chronic hepatitis
TRANSCRIPT
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الرحمن ا الرحمن بسم ا بسمالرحيمالرحيم
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LiverLiver Diseases Diseases
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Chronic hepatitisChronic hepatitisin childrenin children
Dr Tai Al AkawyDr Tai Al Akawy
Alexandria university children hospitalAlexandria university children hospital
Based on Nelson text book of pediatrics and many online articles that will be mentioned on the slides
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DEFINITIONDEFINITION
The term chronic hepatitis means ongoing The term chronic hepatitis means ongoing inflammation of the liver persisting for inflammation of the liver persisting for more more
than six monthsthan six months that is detectable by that is detectable by biochemical and histologic means. biochemical and histologic means.
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Clinical featuresClinical features
-Depend on pathology & aetiology -Depend on pathology & aetiology
--Mild illness Mild illness with dyspepsia & variablewith dyspepsia & variable
increase in liver enzymes without evidenceincrease in liver enzymes without evidence
of chronic liver disease of chronic liver disease
--Florid progressive Florid progressive illness with illness with
evidence of chronic liver disease.evidence of chronic liver disease.
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DiagnosisDiagnosis
Elevated transaminasesElevated transaminases
Minimal elevation of alk. Phos.Minimal elevation of alk. Phos.
Hepatic dysfunctionHepatic dysfunction
- serum bilirubin- serum bilirubin
- serum albumin- serum albumin
- P.T.- P.T. Liver biopsyLiver biopsy
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Chronic hepatitisChronic hepatitis
OLD CLASSIFICATIONOLD CLASSIFICATION
Chronic persistant hepatitisChronic persistant hepatitis
Chronic active hepatitisChronic active hepatitis
Based on histopathological distinctionBased on histopathological distinction
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1-Chronic persistent hepatitis 1-Chronic persistent hepatitis (CPH)(CPH)
-Chronic inflammatory infiltrate-Chronic inflammatory infiltrate
confined to portal tractconfined to portal tract
-Spotty necrosis-Spotty necrosis
-Normal liver architecture -Normal liver architecture
-Cirrhosis is rare -Cirrhosis is rare
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2- Chronic active hepatitis 2- Chronic active hepatitis (aggressive)(aggressive)
-Inflammatory infiltrate in portal tract & -Inflammatory infiltrate in portal tract &
parenchyma (piece meal necrosis)parenchyma (piece meal necrosis)
-Distorted lobular architecture -Distorted lobular architecture
-Septa linking portal tract -Septa linking portal tract
& C.V& C.V
-Subsequent Cirrhosis can -Subsequent Cirrhosis can
follow.follow.
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PRESENT CLASSIFICATION PRESENT CLASSIFICATION of chronic hepatirisof chronic hepatiris
CAUSECAUSE
GRADEGRADE
SEVERITYSEVERITY
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CAUSECAUSE
Chronic viral hepatitisChronic viral hepatitis
Autoimmune hepatitisAutoimmune hepatitis
Drug induced hepatitisDrug induced hepatitis
Metabolic disorders associated with CLDMetabolic disorders associated with CLD
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GRADEGRADE -Histological assessment of -Histological assessment of necroinflammatory activitynecroinflammatory activity
Portal inflammationPortal inflammation
Periportal necrosis Periportal necrosis
Piecemeal necrosis or Piecemeal necrosis or interface hepatitisinterface hepatitis
Bridging necrosisBridging necrosis
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SeveritySeverity
Level of progression of the disease based on Level of progression of the disease based on the degree of fibrosis orthe degree of fibrosis or cirrhosiscirrhosis
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CAUSESCAUSES
Hepatitis B ,C , DHepatitis B ,C , D Autoimmune hepatitisAutoimmune hepatitis Drug-induced hepatitisDrug-induced hepatitis Metabolic :Wilson's disease ,A 1-antitrypsin Metabolic :Wilson's disease ,A 1-antitrypsin
deficiency ,haemochromatosis, glycogen storage deficiency ,haemochromatosis, glycogen storage disease type IVdisease type IV
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Hepatitis B Virus
Hepatitis B (HBV) Hepadnaviridae (1970)
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Hepatit is B Virus (HBV)Hepatit is B Virus (HBV)
