Hepatitis Viral en Niños - Que Conocemos en 2021

SYMPOSIUM: HEPATOLOGY
Viral hepatitis in children: Epidemiology

The WHO estimated that there were 7134 HAV related deaths in
2016, 0.5% of the mortality due to viral hepatitis.2 HAV is more
what do we know in 2021? prevalent in low income countries with 90% children infected by
10 years of age. The middle-income countries with variable
Chayarani Kelgeri sanitary conditions may see more severe disease in adults and
Deirdre Anne Kelly outbreaks.
Higher income countries have low prevalence of HAV; cases
are reported following travelling to endemic areas and food
borne outbreaks. Some cases have been reported among ado-
Abstract
lescents and adults with high-risk behaviour such as men having
Viruses are a common cause of hepatitis in children. Hepatitis A and E
cause acute infections while Hepatitis B, C and D can lead to chronic
sex with men.
infection with increased morbidity and mortality due to chronic liver
Natural history
disease and hepatocellular carcinoma in later life. Acute infections
The incubation period following exposure is around 14e28 days.
may be fulminant causing acute liver failure necessitating a liver trans-
Symptoms following HAV infections are variable with mild
plant. Our understanding of these viruses continues to evolve, and this
symptoms in most children less than 5 years of age. The severity
review aims to summarize the current strategies in diagnosis, preven-
increases with age. ALF and death are infrequent and encoun-
tion and use of anti-viral drugs to treat these infections.
tered more in the elderly or those with an underlying liver con-
Keywords direct acting antivirals; hepatitis A; hepatitis B; hepatitis dition. It may take a few months for complete clinical recovery
C; hepatitis D; hepatitis E; hepatotropic virus; nucleoside analogues; followed by lifelong immunity.
viral hepatitis
Diagnosis
Acute HAV hepatitis is confirmed by positive immunoglobulin
Introduction (Ig) G and IgM antibodies to HAV with raised liver transaminases
and bilirubin (Figure 2). A positive IgM with a negative IgG may
Hepatotrophic viruses causing hepatitis continue to be a major indicate false positive result and needs confirmation with HAV
public health concern worldwide. Hepatitis due to Hepatitis A polymerase chain reaction. Similarly, IgM can be negative if
(HAV) and Hepatitis E (HEV) usually recover after acute infec- tested very early in the disease (within 5 days of onset of
tion. Hepatitis B (HBV), Hepatitis C (HCV) and Hepatitis D (HSV) symptoms). A repeat sample should be obtained if clinical sus-
may progress to chronicity with morbidity and mortality related picion is high.3
to cirrhosis and a lifetime risk of hepatocellular carcinoma (HCC)
(Figure 1).1 Treatment
Symptoms of acute hepatitis are similar for all viruses and There is no specific treatment for HAV hepatitis and is largely
include nausea, vomiting, abdominal pain, jaundice and high supportive with anti-pruritic agents, hydration and fat-soluble vi-
coloured urine. Children with acute hepatitis need monitoring and tamins with prompt referral to transplant centre if ALF develops.
prompt referral to a liver transplant centre if they develop acute
liver failure (ALF). Children with chronic HBV and HCV infections Prevention
who follow precautions do not pose a risk to others and should Improved sanitation and hygiene, food safety, health education
not be restricted from participating in regular activities. and vaccines providing long term immunity are the most effec-
National policies have been guided by the goals and targets set out tive ways to combat HAV. In endemic countries, HAV vaccines
by the World Health Organization (WHO) global health strategy to are included in the childhood immunization schedules while in
eliminate viral hepatitis as a public health threat by 20302 (Table 1). countries with low prevalence, the vaccine is used as an inter-
Management of these viral infections especially HBV and HCV vention during outbreaks, in high-risk populations, contact with
are evolving constantly as new information and effective anti- a known index case and as a travel vaccine to endemic countries.
viral drugs become available for use in children. Prophylaxis with human normal Ig may additionally be required
in immunocompromised children.3
Hepatitis A
HAV is a picornavirus (literally a small RNA virus). This non- Hepatitis B
enveloped ribonucleic acid (RNA) virus is usually transmitted HBV is an enveloped, highly infectious double stranded deoxy-
