HEPATITIS IN CHILDREN

Dr Hamza Bawumia
(BSc. Biochem, MBChB)

Supervisor:
Dr Paabie

Liver is divided histologically into lobules. The center of the

lobule is the central vein. At the periphery of the lobule are portal
triads.

Liver physiology

Liver is a multitask organ

Metabolic Function
Synthesis
Breakdown
Other functions
storage of vitamin
A,D,B12,
Excretion of waste
products from
bloodstream into bile
Storage functions

Protein metabolism
Synthesis of amino acids
Carbohydrate metabolism
Gluconeogenesis
Glycogenesis

Lipid metabolism
Cholesterol synthesis
Lipogenesis

Production of coagulation
factors I, II, V, VII, IX, X and XI, and
protein C, protein S and antithrombin
Produces insulin-like growth factor 1
(IGF-1), a polypeptide protein
anabolic effects

Production of thrombopoetin
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Liver physiology
Produces albumin, the major osmolar
component of blood serum
Synthesizes angiotensinogen,
responsible for raising blood pressure
when activated by renin.

Breaks down insulin and other hormones

Glycogenolysis
Breaks down or modifies toxic substances
Converts ammonia to urea
Storage of iron, vitamins and trace
elements
Others - Hematopoietic organ when required
Excretory organ: bile salts, degraded drugs
/toxins /antibiotics

HEPATITIS = inflammation of liver

HEPATITIS - causes

ACUTE:
Viral hepatitis
Non-viral infection
Alcohol*
Toxins
Drugs
Ischemic hepatits
Autoimmune
Metabolic diseases

CHRONIC:
Viral hepatitis
Alcohol*
Drugs
Non-alcoholic
steatohepatitis
Autoimmune
Heredity

HEPATITIS symptoms and

signs

ACUTE:
Malaise
Muscle and join
ache
Fever
Nausea or vomiting
Loss of apetite
Abdominal pain
Dark urine
Enlarged Tender
Liver

CHRONIC:
Malaise, tiredness,
weakness
Weight loss
Peripheral oedema
Ascites
Jaundice*
Chronic Hepatitis is defined as
sustained inflammatory
disease of the liver lasting for
more than 6 months.

Viral Hepatitis

Viral hepatitis is a systemic disease

with primary inflammation of the liver
by any one of a heterogenous group of
hepatotropic viruses.

Hepatotropic Viruses
PRIMARY

Hepatitis A Virus (HAV)

Hepatitis B Virus (HBV)
Hepatitis C Virus (HCV)
Hepatitis D Virus (HDV)
Requires HBV co-infection

Hepatitis E Virus (HEV)

Hepatitis F Virus
(controversial)
Hepatitis G Virus
(pathogen?)
Others

SYSTEMIC

Cytomegalovirus (CMV)
Epstein-Barr Virus (EBV)
HIV
Adenovirus
Parvovirus B19
Rubella
Coxsackievirus B
Enteroviruses
Human Herpes Viruses
Herpes Simplex Virus (HSV)
HHV-6
Varicella Zoster Virus (VZV)
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Acute Viral Hepatitis

Acute hepatocellular injury/inflammation

Reflected by elevated transaminases (AST or
SGOT, ALT or SGPT)
Clinical manifestations often include fever,
malaise, jaundice, RUQ pain, nausea/vomiting

Typically self-limiting and of short duration

Contrast with: chronic, fulminant

Causative agents
HAV (50% of cases in U.S.), HEV
CMV, EBV, VZV
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Fulminant Hepatitis

Acute, massive hepatocellular necrosis

Impaired synthetic, excretory, and detoxifying
functions of the liver
Cholestasis, ascites, coagulopathy, encephalopathy,
multi-system failure
Initially very elevated transaminases
Falling transaminases and rising bilirubin ominous
Hyperammonemia, hypoalbuminemia, prolonged PT, hypoglycemia

Viral agents (50% of cases)

Most cases of fulminant hepatic failure are caused by
unidentified agent, presumably viral
HAV, HBV+/-HDV, HCV, HEV
HSV, enteroviruses, EBV, CMV, HHV-6, VZV

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Chronic Hepatitis

Prolonged necroinflammatory process

Elevated transaminases for > 6 months
Insidious clinical manifestations
Can include cholestasis (jaundice, pruritus),
ascites, hypoalbuminemia, coagulopathy,
encephalopathy
Can progress to fibrosis and then cirrhosis

Viral agents: HBV (+/- HDV), HCV

Other causes include autoimmune, metabolic
disorders (Wilsons, CF, alpha-1 antitrypsin deficiency),
drug/toxin-mediated, idiopathic
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Type of Hepatitis
A

Source of
virus

Feces

Blood
Blood derived
Body fluids

Blood
Blood derived
Body fluids

Blood
Blood derived
Body fluids

Feces

Route of
Transmission

Feco-oral

Percutaneous
Permucosal

Percutaneous
Permucosal

Percutaneous
Permucosal

Fecooral

Chronic
Infection

No

Yes

Yes

Yes

No

Prevention

Pre Post
Exposure
Immunization

Pre Post
Exposure
Immunization
Blood donor
screening

Blood donor
screening

Pre Post
Exposure
Immunization

Ensure
Safe
Drinking
water

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Hepatitis A
Transmission: faecal-oral
Incubation: 2-6weeks
High-risk countries:

Eastern Europe, Africa, Asia, South America

In these regions almost every child comes into
contact with the hepatitis A virus before the age of 10

