BY DR AFTAB

MODERATOR DR ROHIT CK
 Hepatitis B is an infectious disease caused by
the hepatitis B virus

 It’s a major public health problem , causing

chronic hepatitis, cirrhosis of liver and HCC.

 It’s a member of the HEPADNAVIRUS family.

 HCV - small , positive stranded RNA-
enveloped virus.

 Highly variable genome - classified into six

distinct genotypic groups .

 Genotype 1 - most common (46.2% of all HCV

infections), followed by genotype 3 (30.1%)
 PERCUTANEOUS – Exposure to infectious
blood or body fluids (50 to 100 times more
infectious than HIV).
 PERINATAL- Without intervention, HBsAg +ve
mother has 20% risk of passing the infection
to her offspring at the time of birth. This risk
is as high as 90% if the mother is positive for
HBsAg.
 SEXUAL
 BREAST FEEDING
 HIGH –blood , serum , wound exudates .

 MODERATE-semen, vaginal fluid , saliva .

 LOW-urine , faeces, sweat, tears and breast

milk.
 Assessment can be done by using

1) HBV markers - a) HBsAg

b) HBeAg/anti-Hbe
c)HBV DNA

2) Liver disease – a) Biochemical parameters:

ALT
b) fibrosis markers
non invasive or
liver biopsy (in selected
cases)
 The serum aminotransferases- aspartate
aminotransferase(AST) and alanine
aminotransferase(ALT) increase to a variable
degree during the prodromal phase of acute
viral hepatitis and precede the rise in bilirubin
levels.
 N.B - level of enzymes elevation doesn’t
correlate well with the degree of liver damage
.
 Prothrombin time (PT) measurement is
important in patient with acute viral hepatitis:

 Prolonged value:

 may reflect a severe hepatic synthetic defect

 signify extensive hepatocellular necrosis and
 indicate a worse prognosis.
 Serum bilirubin, ALT and gamma globulin are
only moderately increased.

 Serum albumin is usually normal.

 At time of presentation , feature of hepato-

cellular disease are usually mild.
 Virus–specific antibodies, which appear
during and after hepatitis virus infection, are
both diagnostic and treatment wise very
important.
 Appears in the blood about 6 weeks after
infection
 Usually disappears by 3 months after the
clinical illness.
 Persistence for more than 6 months -
development of a carrier state or progression
to chronicity.
 Inverse correlation - between the serum
concentration of HBsAg and degree of liver
cell damage .
 For example – titres are highest in
immunosuppressed patients, lower in
patients with chronic liver disease, and very
low in patient with fulminant hepatitis .

 This shows that, in hep B , the degree of liver

damage and the clinical course are related to
variations in the patient’s immune response
to HBV rather than to the amount of
circulating HBsAg .
 Correlates with ongoing viral synthesis and with
infectivity.

 Transiently present during the acute attack.

 Persistence for more than 10 weeks strongly

suggests the development of chronicity.

 Its principal clinical usefulness is as an indicator

of relative infectivity.

 Used in selecting the patient for therapy.

 Prognostic for resolution of infection.

 The appearance of anti- Hbe is strong

evidence that the patient will recover
completely .
 HBV DNA is the most sensitive index of viral
replication.
 Serum marker for fibrosis:

 APRI
 FIB-4
 FIBROSCAN

 Performed to rule out advanced fibrosis

 To know the degree of necro-inflammation
and fibrosis

 To help guide the decision to treat.

 Hepatic histology varies widely and includes

chronic hepatitis , cirrhosis and HCC.
 Pegylated Interferon

 Lamivudine

 Adefovir

 Entecavir

 Telbivudine

 Tenofovir
 Route of administration- subcutaneous injection

 180mcg weekly

 Duration of therapy- 48 to 52 week

 S/E-Flu‐like symptoms, fatigue, mood

disturbances, cytopenia, autoimmune disorders
in adults
 Route of administration- oral

 100mg daily

 Duration of treatment - >52 week

 S/E- Pancreatitis, Lactic acidosis

 Route of administration- oral

 10mg daily

 Duration- >48 week

 S/E- Acute renal failure, Lactic acidosis.

 Route of administration- oral

 0.5mg daily

 Duration of therapy- >48 week

 S/E - Lactic acidosis.

 Route of administration- oral

 600mg daily

 Duration of treatment- >52 weeks

 S/E-Creatine kinase elevation and myopathy,

Peripheral neuropathy, Lactic acidosis
 Route of administration- oral

 Tenofovir dipovoxil fumarate300 mg daily or

 Tenofovir alafenamide25 mg daily

 Duration of therapy- >48 weeks

 A/E - Nephropathy, Osteomalacia, lactic acidosis.

 It consists of :

 Identification of high risk population.

 Screening of high risk population.

 Diagnosis

 Treatment
 All persons recommended for HCV screening
should initially be tested for HCV antibody
using an assay approved by the US Food and
Drug Administration (FDA).

 Examples -Abbott HCV EIA 2.0

Advia Centaur HCV
 Serum anti HCV Antibodies – 99% sensitivity and
specificity.

 Serum HCV RNA –

for confirmation of diagnosis
for viral load
for monitoring response to
therapy
 ALT – non specific

 Liver biopsy- for cirrhosis and prognosis.

 Evaluation for advanced fibrosis:
 liver biopsy
is recommended for all
 imaging, and/or persons with HCV infection,
 noninvasive markers
 It helps in making decision regarding HCV
treatment strategy and
 To determine the need for initiating
additional measures for the management of
cirrhosis (eg, hepatocellular carcinoma
screening)
 In acute infection-
 Treatment can be delayed for 8 to 12 weeks
for assess for spontaneous resolution.

 PEG-INF ALFA based therapy for 12 to 24

weeks

 Ribavirin may be added .

 Detected HCV RNA ( with or without elevated
ALT)

 On biopsy/non invasive modality - moderate

to severe inflamation/ necrosis.

 No contraindications to therapy.
 Genotype 1-
1. PEG IFN alfa 2a 180mcg/week plus a daily
dose of 1000mg ribavirin for 48 weeks. (
when weight is less then 75kg)

2. PEG alfa 2b 1.5mcg/ week plus a daily dose

of 1200mg of ribavirin for 48weeks. ( when
weight is more than 75kg )
 Genotype 2 and 3 –
1. PEG IFN alfa 2a 180mcg/week OR alfa 2b of
1.5mcg/week PLUS 800mg of rabavirin for
24 weeks

 Genotype 4 –
Combination therapy with PEG IFN plus
Ribavirin for 48 weeks.
 - At week 12
I. Retest HCV RNA levels
if negative – continue for full 48
weeks
monitor for symptoms , blood
counts and ALT levels at 4 to 8
weeks interval.
if still positive – add a protease
inhibitor
 After therapy –

1. Assess ALT at 2 and 6 months.

2. Repeat HCV RNA , 6 month after stopping

treatment