are lifelong carriers
worldwide
• Low prevalence areas (0.1-2%): New Zealand,
Australia, USA, Canada and Western Europe.
• Intermediate prevalent areas (3-5%) Japan,
Middle East, Latin and South America, central Asia
• high prevalence areas (10-20%) China, Indonesia,
Pacific Islands, south East Asia, sub-Saharan Africa

6. EPIDEMIOLOGY: NIGERIA

7. EPIDEMIOLOGY: NIGERIA
• 70% of population showing evidence of past
infection.
• 7.3-24% (average 13.7%) of the population
has serological evidence of current
infection.
• Going by the 2006 national census, 19
million Nigerians are currently infected and
about 5 million of these are expected to die
as a consequence of the disease.

8. MODES OF INFECTION:
• Perinatal (high prevalence area),
• early childhood household contact,
• unsafe injections (intermediate and high
prevalence areas),
• blood transfusion,
• sex (low, intermediate and high prevalence
areas).
Sex is the overall most common
mode.

9. Concentration of HBV
in Various Body Fluids
HIGH MODERATE LOW/UNDETECTABLE
Blood semen Urine
Serum Vaginal secretions Faeces
Wound exudates saliva Sweat
Tears
breast milk

10. NATURAL HISTORY AND RISK OF
CHRONICITY
• The virus can survive at least 7 days (up to
15yrs at 20oC) outside human body
• The incubation period is 90 days (30-180
days). Virus becomes detectable 30-60
days post infection
• Up to 90-95% of adults recover fully
within 6 months of infection.
• Infected Infants: have a 70-90% risk of
chronicity
• Childhood infections (1-4years) have a
30-50% risk of chronicity.

11. NATURAL HISTORY AND RISK OF
CHRONICITY
• Estimated 10-30% of patients are expected
to progresses to cirrhosis without treatment.
25% of adult who were chronically
infected from childhood die from HBV
cancer or cirrhosis.
• Adults and adolescent have a 1-3% risk of
chronicity.
• Elderly individuals have about 25% risk of
chronicity and only about 0.1-0.5% of adults
have fulminant hepatic failure

12. • Relative Risk of Chronic hepatitis B for
Hepatocellular carcinoma (HCC) is
100 and 10 year risk of HCC may be
as high as 15%
• Hepatocellular carcinoma usually 25-
30years after initial HBV

13. Acute Hepatitis B Virus Infection
Typical Serologic Course
Symptoms
HBeAg anti-HBe
Total anti-HBc
Titer
IgM anti-HBc
HBsAg anti-HBs
0 4 8 12 16 20 24 28 32 36 52 100
Weeks after Exposure

14. Chronic Hepatitis B Virus Infection
Typical Serologic Course
Acute Chronic
(6 (Years)
months) HBeAg anti-HBe
HBsAg
Total anti-HBc
IgM anti-HBc
0 4 8 12 16 20 24 28 32 36
52
Weeks after Exposure

15. OUTCOMES
Infection
Symptomatic
Asymptomatic acute hepatitis
B
95% 95%
Resolved Chronic Resolved Chronic
Immune infection Immune infection
Cirrhosis Cirrhosis
Asymptomatic Asymptomatic
Liver cancer Liver cancer

16. OUTCOMES
• Improvement and Resolution
• Fulminant Hepatic Failure
• Chronic Hepatitis
• Cirrhosis
• Hepatocellular Carcinoma

17. OUTCOME BY AGE OF INFECTION
100 100
80 80
60 Chronic Infection
60
40 40
20 20
Symptomatic Infection
0 0

18. SYMPTOMS
• Hyperacute: hepatic encephalopathy
• Acute(nonspecific symptoms): anorexia, nausea,
vomiting, low grade fever, myalgia, fatigability,
aversion for food and cigar, dark coloured urine.
• Sub-acute: gynaecomastia, hair changes,
testicular atrophy.
• Chronic: peripheral stigmata of chronic liver
disease
• Reactivation of chronic hepatitis: mixed
symptoms
JAUNDICE
• Starts 10days post onset of constitutional
nonspecific symptoms. Lasts 1-3months

