Hepatitis A, B

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INFECTIVE VIRAL HEPATITIS

SNEHA S R
Liver may be subjected to a number of different
infections.
Viral hepatitis must be considered in anyone
presenting with hepatitic liver blood tests(high
transaminases).
CAUSES OF VIRAL HEPATITIS

1.More common:Hepatitis A,B,C,D and E


2.Less common:Cytomegalovirus and Epstein
barrr virus
3.Rare:Herpes simplex and yellow fever.
HEPATITIS A
The hepatitis A virus belongs to picorna group of
enteroviruses.
Highly infectious and is spread by Feco-oral route
Risk of infection is associated with a lack of safe water
and poor sanitation.
Infection may be asymptomatic or produce symptoms
after an incubation period of 28 days
Development of symptom is related to age
Infected individuals excrete the virus in faeces or about
2-3 weeks before the onset of symptoms and then for a
further week or so.
INVESTIGATIONS
Diagonosis based on Antibody testing.
Only one HAV antigen is found and infected people
make an antibody to this antigen(anti-HAV)
Anti-HAV immunoglobulin M antibody is detectable
in the blood 5-10 days before the onset of
symptoms and falls to low levels within 3 months
of recovery.SO it is the diagnostic of acute HAV
infection.
Anti-HAV IgG antibody persists for years after
infection,and is a marker of previous HAV infection.
MANAGEMENT
Infection prevented by improving social
conditions,especially over crowding and poor
sanitation.
Individuals can be protected from infection by
active immunisation with an inactivated virus
vaccine.
Immunisation should be given to people at
high risk like people travelling to endemic
areas,Close contacts of HAV infected patients
etc,those with major liver disease and
Immediate protection can be provided by immune serum
globulin if this is given soon after exposure to the virus.
Intra muscular injection of immune serum globulin is
recommended for close contacts of infected individuals
who are less able to respond to vaccination such as
immunocompromised,>60yrs of age.
It is also effective in a hepatitis outbreak,in a school or
nursery as injection to those at risk prevents spread to
families.
NO ROLE FOR ANTIVIRAL DRUGS IN THERAPY OF HEP A
INFECTION
HEPATITIS B
Conists of a core containing DNA and a DNA
polymerase enzyme needed for virus
replication,surrounded by surface protein.
The virus and an excess of its surface protein
(HBSAg)circulate in the blood.
The virus replicates and assembles with in
hepatocytes.but not cytotoxic.
Hepatocyte damage occurs during immune
medited clearance of infected hepatocytes.
HBV is one of the most common cause of CLD and
hepatocellular carcinoma worldwide.
HEPATITIS B CAUSES ACUTE OR CHRONIC INFECTION
Risk of developing chronic HBV infection depends on
the source and timing of exposure.
Most common cause of chronic infection:Vertical
transmission from mother to child in perinatal period.
Exposure to HBV at older age leads to acute infection.
Chronic hepatitis can lead to cirrhosis or
hepatocellular carcinoma.
CAUSES
INVESTIGATIONS
Assesment of HBV relies on looking at a
combination of viral markers(surface
antigen,e antigen and viral load) and liver
markers (ALT and fibrosis markers)to
determine stage of the disease.
HBV contains several antigen to which the
infected person can make immune response.
These antigens and their antibodies are
important in identifying the stage of disease.
Direct assessment of viral load by PCR for
HEPATITIS B SURFACE ANTIGEN
Main indicator of active infection
Negative test makes infection very unlikely.
Antibody to HBSAg(Anti HBs) usually appears
after about 3-6 months and persists for many
months and perhaps permanently
Anti-HBs implies either a previous infection in
which antiHBc also present or previous
vaccination in which case anti-HBC not
present.
HEPATITIS B CORE ANTIGEN
HBcAg is not found in the blood,but anti body
to it (anti-HBc) appears early in illness rapidly
reaches a high titre ,which gradually subside
and then persists.
Anti-HBc is initially of igM type ,with IgG
antibody appearing later.
HEPATITIS B e ANTIGEN
Is a part of the core antigen and is detectable in
blood.
Indicator of viral replication
Loss of HBeAg and development of anti Hbe
antibody indicates a partial immune control over
the virus and is associated with a signicant drop
in viral load.
Occurs 10-30 years later in perinatally acquired
infections but within 3-6 months in adult
acquired acute infections.
PHASES OF CHRONIC HBV
INFECTION
INTERPRETATION OF
SEROLOGICAL TEST
MANAGEMENT
Management of acute hepatitis
Full spontaneous recovery occurs in more than 95% of
adults following acute HBV infection.
Fulminant liver failure occurs in less than 1 %of cases
but can be life threatening and requires liver
transplantation.
Antiviral therapy is considered only in those with
severe liver injury or a course with persistent
symptom for>4 weeks.
Recovery occurs with in 6 months and is characterised
by the appearance of antibody to viral antigens.
MANAGEMENT OF CHRONIC HEPATITIS B
Treatment aimed at supressing viral
replication to prevent disease progression to
cirrhosis and hepatocellular carcinoma.
Goals include HBeAg
seroconversion,reduction in HBV-DNA and
normalisation of the LFT.
Two different type drugs are used to treat
hepatitis B.:direct acting
nucleoside/nucleotide analogues and
DIRECT ACTING NUCLEOSIDE/NUCLEOTIDE
ANALOGUES
Main stay of therapy
Orally administered.
They inhibit the reverse transcription of pre
genomic RNA to HBV DNA by DNA
polymerase
DRUGS:Lamivudine,entecavir,tenofovir.
LAMIVUDINE
Long term therapy is complicated by
development of HBV DNA polymerase
mutants which leads to viral resistance.
This agent is not commonly used now a days
but may be used prevent reactivation in
patients with past HBV infection.
Entecavir and tenofovir
More effective than lamivudine
Antiviral resistance mutations occur very
rarely
Both drugs have action against HIV virus ,so
their use as monotherapy is contraindicated
in HIV positive patients as it may lead to HIV
antiviral drug resistance
Other management methods
Pegylated interferon α
Pegylated interferon α acts by augmenting the
host immune response. This is most effective
in patients with a pre-treatment low viral load
and serum transaminases greater than twice
the upper limit of normal.

liver transplantation:Done in patients with


advanced liver disease or HCC
PREVENTION
A recombinant hepatitis B vaccine containing HBsAg is
available(Engerix) and is capable of producing active
immunisation in 95% of normal individuals.
The vaccine should be offered to those at increased risk

of infection who are not already immune, as evidenced by


anti-HBs in the blood.
The vaccine is ineffective in those already infected by HBV.
 Following known exposure, infection can also be
prevented or minimised by the intramuscular injection of
specific hepatitis B immunoglobulin (HBIg) prepared from
blood containing anti-HBs.
This should be given within 48 hours, or at
most a week, of exposure to infected blood.
Neonates born to hepatitis B-infected
mothers should be immunised at birth and
given immunoglobulin. Hepatitis B serology
should then be checked at 12 months of age.
Thank you

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