Chronic hepatitis in children can be caused by viral infections like hepatitis B and C, autoimmune disorders, drug reactions, and metabolic diseases. Hepatitis B often becomes chronic if contracted as a newborn. It progresses through immune tolerant, immune active, and inactive carrier phases. Hepatitis C poses a high risk of chronicity in children. Autoimmune hepatitis involves liver inflammation from a misdirected immune response. Common drugs that can cause chronic liver injury include anti-tubercular and anticonvulsant medications. Metabolic diseases such as Wilson's disease and nonalcoholic steatohepatitis account for a significant percentage of chronic liver disease in children. Treatment depends on the underlying cause and may include antiviral therapy,

1. CHRONIC HEPATITIS
IN CHILDREN
Dr. Virendra Kumar Gupta
Assistant Professor

2. DEFINITION
Chronic hepatitis means ongoing
inflammation of the liver persisting for more
than six months that is detectable by
biochemical and histologic means.

3. CAUSES
1.Chronic viral hepatitis
 Hepatitis B, C, D
2.Autoimmune liver disease
 Autoimmune hepatitis
 Sclerosing cholangitis/primary biliary cirrhosis
 Overlap syndrome with sclerosing
cholangitis and autoantibodies
 Systemic lupus erythematosus
 Coeliac disease

4. 3.Drug-induced hepatitis
4.Metabolic disorders associated with chronic
liver disease
 Wilson disease
 Nonalcoholic steatohepatitis
 α1-Antitrypsin deficiency
 Tyrosinemia
 Niemann-Pick disease type 2
 Glycogen storage disease type iv
 Cystic fibrosis
 Galactosemia
 Bile acid biosynthetic abnormalities

6. Clinical presentation
 Can present with acute decompensation
 Asymptomatic
 Signs of chronic liver disease/failure

8. Hepatitis B
 Chronic hepatitis : HBsAg positivity for >6 mo
 Risk : >90% infected <1yr , 30% children &
2% of adults infected will become chronic
carriers.
 Three phases of this chronic infection include
1. Immunotolerant phase - active viral
replication and minimal liver damage.HBsAg &
HBeAg are positive and anti Hbe is negative.
HBV DNA load is high. ALT normal

9. 2. Immuno active phase- host tries to resolve
infection HBsAg & HBeAg are positive and anti
Hbe is negative.
HBV DNA load is low. ALT high & with flares
3. Inactive carrier phase- HBsAg & anti Hbe are
positive and HBeAg is negative.
HBV DNA load is very low. ALT normal.
Sometimes may lead to resolution with HBsAg
being negative and Anti HBs positive.

10. Symptomatic Infection
Chronic Infection
Age at Infection
Chronic Infection (%)
SymptomaticInfection(%)
Birth 1-6 months 7-12 months 1-4 years Older Children
and Adults
0
20
40
60
80
100100
80
60
40
20
0
Outcome of Hepatitis B Virus Infection
by Age at Infection
ChronicInfection(%)

11.  Sexual - sex workers and homosexuals are
particular at risk.
 Parenteral - IVDA, Health Workers are at
increased risk.
 Perinatal - Mothers who are HBeAg positive
are much more likely to transmit to their
offspring than those who are not. Perinatal
transmission is the main means of
transmission in high prevalence populations.
Hepatitis B Virus
Modes of Transmission
Keeffe EB, et al. Clin Gastroenterol Hepatol. 2006;4:936–962.

12. Diagnostic Interpretations of Hepatitis B
markers
HBsAg Non infectious component
of viral coat
Indicator of disease. If > 6
months: chronic HBV
Anti-HBs Antibody response to HBsAg Indicates recovery and/or
immunity
HBeAg Antigen that correlates with
replication and infectivity
High level of infectivity and
replication
Anti-HBe Antibody response to HBeAg Decreasing level of
replication
Remission/resolution
Anti-HBc IgM Non protective antibody to
the HBcAg
Recent HBV infection
Anti-HBc IgG As above Remote exposure to HBV
HBV DNA Replictative genetic
material of HBV; infectious
agent
Viral replication and
continues infection

13. Diagnostic Interpretations of Hepatitis B
markers
HBsAg Non infectious component
of viral coat
Indicator of disease. If > 6
months: chronic HBV
Anti-HBs Antibody response to HBsAg Indicates recovery and/or
immunity
HBeAg Antigen that correlates with
replication and infectivity
High level of infectivity and
replication
Anti-HBe Antibody response to HBeAg Decreasing level of
replication
Remission/resolution
Anti-HBc IgM Non protective antibody to
the HBcAg
Recent HBV infection
Anti-HBc IgG As above Acute or remote exposure
to HBV
HBV DNA Replictative genetic
material of HBV; infectious
agent
Viral replication and
continues infection

14. Symptoms
HBeAg anti-HBe
Total anti-HBc
IgM anti-HBc anti-HBsHBsAg
0 4 8 12 16 20 24 28 32 36 52 100
Acute Hepatitis B Virus Infection with
Recovery Typical SerologicCourse
Weeks after Exposure
Titre

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

16. HBV Scenarios
HBsAg anti-HBs anti-HBc
IgM
anti-HBc
IgG
HBeAg DX
+ - + + +
+ - - + +
- + - - -
- + - + -
- - + - -
- - - + -
Acute
infection
Carrier
Vaccinated
Exposed
Immune
Acute
Window
Exposed
Ab lost