1. Keeffe EB, et al. Clin Gastroenterol Hepatol. 2006;4:936–962.2. Lok AS, McMahon BJ. Hepatology. 2007;45:507–539.
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HBVHBV : Structure: Structure
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Hepatitis B VirusHepatitis B Virus
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Replication of HBV
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Epidemiology of Hepatit is BEpidemiology of Hepatit is B
Prevalent in Asia, Africa, Southern Prevalent in Asia, Africa, Southern Europe and South America (2-20%)Europe and South America (2-20%)
Age of infection Age of infection is important in is important in determining the outcome of the determining the outcome of the disease.disease.
Lok AS, et al. Hepatology. 2007;45:507-539.
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Chronic Hepatit is B InfectionChronic Hepatit is B Infection
Infections acquired perinatally and in early childhood usually becomes chronic
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Symptomatic Infection
Chronic Infection
Age at Infection
Chronic Infection (%)
Sym
pto
matic In
fection
(%)
Birth 1-6 months 7-12 months 1-4 years Older Childrenand Adults
0
20
40
60
80
100100
80
60
40
20
0
Outcome of Hepatitis B Virus Infectionby Age at Infection
Ch
ron
ic Infectio
n (%
)
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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.
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Diagnostic Interpretations of Diagnostic Interpretations of Hepatit is B markersHepatit is B markers
HBsAgHBsAg Non infect ious component of viral coat
Indicator of disease. If > 6 months: chronic HBV
Anti-HBsAnti-HBs Antibody response to HBsAg
Indicates recovery and/or immunity
HBeAgHBeAg Antigen that correlates with replicat ion and infectivity
High level of infect ivity and replicat ion
Anti-HBeAnti-HBe Antibody response to HBeAg
Decreasing level of replicat ionRemission/resolution
Anti-HBc IgMAnti-HBc IgM Non protective antibody to the HBcAg
Recent HBV infect ion
Anti-HBc IgGAnti-HBc IgG As above Remote exposure to HBV
HBV DNAHBV DNA Replictative genetic material of HBV; infectious agent
Viral replicat ion and continues infection
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Diagnostic Interpretations of Diagnostic Interpretations of Hepatit is B markersHepatit is B markers
HBsAgHBsAg Non infect ious component of viral coat
Indicator of disease. If > 6 months: chronic HBV
Anti-HBsAnti-HBs Antibody response to HBsAg
Indicates recovery and/or immunity
HBeAgHBeAg Antigen that correlates with replicat ion and infectivity
High level of infect ivity and replicat ion
Anti-HBeAnti-HBe Antibody response to HBeAg
Decreasing level of replicat ionRemission/resolution
Anti-HBc IgMAnti-HBc IgM Non protective antibody to the HBcAg
Recent HBV infect ion
Anti-HBc IgGAnti-HBc IgG As above Acute or remote exposure to HBV
HBV DNAHBV DNA Replictative genetic material of HBV; infectious agent
Viral replicat ion and continues infection
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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
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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 Exposure
Titre
Progression to Chronic Hepatitis B Virus Infection Typical Serologic Course
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HBV ScenariosHBV ScenariosHBsAgHBsAg anti-HBsanti-HBs anti-HBcanti-HBc
