Topic presentation of Chronic Hepatitis B & Hepatitis C

1. Chronic Hepatitis B & C
PRESENTATION ON
Presented By
Dr. Banaful Roy
Intern Doctor
Dr. Sirajul Islam Medical College & Hospital

2. What is Hepatitis?
Hepatitis is an inflammation of
the liver parenchyma. The condition
can be self-limiting or can progress
to fibrosis, cirrhosis or liver cancer.

3. Causes of Viral Hepatitis
❑Hepatotropic :
◦ Hepatitis A
◦ Hepatitis B ± Hepatitis D
◦ Hepatitis C
◦ Hepatitis E
❑Systemic:
◦ Cytomegalovirus
◦ Ebstein-Barr virus
◦ Herpes simplex
◦ Dengue virus
◦ Yellow Fever

4. According to the duration
Hepatitis can be divided into two
types-
1. Acute hepatitis
2. Chronic hepatitis

5. Acute Hepatitis
Acute infections may occur with limited or no
symptoms or may include symptoms such as-
◦ Jaundice
◦ Dark urine
◦ Extreme fatigue
◦ Nausea
◦ Vomiting
◦ Abdominal pain
Duration is less than 6 months.

6. Chronic Hepatitis
Chronic Hepatitis is the inflammation of the
liver that persists at least 6 months.
Common causes includes hepatitis B and C
virus and certain drugs.

7. Differences between Acute and Chronic
Hepatitis
Traits Acute Hepatitis Chronic Hepatitis
1. Duration Less than 6 months More than 6 months
2. Prodromal phase Present Absent
3. Causative agent Hepatotropic virus Hepatitis B, C and D viruses
4. Outcome
Spontaneous recovery
Chance of acute hepatic failure
Spontaneous recovery and may
develop liver cirrhosis &
hepatocellular carcinoma

8. Chronic Hepatitis B
Hepatitis B is the most common cause of chronic
liver disease and hepatocellular carcinoma
worldwide.
Properties of Hepatitis B Virus:
▪Partially double – stranded circular DND virus
▪Enveloped
▪42 nm
▪Hepadnavirus

10. Sources of Hepatitis B Infection and Risk of
Chronic Infection:
Vertical Transmission (90%)
⮚Hepatitis B surface antigen (HBsAg)- Positive mother
Horizontal Transmission (10%)
◦ Injection drug use
◦ Infected unscreened blood product
◦ Tattoos/Acupuncture needles.
◦ Sexual transmission

11. Investigations
1. Liver function tests:
●Serum bilirubin: High
●ALT (SGPT) & AST (SGOT): High
●Alkaline phosphatase; Slightly high
●Serum albumin level
●Prothrombin time
2. Viral markers:
●HBeAg, anti-HBeAg antibody
● HBsAg, anti-HBsAg antibody
● Anti-HBcAg antibody

12. 3. Viral Load:
HBV-DNA can be measured by
polymerase chain reaction (PCR) in the
blood.
4. Ultrasonogram of hepatobiliary system.
5. Liver biopsy

13. Hepatitis B Surface Antigen
➢ Hepatitis B surface antigen (HBsAg) is an
indicator of active infection.
➢ It can persist 3-4 weeks up to 5-6 months
➢ The persistence of HBsAg for longer than 6
months indicates chronic infection or chronic
carrier.
Antibody to HBsAg
➢ It usually appears after about 3-6 months and
persist for many years or perhaps permanently

14. Hepatitis B core antigen
Hepatitis B core antigen is not found in the blood but
antibody to it appears early in the illness and reach high
titre. Anti Hbc can sometime reveal an acute Hb infection
when the HBsAg has disappeared and before Anti HBs is
developed. This period is known as window period.
Hepatitis B eAg
HBeAg is an indicator of viral replication. The absence of
HBeAg usually implies low viral replication.
Chronic HBV infection is marked by the presence of
HBsAg and Anti Hbe is also present.
There is also exceptions such as HBeAg negative chronic
hepatitis B also called precore mutant infection in which
high level of viral replication, serum HBV-DNA and
hepatic necroinflammation are seen,despite negative
HBeAg.