19. DIAGNOSIS AND LIVER DISEASE
STAGING
Phase one:
• Liver function tests (ALT, AST, ALP, PT,
Total protein and Albumin) and viral markers
of possible hepatotoxic viruses (HDV, HEV,
HAV, HIV)
• Full blood count and platelets & Urinalysis
• Hepatic ultrasound and other liver imaging
techniques
Phase two:
• Molecular biology: HBV DNA
• Liver biopsy and staging:

20. HBsAg Anti Anti Interpretation of Results
HBs HBe
+ve -ve -ve Characteristic of early acute HBV
infection
+ve +ve/-ve +ve Implies either acute or chronic HBV
infection which may be differentiated
with respect to IgM anti HBc
-ve +ve +ve Characteristic of previous HBV
infection and current immunity to the
virus
-ve -ve +ve No clear interpretation
Could be due past HBV infection
Low level of HBV infection
False +ve /non specific reaction
-ve -ve -ve Suggests liver toxicity due to other
agents other than HBV
-ve +ve -ve Typical of vaccinated individual

21. OTHER TESTS
• Thyroid function test
• Body mass index
• Fasting blood sugar and insulin assay
for resistance
• Neropsychiatric evaluation
• Alcohol and drug abuse evaluation

22. CLINICAL STATES
• Acute,
• Sub-acute,
• Chronic active,
• Chronic asymptomatic carrier state
• Decompensated end-stage liver
disease

23. WHO TO SCREEN?

24. WHO TO SCREEN?
• All Nigerians HBsAg and HBcAg are used for
sreening:
• every new visit to the clinic,
• pre-school, pre-employment, pre-insurance,
• pre-blood donation,
• pre-marriage and pregnancy,
• sexual history, STI,
• illegal drug users,
• healthcare workers, morgue works,
• chronic alcoholics,

25. WHO TO SCREEN?
• Children or spouses of HBsAg positive
individuals
• All HIV positive patients
• Cirrhosis patients or nodular liver or big liver
• Jaundiced patients especially after blood
transfusion
• Patients with bleeding problems especially if
it started after blood transfusion.
• Chronic Renal Failure patients especially
after haemodialysis.

26. TREATMENTS
• Generally, there is no specific treatment for
HBV infection. Comfort, nutritional balance,
avoidance of hepatotoxic drugs, etc., are
essential.
• HBV drugs are expensive and not readily
available
• Chronically infected people respond less
and patient with significant cirrhosis respond
less with increased chance for serious side
effects.

27. DRUGS
• pegylated IFN,
• lamivudine,
• telbivudine,
• adefovi,
• entecavir,
• tenofovir.

28. INTERFERONS IFN (PEGYLATED)
• IFN is given as S/C injection, 180mcg
weekly for 4months (up to 12months in
patients with high viral loads and patients
with negative HBeAG). 30-40% on treated
patients sustained suppression of HBV.
Some will also lose their HBsAg.
• There yet no known resistance to the drug
• Marketed as PEGASYS®
• Avoid in advanced stage (decompensated
disease)

29. LAMIVUDINE
– Use when PEGASYS is not available or
affordable
– Taken as Tab 100mg daily and is well
tolerated orally
– Can be used in decompensated patients
DISADVANTAGE
– High rate of drug resistance (15-30% in 1yr,
50% in 3yrs, 70% in 5yrs).
– Infinite duration of treatment (cannot stop
until at least 1yr after HBeAg seroconversion
occurs)

30. DIETARY LIMITATIONS

31. DIETARY LIMITATIONS
• Patients with acute or chronic HBV infection
without cirrhosis have NO dietary
restrictions.
• For individuals with decompensated
cirrhosis (portal hypertension,
encephalopathy), a low sodium/salt diet
(1.5gm/d), high protein diet (i.e. white meat
like pork, turkey, fish), and, in cases of
hyponatremia, fluid restriction (1.5L/d) are
indicated.