IgMIgManti-HBcanti-HBc
IgGIgGHBeAgHBeAg DXDX
++ -- ++ ++ ++
++ -- -- ++ ++
-- ++ -- -- --
-- ++ -- ++ --
-- -- ++ -- --
-- -- -- ++ --
Acute infection
Carrier
Vaccinated
ExposedImmune
AcuteWindow
ExposedAb lost
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Possible Outcomes of HBV InfectionPossible 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 failure Hepatocellular carcinoma
Liver transplant
6-15% in 5 years 20-23% in 5 years
DeathDeath
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Chronic Hepatit is B Chronic Hepatit is B Infection in PediatricsInfection in Pediatrics
•Mostly asymptomaticMostly asymptomatic
•Normal growthNormal growth
•Liver damage is mild during childhoodLiver damage is mild during childhood
•Cirrhosis, hepatocellular carcinoma at any age Cirrhosis, hepatocellular carcinoma at any age (rare)(rare)
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Zacharakis G. J Pediat Gastr Nutr; 44:84-91.2006
Natural History of Chronic HBV Natural History of Chronic HBV (in children)(in children)
•HBeAb seroconversion rate 55% in HBeAb seroconversion rate 55% in 12 years12 years
•Lower seroconversion in vertical Lower seroconversion in vertical transmision (38.5%) Vs. horizontal transmision (38.5%) Vs. horizontal (74%)(74%)
•Loss of HBsAg seen in 5%Loss of HBsAg seen in 5%
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Courtesy of Jerrold R. Turner, M.D., Ph.D.
Hepatit is B Liver BiopsyHepatit is B Liver Biopsy
This patient has cirrhosis due to hepatitis B virus (HBV)
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Courtesy of Jerrold R. Turner, M.D., Ph.D.
Hepatit is B Liver BiopsyHepatit is B Liver Biopsy
The portal area is expanded, and the regenerative nodule is encircled by collagen
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Courtesy of Jerrold R. Turner, M.D., Ph.D.
Hepatit is B Liver BiopsyHepatit is B Liver Biopsy
Ground-glass hepatocytes represent cells with cytoplasm swollen by viral particles.
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Courtesy of Jerrold R. Turner, M.D., Ph.D.
Hepatit is B Liver BiopsyHepatit is B Liver Biopsy
Immunoreactive HBsAg(stained red) is deposited in the cytoplasm
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Who to treat?Who to treat?
High ALTHigh ALT Inflammation in biopsyInflammation in biopsy Low HBV DNALow HBV DNA Late acquisit ion of Late acquisit ion of
infectioninfection
Better Better Response Response
to to treatmenttreatment
Mei-Hwei Chang. Pediatric Gastroint Dis. 2004
Children with chronic HBV (HBsAg > 6 months)Children with chronic HBV (HBsAg > 6 months)
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Goals of treatment in Pediatric Goals of treatment in Pediatric populationpopulation
Reducing the risk of HBV related Reducing the risk of HBV related cirrhosiscirrhosis and and HCCHCC
Elimination of Elimination of HBeAg HBeAg may may
considerably improve prognosisconsiderably improve prognosis
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How to treat?How to treat?
PediatricsPediatrics
IFN-IFN- αα LamivudineLamivudine
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How to treat?How to treat?
PediatricsPediatrics
IFN-IFN- αα LamivudineLamivudine
AdefovirAdefovirEntecavirEntecavir
Successful response to treatment will result in the disappearance of HBsAg,
HBV-DNA, and seroconversion of HBeAg.