The proportion of symptomatic forms

and complications increase with age

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Hepatitis A

Diagnosis:

AST, ALT, IgM, IgG

Prevention: hygienic measures

passive immunization ( gives <3 months
immunity to those at risk)
active immunization

Treatment: nonspecific, dietary food and long rest

CHRONIC

LIVER DISEASE DOES NOT OCCUR with

Hepatitis A infection.
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Hepatitis B:
ACUTE

CHRONIC- 5-10%
(infection >6months)

Worldwide (W.H.O.

estimates)

More than 2 BILLION people alive today have

been infected with HBV at some time in their
lives. Of these, about 350 million remain infected
chronically and become carriers of the virus.
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18

Chronic Hepatitis B
2 types
Chronic persistent hepatitis
Chronic active hepatitis

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Chronic Persistent Hepatitis

Histology
- Normal hepatic lobular architecture with
infiltration of monocytes in portal areas
b) Elevated plasma transaminase levels with
normal PT, Alkaline phosphate, albumin,
globulin, GGT
Treatment
Close observation
Excellent prognosis ( rarely progresses to
CAH or cirhosis)
a)

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21

Chronic Active Hepatitis

Histology
-Patchy hepatocellular necrosis with
destruction of lobular architecture and
regenerating hepatocytes with multiple nuclei
-Raised transaminase, bilirubin, ANA(75%)
Treatment
Immunosuppresive therapy
- Prednisolone
- Azathioprine
- Interferon for Hep B
These may prevent progression to serious liver damage and cirhosis
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23

Transmission: blood and body fluids, iv drug

abusers, sexual transmission

Incubation: 1-6 months

Hepatitis B virus primarily interferes with functions

of the liver by replicating in liver cells
During HBV infection, the host immune response
causes both hepatocellular damage and viral
clearance

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HBV Diagnosis

Hochman J, Balistreri WF. Pediatr Rev. 2003; 24: 399-410.

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HBV Treatment

Lin KW, Kirchner JT. Am Fam Physician 2004; 69:75-82.

GOALS of TREATMENT

- Suppress HBV replication

- Seroconversion from eAg to e Ab
- Prevent long-term sequelae

Interferon-alfa
Lamivudine
Adefovir
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Prevention: vaccination
Treatment: chronic- interferon-2, antiviral

drugs (lamivudine...)

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When HBV infection is acquired at birth (vertical

transmission) or early childhood there is a high
level of immunological tolerance and cellular
immune response does not occur, thus chronic
infection is the norm.

This immune tolerant phase is characterized by

minimal hepatic inflammatory activity and normal or
near normal serum ALT despite positive Hbe Ag
and high levels of HBV replication.

This phase persists for 2-3 decades before an

active hepatitis develops that might lead to fibrosis
and cirrhosis.
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AGE

At Birth

Immunization
schedule
in
Ghana
Showing Hep B
immunization

6 weeks

10 weeks

14 weeks

6 months
9 months

12 months
18 months

18 months

PICTURE

VACCINES

DOSE

ROUTE AND SITE OF

ADMINISTRATION

BCG

0.05ml

intra-dermal, right upper arm

OPV 0

2 drops

oral

Hepatitis B

0.5ml

intra-muscular, right thigh

OPV 1

2 drops

oral

DPT-HepB-Hib 1

0.5ml

intra-muscular, left thigh

Pneumococcal 1 0.5ml

intra-muscular, right thigh

Rotavirus 1

1.0ml

oral

OPV 2

2 drops

oral

DPT-HepB-Hib 2

0.5ml

intra-muscular, left thigh

Pneumococcal 2 0.5ml

intra-muscular, right thigh

Rotavirus 2

1.0ml

oral

OPV 3

2 drops

oral

DPT-HepB-Hib 3

0.5ml

intra-muscular, left thigh

Pneumococcal 3 0.5ml

intra-muscular, right thigh

Vitamin A

100,000 I.U

oral

Measles 1

0.5ml

sub-cutaneous, left upper arm

Yellow Fever

0.5ml

sub-cutaneous, right upper arm

Vitamin A

200,000 I.U

oral

Measles 2

0.5ml

sub-cutaneous, left upper arm

Vitamin A
Long Lasting
Insecticidal Net
(LLIN)

200,000 I.U

oral

NB: After 18 months vitamin A will be given every six months till child is five years old

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Hepatitis D

Subviral satellite because it can propagate only in

the presence of hepatitis B
coinfection

superinfection

Transmission: parenteral (intravenous drug

use mostly)

> 60% develop cirrhosis

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Hepatitis C
ACUTE

CHRONIC 50-80%

first 6 months after infection

60-70% asymptomatic
most patients develop chronic
HCV

more than 6 months

often asymptomatic
1/3 progress to cirrhosis in 20y

Infects 3-4 million people per year worldwide.

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Hepatitis C
Transmission: blood
Incubation: 2weeks - 6months

No vaccine!

35% of patients infected with HIV are also infected

with hepatitis C virus.

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Thank you

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References

Nelsons Textbook of Pediatrics

Essentials of clinical medicine Kumar and Clark
http://www.emedicinehealth.com/hepatitis
http://www.hepatitis.org/hepatalcool_angl.htm
Oxford handbook of clinical medicine

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North American Society for Pediatric

Gastroenterology, Hepatology and Nutrition

www.naspghan.org

www.cdhnf.org

www.hepb.org

www.aasld.org
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Acknowledgement

Dr Paabie

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