by the faecal-oral route through contaminated food and water. ribonucleic acid (DNA) virus transmitted via blood and bodily
fluids, causing acute and chronic liver disease. 10 genotypes (A-
J) are known with distinct geographical distribution.
Chayarani Kelgeri MD MRCPCH, Consultant Paediatric Hepatologist,
Liver Unit, Birmingham Women’s and Children’s Hospital, UK. Epidemiology
Conflicts of interest: none declared. 257 million people (3.5%) worldwide are infected with HBV,
Deirdre Anne Kelly MD FRCP FRCPI FRCPCH, Consultant Paediatric 68% of these being in the African or western Pacific regions.1 An
Hepatologist, Liver Unit, Birmingham Women’s and Children’s effective vaccine to prevent HBV infection is available which has
Hospital, UK. Conflicts of interest: none declared. reduced chronic HBV infection in children from 4.7% to 1.3% in
PAEDIATRICS AND CHILD HEALTH xxx:xxx 1 Crown Copyright Ó 2021 Published by Elsevier Ltd. All rights reserved.
Please cite this article as: Kelgeri C, Kelly DA, Viral hepatitis in children: what do we know in 2021?, Paediatrics and Child Health, https://doi.org/
Descargado para Anonymous User (n/a) en Pontifical Xavierian University de ClinicalKey.es por Elsevier en octubre 29, 2021. Para uso
10.1016/j.paed.2021.09.002
personal exclusivamente. No se permiten otros usos sin autorización. Copyright ©2021. Elsevier Inc. Todos los derechos reservados.
0.8
3.3
30
HAV
HBV
HCV
HEV
Acute
66 hepatitis
Cirrhosis
HCC
Figure 1 Deaths from Viral hepatitis - by virus and type of sequelae as globally estimated by World health organization in 2015 and published in
2016.1
Natural history
WHO targets for eliminating viral hepatitis as public Vertical (Mother to child) transmission accounts for majority of
health threat by 2030. Data from2 HBV infections in children and the risk is increased if mother is
HBV e Antigen (HbeAg) positive with high HBV DNA load. Some
WHO Impact targets by 2030
infections are acquired through horizontal transmission because
Incidence of new cases of chronic 90% reduction
of close contact with an infected index case. Sexual contact,
HBV and HCV (equivalent to 0.1%
tattooing, body piercing, drug abuse with shared needles and
prevalence of HBsAg in
syringes may account for HBV infections seen in the adolescent
children)
period.4
Mortality due to HBV and HCV 65% reduction
Perinatal infections are largely indolent, but ones acquired
Preventive targets
later, have an incubation period of around 75 days (30
HBV childhood vaccine coverage 90%
e180 days) and may have symptoms of mild to severe fulminant
Prevention of Vertical transmission 90%
hepatitis in the acute stage. The risk of ALF in babies is higher if
of HBV infection
mothers are HBV e antibody positive (anti HB e) as they may
Blood donation safety screening 100%
carry a mutant HBV strain. Co-infection or superinfection with
Safe injections in and out of health 90%
HDV also increases the risk of ALF, which is likely to require
facilities
liver transplantation.
Supply of sterile needles and syringes 300
The tendency for chronic infection depends critically upon the
per intravenous drug abuser
age of infection. About 90% of infants infected below one year of
Testing targets
age, 25e50% of those infected between 1 and 5 years of age and
HBV and HCV diagnosis 90%
less than 5% if infected beyond 5 years of life will develop
Treatment targets
chronic HBV infection, defined as persistence of HBV surface Ag
HBV and HCV treatment for eligible 80%
(HBsAg) beyond 6 months of infection. The trajectory of disease
people
progression thereafter is a complex interplay between HBV and
Table 1 the host immune system passing through fluctuating phases of
variable duration and is not well delineated in children
(Figure 3).
Advanced liver disease with its related complications, HCC
2015.1 HBV infection is less prevalent in developed countries but and HBV-related immune manifestations like glomerulonephritis
is increasing because of migration and adoption of children from and cryoglobulinemia are not common in children.4 Risk factors
endemic countries. for progression to advanced liver disease and HCC are perinatal
10.1016/j.paed.2021.09.002
Jaundice
SEROLOGY
IgG
IgM
VIRAL DYNAMICS
Viraemia
Faecal shedding
EPIDEMIOLOGY
Case interval
Incubation
Hepatic illness
Potential high infectivity
Recovery
0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
Weeks
Figure 2 Immunological response to Hepatitis A,4 IgG: Immunoglobulin G IgM: Immunoglobulin