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INF-INF- αα
Approx 58% of patient show Approx 58% of patient show responseresponse
Advantage:Advantage: More durable responseMore durable response Lack of resistant mutantsLack of resistant mutants
Disadvantage:Disadvantage: Weekly SC administrat ionWeekly SC administrat ion Very expensiveVery expensive Adverse reactions:Adverse reactions: Flu-l ike symptoms, depression, Flu-l ike symptoms, depression,
anorexia, bone marrow suppressionanorexia, bone marrow suppression
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LamivudineLamivudine
Virologic response in children, 23% Virologic response in children, 23% compared to 13% in placebocompared to 13% in placebo
Ad:Ad: OralOral Well toleratedWell tolerated CheapCheap
Dis:Dis: Less durability of responseLess durability of response Increased risk of drug resistant , 70% by 5 yearsIncreased risk of drug resistant , 70% by 5 years
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HEPATITISHEPATITIS - C - C
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Courtesy of the C. Everett Koop Institute at Dartmouth
Hepatit is C Virus Hepatit is C Virus (HCV)(HCV)
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hypervariableregion
capsid envelopeprotein
protease/helicase
RNA-dependent
RNA polymerase
c22
5’
core E1 E2 NS2
NS3
33c
NS4
c-100
NS5
3’
Hepatitis C Virus
Hepatitis C (HCV) Flaviviridae (1988)
Structural genes at the 5' end, the non-structural genes at the 3' end
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HCV replicates exclusively in the cytoplasmvia an RNA intermediate
Nucleus
Viral entry & uncoating
Translation & processing(+)
(+)
(-)
(+)
HCV RNAreplicationVirus particle
assembly Replicativeintermediate
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El-Kamary SS. J Pediatr. 143:54-9, 2003.
Jonas MM. J Pediatr. 131:314-6, 1997.
Yeung LT. Hepatology. 34:223-9, 2001.
Aletr MJ. N Engl J Med. 341; 556-62. 1999
Prevalence of Hepatit is Prevalence of Hepatit is CC
•1.8% prevalence in US 1.8% prevalence in US
•10,000-60,000 newborn wil l be infected 10,000-60,000 newborn wil l be infected worldwide yearlyworldwide yearly
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Prevalence of Hepatit is Prevalence of Hepatit is CC
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Genotype Distribution of Genotype Distribution of Hepatit is CHepatit is C
Gower E, Estes C, Blach S, et al. Global epidemiology and genotype distribution of the hepatitis C virus infection. J Hepatol 2014.
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Mode of Transmission Mode of Transmission of Hepatit is Cof Hepatit is C
•Transfusion of blood or contaminated Transfusion of blood or contaminated products (prior to 1992)products (prior to 1992)
•Use of intravenous drugsUse of intravenous drugs
•SexualSexual
•VerticalVertical (most important among children) (most important among children)
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Mast EE. J Infect Dis. 192:1880-1889, 2005
Perinatal Transmission Perinatal Transmission of Hepatit is Cof Hepatit is C
•3.7% of the infants(born to HCV infected 3.7% of the infants(born to HCV infected mothers) acquired HCV.mothers) acquired HCV.
•Infection rate in HIV posit ive mothers, 25%Infection rate in HIV posit ive mothers, 25%
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Breast feeding and Breast feeding and transmission of Hepatit is Ctransmission of Hepatit is C
• HCV detected in breast milk and colostrumHCV detected in breast milk and colostrum
• Rate of transmission is identical to bott le-fed Rate of transmission is identical to bott le-fed infantsinfants
• Safety based on the absence of traumatized, Safety based on the absence of traumatized, cracked or bleeding nipplescracked or bleeding nipples
Yeung LT. Hepatology.34:223-9, 2001.
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Risk Factors for Vertical Risk Factors for Vertical Transmission of Hepatit is CTransmission of Hepatit is C
Breast feedingBreast feeding Vaginal deliveryVaginal deliverydoes not increasedoes not increase vertical transmission vertical transmission
Mast EE. J Infect Dis. 192:1880-1889, 2005
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Risk Factors for Vertical Risk Factors for Vertical Transmission of Hepatit is CTransmission of Hepatit is C
Does increaseDoes increase vertical transmission: vertical transmission: Use of internal fetal monitoring Use of internal fetal monitoring
devicesdevices High viral loadsHigh viral loads Prolonged rupture of membranes (>6 Prolonged rupture of membranes (>6
h)h) HIV co-infectionHIV co-infection
Mast EE. J Infect Dis. 192:1880-1889, 2005
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Natural History of Hepatit is CNatural History of Hepatit is C
ExposureExposure
No No infectioninfection
AcuteAcuteChronicChronic
SpontaneouSpontaneous clearance s clearance
(early)(early)•Cirrhosis Cirrhosis (20-40%)(20-40%)
•HCC HCC (1-4%/year)(1-4%/year)
<75%<75%
>20%>20%
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England K. J Pediatr. 147:227-32, 2005.
