This document summarizes chronic hepatitis, defining it as hepatitis lasting more than 3-6 months or presenting with signs of liver decompensation or failure. The causes discussed include chronic viral hepatitis (types B, C, and D), autoimmune liver diseases, drug-induced hepatitis, and various metabolic disorders. Clinical presentation can range from being asymptomatic to acute decompensation or signs of chronic liver disease. Management involves diagnostic testing to determine the cause and severity of liver dysfunction, with treatment being specific to the underlying condition such as antiviral medication for hepatitis B or immunosuppressants for autoimmune hepatitis.

1. CHRONIC HEPATITIS
DR LALITHA, AP ,Dept of Pediatrics

2. Definition
 Chronicity is determined
- duration >3-6 months or
-evidence of hepatic decompensation
(hypoalbuminemia,encephalopathy,
coagulopathy)
- Physical stigmata of chronic liver disease
Can lead to cirrhosis/ESLD/hepatocellular
carcionoma

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

4.  Drug-induced hepatitis
 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

9. MANAGEMENT
 DIAGNOSIS: to determine cause and assess
extent of liver dysfunction and complication
 Investigations include: LFT, USG abdomen,
liver biopsy
 Specific to cause: viral markers,autoantibodies
, metabolic workup

10. 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

11. 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.

12. 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)

13. 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

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

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

16. 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.

17. 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

19. 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

20. 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.

21. 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

22.  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

23. 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.

24. 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

25. 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

26. 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

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

28. 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.

29.  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

30. THANK YOU