M. Reproduced from reference 3 with permission.
acquisition, high HBV DNA load, and late seroconversion of classify the different phases and guides treatment and prognosis
HBeAg with prolonged periods of hepatitis. (Figure 3). HBeAg is a marker of virus replication and infectivity.
Occult HBV DNA persists in the liver even after spontaneous Liver biopsy is not routinely indicated unless other causes of liver
sero-clearance and may reactivate when the balance between disease are suspected.
HBV and the host immune response changes for example during
periods of immunosuppression. Treatment
Treatment of acute HBV infection is supportive. Prompt referral
Diagnosis or discussion with a transplant centre is required if ALF develops.
HBV infection is diagnosed by detecting HBsAg in blood. Further Management of chronic HBV in children continues to evolve
serology (Table 2), HBV DNA titres and liver biochemistry help and therapy should be guided by international and national
HBsAg Positive HBsAg
HBV DNA
20000 IU/mL
ALT
Normal ALT
HBeAg Positive HBeAg, Negative anti HBe Positive anti HBe, Negative HBeAg
HBeAg positive HBeAg positive HBeAg negative HBe Ag negative
Phase of
Infection Chronic Infection Chronic Hepatitis Chronic Infection Chronic hepatitis
Generally, not May be indicated Not indicated May be indicated
Treatment indicated
Figure 3 Phases of chronic HBV infection. ALT: alanine transaminase, HBeAg: HBV e antigen, anti HBe: HBV e antibody, HBsAg: HBV surface
antigen.
10.1016/j.paed.2021.09.002
immunodeficiency virus (HIV) infection, extra hepatic manifes-