Clinical Features of Clinical Features of Hepatit is C in Hepatit is C in
PediatricsPediatrics•Normal growthNormal growth
•Mostly are asymptomaticMostly are asymptomatic
•HepatomegalyHepatomegaly
•Elevated l iver enzymesElevated l iver enzymes
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Diagnosis of Hepatit is Diagnosis of Hepatit is CC
HCV HCV antibodies antibodies (IgG)(IgG)
HCV RNA PCR HCV RNA PCR (quantitative/qualitative)(quantitative/qualitative)
Init ial screeningInit ial screening
DiagnosisDiagnosis
Confirmation of DiagnosisConfirmation of Diagnosis (qualitative)(qualitative)
Pretreatment Pretreatment evaluationevaluationPost treatment monitorPost treatment monitor
Fried MW, et al. N Eng J Med. 2002;347:975-982.
Manns MP, et al. Lancet 2001;358:958-965.
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Kelly DA. Hepatology; 34:680A. 2001
Wirth S. Hepatology; 36:1280-4. 2002
Davis GL. N Engl J Med; 339:1493-9.1998
McHutchinson JG. N Engl J Med; 339:1485-92.1998
Antiviral Therapy for Hepatit is Antiviral Therapy for Hepatit is CC
•Combined PEGCombined PEG Interferon and RibavarinInterferon and Ribavarin•45-62% sustained virological response45-62% sustained virological response
•Better responseBetter response
•Ribavir in Side effectsRibavir in Side effects
•Anemia/ThrombocytopeniaAnemia/Thrombocytopenia
•Fetal malformationsFetal malformations
(teratogenic)(teratogenic)
Genotype 2, 3Genotype 2, 3
Low pretreatment viral loadLow pretreatment viral load
Younger ageYounger ageAbsence of cirrhosisAbsence of cirrhosis
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Hepatitis C VirusHepatitis C VirusFate of Acute InfectionFate of Acute Infection
15%
Chronic
85%
Spontaneousresolution
Alter MJ, et al. N Eng J Med. 1999;341:556-562.
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Symptoms
anti-HCV
ALT
Normal
0 1 2 3 4 5 6 1 2 3 4
Hepatitis C Virus InfectionTypical Serologic Course
Titre
Months Years
Time after Exposure
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Hepatitis C Virus InfectionHepatitis C Virus InfectionNatural HistoryNatural History
Stable80% (68%)
HCCLiver failure25% (4%)
Slowlyprogressive75% (13%)
Resolved15% (15%)
Acute HCV
Cirrhosis20% (17%)
Chronic HCV85% (85%)
Liver cancer and liver failure occur in 4% of patients who are exposed to HCV over a 20- to 25-year period.
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Chronic Viral Hepatitis in Chronic Viral Hepatitis in PediatricsPediatrics
PreventionPrevention
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The Good News: Hepatitis BThe Good News: Hepatitis B (HBV)(HBV)
VaccineVaccineHBsAg recombinant DNA technology HBsAg recombinant DNA technology
90%-95% efficacy (anti-HBs titers 90%-95% efficacy (anti-HBs titers >> 10mIU/ml) 10mIU/ml)Long-term protection Long-term protection
Post Exposure Prophylaxis(PEP)Post Exposure Prophylaxis(PEP)Hep B Immunoglobulin(HBIG),passively acquired anti-HBs Hep B Immunoglobulin(HBIG),passively acquired anti-HBs
Infants born to HBsAg+ mothers Infants born to HBsAg+ mothers (HBIG & vaccine, efficacy 95% )(HBIG & vaccine, efficacy 95% )
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HBV: ACIP 2005 RecommendationsHBV: ACIP 2005 Recommendations
Birth Dose Birth Dose ““For all medically stable infants weighing ≥2,000 grams For all medically stable infants weighing ≥2,000 grams
at birth and born to HBsAg at birth and born to HBsAg negative negative mothers, the first mothers, the first
dose of HB vaccine should be administered before dose of HB vaccine should be administered before
hospital discharge.” hospital discharge.”