15. The five phases of chronic hepatitis B virus (HBV)
infection:

16. Treatment
The goals of treatment are-
⮚HBeAg seroconversion
⮚Reduction in HBV-DNA and
⮚Normalisation of LFTs
Treatments are still limited, with no drug able to
eradicate hepatitis B infection completely.
The indication for treatment is a high
viral load in the presence of active
hepatitis, as demonstrated by elevated
serum transaminase and/or
histological evidence of inflammation.

17. Two different types of drugs are used
to treat Hepatitis B:
1. Direct acting nucleoside/nucleotide antiviral
agents-
Orally administered nucleoside/nucleotide antiviral
agents are the mainstay of therapy.
a) Lamivudine
b) Entecavir and tenofovir
2. Interferon alfa-
This is the most effective in patients with a low viral
load and serum transaminase greater than twice the
upper limit of normal in whom it acts by augmenting a
native immune response.

18. Liver transplantation
❑Usually contraindicated in HB patient due to graft
infection.
❑The use of post liver transplant prophylaxis with
direct acting antiviral agents and HB Ig reduce the
reinfection rate to 10% and increase 5 years
survival to 80%.

19. Prevention of HBV
infection
1. Recombinant hepatitis-B vaccine containing HBsAg
2. Intramuscular injection of hyperimmune serum
should be given within 24 hours of-
⮚Exposure to infected blood in circumstances likely to
cause infection (e.g. needle stick injury, contamination
of cuts or mucus membranes).
3. Neonates born to hepatitis B-infected mothers
should be immunized at birth and given
immunoglobulin.

20. 4. Other measures
⮚All blood donors should be screened for HBV infection
and blood positive HBsAg should be rejected.
⮚Adequate sterilization of all the surgical instruments.
⮚Use of barrier methods of contraceptives with an
infected patient.
⮚Not to share razors and tooth brushes.

21. CHRONIC HEPATITIS C
Properties:
• Small stranded RNA virus
• Enveloped
• 50-60 nm
• Probably a distant relative of the flavi
virus

22. Risk factors
●Intravenous drug misuse
●Unscreened blood products
●Vertical transmission
●Needlestick injury
●Iatrogenic parenteral transmission
●Sharing toothbrushes/razors

23. Clinical features
• May be asymptomatic.
• Mild, slowly progressive hepatitis
Investigations
1. Serology: Anti-HCV antibody
2. Virology: Hepatitis-C viral RNA
3. Molecular analysis: 6 common viral genotypes
4. Liver function tests
5. Liver biopsy and histopathology

24. Treatment
3. Liver transplantation
1. Supportive care
2. Drugs: Direct-acting antiviral agents for hepatitis C
Drug Class Therapeutic Target Selected Drus
Protease inhibitors
(Pls)
Non-structural viral protein
NS3/4A (protease that cleaves the HCV polyprotein)
Telaprevir
Boceprevir
Simeprevir
Paritaprevir
Grazoprevir
Nucleoside
polymerase
inhibitors (NPls)
Non-structural viral protein
NS5B (RNA-dependent RNA polymerase needed for
viral replication)
Sofosbuvir
Nucleoside
polymerase
inhibitors (NNPls)
Non-structural viral protein
NS5B (RNA-dependent RNA polymerase needed for
viral replication)
Dasabuvir
NS5A Replication
complex inhibitors
Non-structural viral protein
NS5A (assembly of viral replication complex)
Daclatasvir
Velpatasvir
Ledipasvir
Ombitasvir
Elbasvir
Host-targeting
antiviral drugs
(HTAs)
Cyclophilin (pharmacological inhibitor targets host
cell functions involved in the HCV life cycle)
Alisporivir
(HCV = hepatitis C virus)

25. Treatment outcome:
The aim of treatment is to eradicate the infection. In
recent years, there have been substantial advances, so
much so that rates of viral clearance achieved 6
months after finishing treatment ( termed sustained
virological response SVR) have risen from less than
40% a decade ago to levels approaching 100% with
some of the newer direct acting antivirals. The infection
is cured in more than 99% of patients who achieve an
SVR.

26. Complications
⮚Chronic hepatitis
⮚ Cirrhosis of liver
⮚ Hepatocellular carcinoma

27. Fig: Outcome of HBV & HCV Infection