Interpretation of HBV markers tations, fibrosis or cirrhosis on histology, persistent abnormal
Viral markers Interpretation fibro scan readings done twice 6 months apart and family history
of HCC.
HBsAg e Susceptible The drugs currently recommended for use in chronic HBV
Anti HBc total e hepatitis are nucleos(t)ide analogues (NA).4 Entecavir has a good
Anti HBc IgM e safety profile, with high barrier of resistance and is the preferred
Anti HBs - drug in children. Tenofovir is an alternative NA with high barrier
HBsAg þ Early acute infection, transiently after HBV of resistance but is only licensed for use above 12 years of age.
Anti HBc total e vaccination Long term use has been associated with renal tubular damage
Anti HBc IgM e and decrease in bone mineral density and so a safer form,
Anti HBs - Tenofovir alafenamide is preferred. Other NA like Lamivudine,
HBsAg þ Acute infection Adefovir and Telbivudine are no longer used because of low
Anti HBc total þ barrier of resistance, while immunomodulators (Interferon
Anti HBc IgM þ a2b, Peg interferon a2) are invasive and have unpleasant side
Anti HBs - effects.
HBsAg e Acute resolving infection Children on NA need to be monitored for drug resistance and
Anti HBc total þ emergence of mutant strains. The ideal therapeutic endpoint is
Anti HBc IgM þ undetectable HBsAg with eradication of HBV DNA including
Anti HBs þ/- intrahepatic CCC DNA and integrated HBV DNA. This is, how-
HBsAg e Immune due to natural Infection ever, often not achieved even after years of drug therapy.
Anti HBc total þ The European Association for Study of Liver guidelines
Anti HBc IgM e currently recommend cessation of NA in HBeAg negative non-
Anti HBs þ cirrhotic adults who have had virological suppression with
HBsAg þ Chronic infection normal transaminases for more than 3 years provided close
Anti HBc total þ monitoring for viral rebound can be ensured. Most will remain in
Anti HBc IgM e sustained virological remission (SVR) and about 20% will
Anti HBs - eventually lose their HBsAg.
HBsAg e Past infection (most common), false positive, Treatment with NA can also be considered in children with
Anti HBc total þ low level chronic infection, passive transfer chronic or past evidence of HBV infection who will be
Anti HBc IgM e from mother in an infant commencing immunosuppressive drugs and are at moderate to
Anti HBs - high risk of HBV reactivation.
HBsAg e Post HBV vaccination, after immunoglobulin It is unlikely that HBV will be eradicated without the devel-
Anti HBc total e administration opment of combination drug therapy that can act on the different
Anti HBc IgM e stages of the HBV life cycle and reduce risk of drug resistance.
Anti HBs þ
Prevention
HBsAg: HBV surface antigen; Anti HBc: HBV core antibodies; Anti HBs: HBV sur-
There are effective HBV vaccines and one of the WHO preventive
face antibodies.
targets is to achieve childhood HBV vaccine coverage of 90% by
Table 2 2030. As a response to this, most countries have now integrated
HBV vaccine in their primary vaccination schedules (0, 1,
6 months with additional boosters if the anti HBs antibodies are
guidelines with input from a paediatric hepatologist. No drugs less than 10 mIU/L). Unvaccinated children and adults should be
are available yet that can cure or eradicate the virus as the HBV immunized if high-risk or in contact with HBV infection. Hepa-
covalently closed circular DNA (cccDNA) integrates into host titis B Immunoglobulin (HBIG) may be indicated for post expo-
genome and continues replication. sure prophylaxis in some cases.
Children are monitored every 6e12 months with HBV viral Perinatal transmission of HBV depends on screening pregnant
markers, HBV DNA titres, liver function tests, alpha fetoprotein mothers antenatally. Babies of mothers with chronic HBV
(AFP) and a fibroscan. The latter is a type of ultrasound that infection should receive the first dose of HBV vaccine within 24
specifically measures the stiffness of the liver. This allows early hours of life, with HBIG within 12 hours to babies born to HBeAg
detection of progressive liver disease, identifies the need for positive mothers. It is likely that use of NA in third trimester of
treatment and looks for seroconversion. Standard liver ultra- pregnancy in mothers with high HBV DNA load, will further
sound (USS) is recommended every 5 years for HCC surveillance. reduce vertical transmission.
Monitoring is more frequent if alanine transaminase (ALT) is Despite HBIG and vaccine, vertical transmission still occurs in
above upper limits of normal (ULN). 2e10% possibly because of intrauterine infection in mothers
Children with normal ALT are managed conservatively and with high HBV DNA or vaccine administration failure. The sec-
decision to commence treatment is guided by age of the child, ond and third dose of HBV vaccine are administered at one-
HBV DNA titres, HB e Ag positivity, ALT more than ULN for at month intervals (0, 1 and 2 months) using the accelerated
least 6 months, co-existing liver disease, co-existing Human schedule.
10.1016/j.paed.2021.09.002
DAA drugs for chronic HCV infection

Class of DAA Drugs
NS3/4 Protease inhibitors High Potency, Limited genotype coverage, Low Grazoprevir, Voxelaprevir, Glecaprevir
barrier to resistance
NS5B Nucleoside polymerase inhibitor Intermediate potency, Pan genotype, High Sofusbuvir
NS5A Nucleoside polymerase inhibitor High Potency, Multi genotype, Intermediate Ledipasvir, Elbasvir, Pibrentasvir, Velpasvir
Drug combinations Genotype and age recommendations
LedipasvirþSofusbuvir (Harvoni) Genotype 1,4,5,6 and 3 years