ACIP= Advisory committee of immunization practice
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HepatitisHepatitis C C Prevention Prevention The Less Good News:The Less Good News:
There is NO effective vaccineThere is NO effective vaccineBUT;BUT;
Spontaneous clearance of HCV can occur in Spontaneous clearance of HCV can occur in 20-30% of acute infections20-30% of acute infections
Immunity against persistent HCV can be acquiredImmunity against persistent HCV can be acquired
England K. J Pediatr. 147:227-32, 2005.
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Prevention HCVPrevention HCVImmune Correlates of Viral ClearanceImmune Correlates of Viral Clearance
Humoral Immunity Humoral Immunity Neutralizing antibodies, in vitro, are not necessary for Neutralizing antibodies, in vitro, are not necessary for
resolution of HCV infection.resolution of HCV infection.
Cellular ImmunityCellular Immunity Vigorous polyclonal CD4+ and CD8+ T-cell responses Vigorous polyclonal CD4+ and CD8+ T-cell responses
Weak and narrow in chronically infectedWeak and narrow in chronically infected
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HCVHCV Cellular Immune Response in Acute Cellular Immune Response in Acute
InfectionInfection
Bowen and Walker, Nature 2005
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HCV Prevention StrategyHCV Prevention Strategy
Increased screening and knowledge of HCV status Increased screening and knowledge of HCV status reduces HCV transmissionreduces HCV transmission
2/3 of people with chronic HCV are not 2/3 of people with chronic HCV are not diagnoseddiagnosed
10% of people with HCV infection have 10% of people with HCV infection have no recognized source for their infection no recognized source for their infection
Hagan 2001 Am J Pub HealthHagan 2001 Am J Pub Health
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73
HBsAg
RNA
δ antigen
Hepatitis D (Delta) Virus
Hepatitis D (HDV) ? (1977)
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Hepatitis DHepatitis D
Requires coexistent Hep BRequires coexistent Hep B CoinfectionCoinfection: does not worsen acute Hep B or : does not worsen acute Hep B or ⇑⇑
risk for chronic staterisk for chronic state SuperinfectionSuperinfection::
– usually develop chronic HDV infection.usually develop chronic HDV infection.– high risk of severe chronic liver disease.high risk of severe chronic liver disease.
Diagnosis: Anti-HDV IgMDiagnosis: Anti-HDV IgM
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75
Jaundice
Symptoms
ALTTotal anti-HDV
IgM anti-HDV
HDV RNA
HBsAg
HBV – HDV SuperinfectionTypical Serologic Course
Time after Exposure
Titre
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HBV-HDV Coinfection
Pre or post exposure prophylaxis to prevent HBV infection.
HBV-HDV Superinfection
Education to reduce risk behaviors among persons with chronic HBV infection.
Hepatitis D - Prevention
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Immune disordersImmune disorders
Autoimmune disease can affect the hepatocyte Autoimmune disease can affect the hepatocyte or bile duct or bile duct
And, is characterized by And, is characterized by The presence of The presence of autoantibodies autoantibodies Increased Increased Ig Ig levels.levels.
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DefinitionDefinitionAutoimmune HepatitisAutoimmune Hepatitis
Unresolving inflammation of the liver of unknown Unresolving inflammation of the liver of unknown cause.cause.