17. 17
Possible Outcomes of HBV Infection
Acute hepatitis B infection
Chronic HBV infection
3-5% of adult-
acquired infections
95% of infant-
acquired infections
Cirrhosis
Chronic hepatitis
12-25% in 5 years
Liver failureHepatocellular
carcinoma
Liver transplant
6-15% in 5 years 20-23% in 5 years
DeathDeath

18. Treatment
 Only useful for immunoactive phase as it will
reduce risk of hepatic cancer and cirrhosis
 Treatment for children is only by :
 Interferon(IF alpha 2b,peg IF) AND lamivudine
after thorough investigations and classification
of stage of disease.
 Adefovir ,entecavir and tenofovir are used in
older children(>12 years)

19. Chronic hepatitis C
 Prevalence low in children
 Risk of perinatal transmission:5%
 Increases to 20% if mother coinfected with HIV
 Poses 85 % risk of developing chronicity but
no good evidence in children

20.  Mostly asymptomatic with fluctuating /normal
transaminases levels
 Slow progression to fibrosis/cirrhosis/CLD
 Associated with extrahepatic manifestations

21. Natural History of Hepatitis C
Exposure
No infection
Acute
Chronic
Spontaneous
clearance
(early)
•Cirrhosis
(20-40%)
•HCC
(1-4%/year)
<75%
>20%

22.  Diagnosis: HCV RNA and genotype , liver
biopsy
 Treatment:
PEG INTERFERON ALPHA 2b and
RIBAVIRIN
(in > 3yrs of age) for 2 year duration

23. Autoimmune liver disease
Autoimmune liver disease is a clinical
constellation that suggests an immune-
mediated process characterized by :
 hypergammaglobulinemia,
 circulating autoimmune antibodies,
 necro inflammatory histology &
 responsive to immunosuppressive therapy .
 They include autoimmune hepatitis,
autoimmune sclerosing cholangitis & de
novo hepatitis.

24. Pathophysiology
 Triggering factors : molecular mimicry,
infections, drugs, environment (toxins) in a
genetically susceptible host
 Inflammatory cells invades the surrounding
parenchyma.
 HLA DR3, DR4, and DR7 isoforms confer
susceptibility to autoimmune hepatitis

26. Clinical manifestations
 Acute viral hepatitis like picture(40%) can
progress to ALF esp in Type 2
 Insidious onset of liver disease with fatigue,
relapsing or prolonged jaundice.
 Chronic liver disease and its complications
 Extrahepatic manifestations: arthritis,
vasculitis, nephritis, throiditis, anemia, rash

27. Management
 Diagnosis is done by:
elevated transaminases, positive auto
antibodies , raised gammaglobulins and IgG
levels, liver biopsy, absence of known etiology
and response to immunosuppressive drugs.
 Steroids, Azathioprine are first line drugs
 Cyclosporine and mycophenolate mofetil are
second line drugs
 Liver transplantation as and when required.

28. Drug induced liver disease
 Drugs commonly used in children that can
cause chronic liver injury include isoniazid,
methyldopa, pemoline, nitrofurantoin,
dantrolene, minocycline, pemoline, and the
sulfonamides.
 Anti tubercular and anticonvulsant drugs are
major causes
 Can be chemical hepatotoxicity/idiosyncratic
heapatotoxicity

29.  They can mimic any form of liver
disease(acute &chronic hepatitis, ALF, portal
hypertension)
 Good history taking and high index of
suspicion is required
 Treatment is by withdrawal of drug and
supportive care

30. Metabolic causes
 Can account for 15-20% of liver diseases in
India
 Most common is Wilsons disease.
 Most symptoms are due o hepatocyte injury or
secondary to hypoglycemia or
hyperammonemia
 Treatment is cause specific.

31. Wilsons disease
 a/k/a hepatolenticular degeneration
 Toxic accumulation of copper in
liver,brain,cornea and other tissues
 Due to abnormal gene, ATP 7B in
chromosome 13

32. Clinical features
 Various forms of hepatic disease:
 Asymptomatic hepatomegaly
 subacute/chronic hepatitis
 Acute hepatic failure with/without hemolytic
anemia
 Others: neuropsychiatric disease, KF
Ring,sunflower cataract , coombs negative
hemolytic anemia, arthritis, pancreatitis,
nephrolithiasis, cardiomyopathy
,endocrinopathies

33. diagnosis
 Serum ceruloplasmin(<20mg/dl)
 24 hr urinary copper excretion(>100mcg/day)
with penicillamine challenge
test(>1600mcg/day)
 KF ring(slit lamp)
 Liver biopsy: hepatic copper (>250mcg/g)
 Family screening

34. Treatment
 Dietary restriction of copper
 Copper chelating
agents(penicillamine/triethylene tetramine
hydrochloride, zinc, ammonium
tetrathiomolybdenate)
 Liver transplantation

35. Nonalcoholic steatohepatitis
 Usually associated with obesity and insulin
resistance
 Most children are asymptomatic
 May have vague abdominal pain.
 o/e: hepatomegaly , features of insulin
resistance like striae, acanthosis nigricans
obesity and hepatomegaly.
 It can progress to cirrhosis.

36.  Diagnosis is usually clinicopathological
correlation . Other causes to be excluded
 Treatment is by weight reduction and dietary
modifications.
 Ursodeoxycholic acid and vitamin E have
promising results

37. THANK YOU