SofusbuvirþVelpatasvir (Epclusa) Pan genotype and 6 years
GlecaprevirþPibrentasvir (Maviret) Pan genotype and 3 years
SofusbuvirþRibavarin Genotype 2,3 and 3 years
Table 3
Infected children and families should be educated regarding is recommended that infants with positive anti HCV are tested
care of bleeding wounds, use of sterile needles, syringes and safe with HCV RNA beyond 3 months of age and repeated at 6
sex by using barrier contraception to prevent spread of the virus. e12 months to diagnose chronicity.
Children with chronic HCV infection are monitored annually
Hepatitis C for clinical symptoms, liver biochemistry, AFP, HCV RNA (for
spontaneous clearance). Older children should have a fibroscan.
HCV is a single stranded RNA virus transmitted through blood and
They should have a liver ultrasound scan every 3e5 years.
sexual contact. Six genotypes with various subtypes are known
that differ in drug susceptibility influencing medical therapy.
Treatment
One of the success stories of this century is the availability of safe
Epidemiology
and effective direct acting antiviral (DAA) drugs that eliminate
Approximately 70 million people are thought to be chronically
the virus achieving cure in adults with chronic HCV infection.6
infected with HCV worldwide,1 3.5 to 5 million are children.
These results are replicated in children as evidenced by recent
Natural history clinical trials. FDA and EMA approved DAA regimens (Table 3)
HCV infection in children is commonly acquired through peri- are now available for children with chronic HCV aged 3 years or
natal transmission. Blood products and iatrogenic transmission more. Though children are asymptomatic it is cost effective to
through infected needles and surgical instruments occur in low- treat them early to avoid progression of liver disease and long-
income countries while tattooing, illicit intravenous drug use term complications. Children with extrahepatic manifestations,
and sexual contact may be the route of infection in adolescents. advanced fibrosis or cirrhosis, co morbidities should be priori-
There is an incubation period of 7e9 weeks. tized for treatment.
The risk of perinatal transmission is about 5% and the risk is Treatment should be in collaboration with a specialist team
greater with maternal high HCV RNA tires or HIV co infection. Of who have expertize in treating and monitoring children. The
these, 80% will remain chronically infected. As infections in choice of DAA and duration of therapy is guided by age and weight
children are asymptomatic, many are unaware of being infected. of the child, HCV genotype, presence or absence of cirrhosis, prior
ALT may be normal or may fluctuate above ULN. Extrahepatic treatment with interferon and ribavirin. The duration of therapy is
manifestations like cryoglobulinemia, glomerulonephritis, joint longer in children with cirrhosis. A paediatric multidisciplinary
pain and skin rashes may be seen in a few children. Liver fibrosis Operational Delivery network was launched in April 2021 by
is minimal in childhood unless associated with co morbid factors National Health Service in England to offer HCV treatment advice
like obesity or concomitant use of hepatotoxic drugs. Although and support to clinicians and families in England.
rare in children, chronic liver disease will develop in about 30%
and HCC in 5% of adults.5 Prevention
There is no vaccine for HCV. As chronic HCV infections are
Diagnosis asymptomatic in children, screening of populations at risk
Children at risk are screened for HCV infection by testing for HCV including antenatal screening is an effective strategy for early
antibody (anti-HCV) and if positive with HCV RNA and genotype diagnosis and treatment.
to distinguish between a chronic and a resolved infection.6 HCV Effective donor screening for blood donation exists in devel-
antibodies remain positive in infants born to infected mothers up oped countries but this is still a risk factor in some countries and
to 18 months of age due to trans placental passage and HCV RNA one of the preventive targets by WHO is to achieve 100% safe
may take up to a few weeks to reach detectable levels. Hence, it donor screening by 2030.1
10.1016/j.paed.2021.09.002
Hepatitis D transmission through blood products donated during viraemic