Reflect a complex interaction between Reflect a complex interaction between Triggering factorsTriggering factors :Infections, medications, toxins, :Infections, medications, toxins,
molecular mimicry?molecular mimicry?
AutoantigensAutoantigens Genetic predisposition:Genetic predisposition:Antigen presentation/immunocyte Antigen presentation/immunocyte
activation, DRB1,activation, DRB1, TNF*2A, TNF*2A, HLA B14, HLA DR3,DR4 HLA B14, HLA DR3,DR4
Immunoregulatory mechanismsImmunoregulatory mechanisms
Krawitt. N Engl J Med 2006;354:54
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Autoimmune HepatitisAutoimmune Hepatitis Characterized by the presence of interface Characterized by the presence of interface
hepatitis & portal plasma cell infiltration in hepatitis & portal plasma cell infiltration in histological examinationhistological examination
hypergammaglobulinaemia hypergammaglobulinaemia auto antibodiesauto antibodies
Manns et al. Hepatology 2006;43:S132
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epidemiologyepidemiology
In northern EuropeansIn northern Europeans Annual incidence 1.9/100,000Annual incidence 1.9/100,000 Prevalence 16.9/100,000Prevalence 16.9/100,000 2.6% of liver transplant2.6% of liver transplant Female affected more than males Female affected more than males
gender ratio 3.6:1gender ratio 3.6:1
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classificationclassification
3 main subtypes3 main subtypes
Based on difference in their Based on difference in their immunological immunological markersmarkers
Czaja et al. Hepatology 2002;36:479
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Type 1 AIHType 1 AIH The most common The most common
form of the disease form of the disease worldwideworldwide
Associated with Associated with ANAANA and/or and/or SMASMA
HLA DR3 & DR4HLA DR3 & DR4 Over 70% are Over 70% are
female and over female and over 40%40% younger age younger age groupgroup..
Czaja et al. Hepatology 2002;36:479
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Type 2 AIHType 2 AIH More common in More common in
Europe and south Europe and south America.America.
Associated with Associated with anti-LKManti-LKM
Described in Described in paediatrics patient paediatrics patient but in Europe 20% but in Europe 20% are adultsare adults
Krawitt. N Engl J Med 2006;354:54Czaja et al. Am J Gastroenterol 1995;90:1206
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Type 3 AIHType 3 AIH
Is the least Is the least established form of established form of the disease.the disease.
Associated with Associated with anti-SLA/LPanti-SLA/LP
ReclassificationReclassification: : Variant type 1 AIHVariant type 1 AIH
(soluble liver antigen/ liver-pancreas antigen)
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Diagnostic criteriaDiagnostic criteria
Diagnosis require presence of Diagnosis require presence of characteristics features characteristics features & & exclusion of other exclusion of other condition that resemble AIHcondition that resemble AIH
All patients must be evaluated for All patients must be evaluated for hereditaryhereditary, , infectiousinfectious and and drugdrug induced induced liver injury.liver injury.
Interface hepatitis Interface hepatitis is the histologic hall is the histologic hall mark of the syndrome & mark of the syndrome & portal plasma portal plasma infiltration typifies the disorder, but infiltration typifies the disorder, but neither neither are specific.are specific.