32. WHY TREAT THE HBV PATIENT?
• To limit active liver disease and prevent liver
disease progression to cirrhosis, liver failure
or cancer
• To prevent transmission of HBV infection
• To improve quality of life
• To limit active viral replication and achieve
sustained virological response

33. GENERAL INDICATIONS FOR
TREATMENT/MANAGEMENT
Chronic HBeAg Chronic HBeAg
positive patients negative patients
HBV DNA >20,000 I.U/ml (105 HBV DNA >2000 I.U/ml (104
copies/ml and when ALT is ↑ for copies/ml and when ALT is
3-6months ↑(>20 U/L in females; 30 U/L in
males ) for 3-6months
All patients with histologic All patients with histologic
evidence of active liver evidence of active liver
disease/inflammation disease/inflammation

34. PREVENSION AND VACCINE:
• HBV vaccine has been available since 1982 and is
about 95% effective. In 1992 31 countries have
HBV vaccination schedule. In 2011, the number
has increased to 179 countries.
• protects for 5-10 yrs. Use HB Ig for sudden
needle pricks.
 Rate of HBV transmission after an occupationally
related needle stick injury is 30% in unvaccinated
health worker (unlike 0.3 % in HIV, 3% in HCV
infection)

35. PREVENSION AND VACCINE:
• Take at birth, 6weeks and 10 weeks of life
• Uninfected and unvaccinated adults will take
3 subcutanous injections at intervals
unmissed or would start again.
• A booster dose in 10yrs

36. PATIENT MORNITORING AND
EVALUATION
• FBC: every 4-8 weeks
• ALT (LFT): every 4-8weeks
• HBV DNA: at 12, 24 and 48 weeks
• HBeAg and anti-HBeAg: every 6months till
seroconversion
• Liver histology: NOT CURRENTLY
RECOMMENDED FOR ROUTINE
MONITORING

37. TREATMENT RESPONSE
• Primary response: ↓ viral load more than 10 folds
after 12 weeks of treatment.
• Primary non-response: ↓ viral load less than 10
folds after 12 weeks of treatment.
• Complete response: undetectable viral load after
24 weeks of treatment
• Partial response: detectable but ↓ viral load
<10,000copies/ml after 24 weeks of treatment
• Inadequate response: detectable but ↓ viral load
>10,000copies/ml after 24 weeks of treatment
• Sustained virological response (Virological
breakthrough): undetectable virus for >6months
• Treatment failure

38. CONTRAINDCATION TO
TREATMENT
• Pregnancy*
• continued alcohol abuse
• sever cardiac disease
• uncontrolled psychiatric illness
• uncontrolled seizure disorder
• untreated thyroid disorder

39. DRUD SIDE EFFECTS
• flu-like syndrome
• fatigue, weight loss, anorexia, diarrhoea, alopecia
• haematological derangements: ↓PCV, ↓WBC,
↓platelets, ↓neutrophils
• neuropsychiatric disorders: mood swings,
depression, suicidal ideation, insomnia, psychosis
• metabolic abnormalities: diabetes, thyroid disorders
• lung complications: pneumonitis, pneumonia
• dermatological problems: rashes
• eye complications: retinal vessels occlusion, retinal
hemorrhages

40. SPECIAL CATEGORIES

41. SPECIAL CATEGORIES
• Pregnancy and newborns: Those born to
mothers with active HBV infection must be
vaccinated with HBIG within 12hrs of birth
and the vaccinated with HBV vaccine
• HIV/HBV co-infection: both diseases must
be treated together. Tenofovir +
emtricitabine (Truvada®)/Lamivudine with a
NNRTI or PI is preferred.
• Diabetes: current guideline recommends
that all patients with diabetes (type 1 or 2)
from 19-59 yrs should be vaccinated with
HBV vaccine.

42. OTHER SIDE EFFECTS OF HBV
INFECTION
• Pleural effusion, hepatopulmonary and
portopulmonary syndrome may occure in patients
with cirrhosis
• Myocarditis and pericarditis and arrhythmias may
occur primarily in patients with fulminant hepatitis
• DIC may occur in patients with fulminant hepatitis.
• Athralgias and arthritis (serum sickness) with
subcutaneous nodules may occur, but are very rare
• Encephalitis, aseptic meningitis, Guillain-Barre
syndrome and mononeuritis complex may occur in
patients with acute hepatitis B

43. OTHER SIDE EFFECTS OF HBV
INFECTION
• Aplastic anaemia is uncommon and
agranulocytosis is very rare
• Pancreatitis
• Chronic renal failure
• Polyarteritis nodosa
• Fleeting rash and hives (common in women)
• Popular acrodermatitis may be seen in acute
infection in children (Gianotti-Crosti syndrome)

44. THANK YOU