phase has also been reported. The WHO estimates HEV to have
HDV is a single stranded RNA that uses HBsAg from HBV as its
caused 44000 deaths in 2015.
coat or envelope hence can occur only with HBV infection. Its
transmission is like HBV and can occur simultaneously as a co- Natural history
infection with HBV infection or as a super infection in some HEV acute hepatitis is generally asymptomatic or mild and self-
one already infected with HBV infection. Eight genotypes are limiting, rarely progressing to ALF. The outcomes are however
known with no geographical variation or difference in clinical worse in pregnant women with a third dying, especially if con-
course.7 tracted in the third trimester. The incubation period is about
40 days.
Epidemiology
HEV infection can cause acute decompensation in patients with
It is difficult to estimate the true prevalence of HDV infection
underlying chronic liver disease. Chronic HEV infections are re-
because of inadequate screening and standardization of testing but
ported only in the immunosuppressed especially organ transplant
HDV is seen globally with varying reports estimating 12e72 million
recipients. They are asymptomatic but may have persistent mild to
people to be infected. The epidemiology is changing because of
moderate transaminases. Extrahepatic manifestations with neuro-
effective HBV vaccination. Areas of high prevalence identified are
logic symptoms, glomerulonephritis and haematological disorders
Mongolia, Republic of Moldova, western and middle Africa.
have been reported with acute and chronic HEV infection.
About 5% of chronic HBV infection are estimated to have
HDV and is more common in intravenous illicit drug users. Diagnosis
Serology with anti-HEV IgM antibody with a positive HEV RNA
Natural history
confirms diagnosis of acute HEV infection. Liver biochemistry
HDV can cause acute and chronic HDV infection. The risk of
and coagulopathy are monitored with prompt referral to Trans-
ALF, severity of chronic liver disease, progression to cirrhosis
plant centre if ALF develops. Positive Anti-HEV IgG antibody
and HCC is higher with dual infection. Less than 5% of co-
with negative anti-HEV IgM and HEV RNA is indicative of a past
infection and 80% with superinfection (incubation period 2
infection. Antibodies may not be detectable in immunosup-
e8 weeks) will develop chronic HDV infection. The incubation
pressed individuals and HEV RNA is required for diagnosis.
period for co infection is the same as HBV. It is usual to find
negative HBeAg with low HBV DNA as HDV suppresses HBV Treatment
replication. However, HBeAg positivity and HDV infection is No drugs are currently approved for use in acute HEV infection
seen more frequent in Intravenous drug users. and treatment is largely supportive. Liver transplant may be
required if patients fail to recover from ALF. Viraemia, which is
Diagnosis
seen in a third of organ transplant patients with chronic HEV, can
HDV infection is diagnosed by presence of HDV antibodies and
be cleared by decreasing the immunosuppression in some in-
confirmed by detection of HDV RNA in serum. All children with
dividuals. Others may require drug therapy with ribavirin or
chronic HBV infection should be tested for HDV at diagnosis and
pegylated interferon.
rechecked with symptoms of severe hepatitis. Liver biochemistry
and coagulopathy should be checked and referred to liver Prevention
transplant centre if ALF develops. Improving sanitation, hand washing and access to clean drinking
water will decrease the incidence of new infections. Vaccinina-
Treatment
tion against HEV is available but is currently licensed for use only
Pegylated interferon may be used to slow the disease progression
in China. The WHO provides guidance to public health author-
but the rate of SVR is poor (around 25%) with frequent relapses
ities during periods of outbreak. Immunosuppressed individuals
following cessation of therapy.
are advised to avoid consumption of uncooked meat. Blood
New drugs that have shown proof of concept in clinical trials
donation is screened in some countries and should be done
either as monotherapy or in combination (with interferon or NA)
universally for parental acquired infections.
include Farnesyl transferase inhibitor Lonafarnib, Sodium Taur-
ocholate co transporting polypeptide receptor blocker Bulevirtide
and nucleic acid polymers. Conclusion
Of the 5 known hepatotropic viruses, HBV, HCV and HDV may
Prevention become chronic causing cirrhosis and HCC and account for about
The same measures that prevent HBV apply for HDV infection. 96% of viral hepatitis related deaths.1 Vaccination, screening,
Vaccines conferring immunity against HBV will be effective in early diagnosis, effective monitoring, treatment and education
preventing HDV infections. has changed the trajectory of these diseases. Antivirals are
indicated in specific children with chronic HBV infection to slow
Hepatitis E the progression of liver disease. Chronic HCV infection is curable
HEV is an RNA virus with seven known genotypes infecting with DAA, and all children at risk should be screened and
humans and animals. Genotype 1 and 2 cause infections in treated. Effective vaccines with long term immunity are available
humans and is transmitted through faeco-oral route through for HAV and HBV, but not for HCV. Worldwide, countries have
contaminated water. Other genotypes may be transmitted from accelerated their national responses in line with WHO global
animals to humans via milk or undercooked meat. Parental health strategy to tackle and to eradicate viral hepatitis. A
10.1016/j.paed.2021.09.002
REFERENCES Indolfi G, Abdel-Hady M, Bansal S, et al. Management of hepatitis B

1 Global hepatitis report. 2017. WHO, http://apps.who.int/iris/ virus infection and prevention of hepatitis B virus reactivation in
bitstream/10665/255016/1/9789241565455-eng.pdf?ua¼1 children with acquired immunodeficiencies or undergoing immune
(accessed 14 July 2021). suppressive, cytotoxic, or biological modifier therapies. J Pediatr
2 Global health sector strategy on viral hepatitis, 2016e2021: to- Gastroenterol Nutr 2020; 70: 527e38.
wards ending hepatitis. 2016. Geneva: World Health Organization, Indolfi G, Easterbrook P, Dusheiko G, et al. Hepatitis B virus infection
https://apps.who.int/iris/bitstream/handle/10665/246177/WHO- in children and adolescents. Lancet Gastroenterol Hepatol 2019; 4:
HIV-2016.06- eng.pdf; 466e76.
jsessionid¼C218A471F69D97C680E0940470EB5455? Modin L, Arshad A, Wilkes B, et al. Epidemiology and natural history of
sequence¼1 (accessed 14 July 2021). hepatitis C virus infection among children and young people.
3 Public health control and management of hepatitis A, 2017 J Hepatol 2019 Mar; 70: 371e8.
guidelines, Public Health England. Public health control and Rizzetto M, Hamid S, Negro F. The changing context of hepatitis D.
management of hepatitis A (publishing.service.gov.uk) https:// J Hepatol 2021; 74: 1200e11.
assets.publishing.service.gov.uk/government/uploads/system/
uploads/attachment_data/file/727411/Public_health_control_
and_management_of_hepatitis_A_2017.pdf (accessed on
July 14 2021). Practice points
FURTHER READING C Hepatitis A and E are transmitted mostly through the faeco-
Abdel-Hady M, Kelly DEDS, Kuipers EJ. Hepatitis B and C in children oral route while Hepatitis B, D and C through parental and
in: encyclopaedia of gastroenterology 2nd edition 2019; vol. 3; sexual route.
113e21. C Nucleoside analogues are indicated in a select few children
Dalton H, Webb G. Hepatitis E: an underestimated emerging threat. with Hepatitis B to achieve functional cure.
Ther Adv Infect Dis 2019; 6: 1e18. C Direct acting antiviral drugs are now licenced and available
HCV Guidance: Recommendations for Testing, Managing, and to treat Hepatitis C in children above 3 years of age.
Treating Hepatitis C https://www.hcvguidelines.org/.
10.1016/j.paed.2021.09.002

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SYMPOSIUM: HEPATOLOGY

Viral hepatitis in children: Epidemiology

Figure 2 Immunological response to Hepatitis A,4 IgG: Immunoglobulin G IgM: Immunoglobulin

HBsAg Positive HBsAg

immunodeficiency virus (HIV) infection, extra hepatic manifes-

DAA drugs for chronic HCV infection

LedipasvirþSofusbuvir (Harvoni) Genotype 1,4,5,6 and 3 years

Hepatitis D transmission through blood products donated during viraemic

REFERENCES Indolﬁ G, Abdel-Hady M, Bansal S, et al. Management of hepatitis B

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