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Autoimmune HepatitisClinical Manifestations
Fatigue Fever Jaundice(+/-) RUQ pain Myalgia/arthralgia Anorexia Hepatosplenomegaly Spider angiomata Cushingoid features
Hirsuitism Acne Portal hypertension
– Ascites
– Varices– Encephalopathy
FHF HCC Asymptomatic
Desmet et al. Hepatology 1994;19:1513
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Autoimmune HepatitisExtrahepatic Autoimmune Diseases
Autoimmune thyroiditis
Grave’s disease Connective tissue
diseases Inflammatory bowel
disease Celiac disease Adrenal insufficiency
Autoimmune hematologic disorders
Type 1 DM Sjogren’s syndrome Fibrosing alveolitis Vitiligo Vasculitis Nephritis
Krawitt. N Engl J Med 2006;354:54Czaja et al. Hepatology 2002;36:479
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Interface hepatitis and bridging necrosis in severe type 1 autoimmune hepatitisInterface hepatitis and bridging necrosis in severe type 1 autoimmune hepatitis
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Autoimmune HepatitisHistology
Lymphoplasmacytic infiltrate
Interface hepatitis
Portal inflammation and invasion of limiting plate
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Plasma cell infiltration of the portal tracts in type 1 autoimmune hepatitisPlasma cell infiltration of the portal tracts in type 1 autoimmune hepatitis
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Autoimmune HepatitisCirrhosis to Hepatocellular Carcinoma
Netter’s Gastroenterology, 2nd ed., Elsevier Inc., 2010, all rights reserved
HCC
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The diagnosis of AIH requires The diagnosis of AIH requires
Determination of Determination of elevated aminotransferase elevated aminotransferase and and gamma globulins gamma globulins
Detection of Detection of ANAANA and/or and/or SMASMA or in their or in their absence, absence, anti-LKManti-LKM
liver tissue examinationliver tissue examination
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Indications for treatmentIndications for treatment
Czaja et al. Hepatology 2002;36:479
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Treatment regimensTreatment regimens
Two regimens comparable with each other Two regimens comparable with each other Prednisone alone orPrednisone alone orlower dose of prednisone in conjunction with lower dose of prednisone in conjunction with azathioprineazathioprineAll patients should be monitored for the All patients should be monitored for the development of drug side effectdevelopment of drug side effect
Czaja et al. Hepatology 2002;36:479Krawitt. N Engl J Med 2006;354:54
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Czaja et al. Hepatology 2002;36:479
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Autoimmune HepatitisAutoimmune HepatitisDisease RemissionDisease Remission
Disappearance of symptomsDisappearance of symptoms Normalization or near normalization of AST Normalization or near normalization of AST
to < 2 x ULNto < 2 x ULN GG and bilirubin: normalGG and bilirubin: normal Minimal or no hepatic inflammationMinimal or no hepatic inflammation
10 year survival: 90%10 year survival: 90%Czaja et al. Hepatology 2002;36:479Krawitt. N Engl J Med 2006;354:54
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relapserelapse
Relapse is common after drug withdrawalRelapse is common after drug withdrawal Patients Patients should be monitored should be monitored by serum by serum
aminotransferase ,bilirubin and gamma aminotransferase ,bilirubin and gamma globulin levelglobulin level
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IBD AS A CAUSE OF CHRONIC IBD AS A CAUSE OF CHRONIC LIVER DISEASESLIVER DISEASES
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Primary sclerosing cholangitis
• PSC is an idiopathic inflammatory disease resulting in intra and extra hepatic biliary strictures and cholestasis
cirrhosis;often assoc.with ulcerative cholitis
• It can occur in infancy and childhood
•This is a cholestatic disease whose etiology is unknown
• This disease differs from primary biliary cirrhosis in that the large bile ducts, the extra hepatic biliary tree ,are affected
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Symptoms:FatiguePruritisJaundiceFeverWeight loss
Diagnosis: Liver function tests CT scan Ultrasound ERCP is the diagnostic tool of choice. (Endoscopic retrograde cholangiopancreatography) Liver biopsy
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Immunosuppressants and steroids
Ursodeoxycholic acid Endoscopic dilation of dominant strictures, with or without stenting
Treatment
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Drug induced Chr. hepatitisDrug induced Chr. hepatitis
(Medication-induced liver diseases)(Medication-induced liver diseases) History of medicines , herbals and alternate History of medicines , herbals and alternate
medicinesmedicines
Mild to very severe hepatic dysfunctionMild to very severe hepatic dysfunction
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Drug induced chr. Liver DiseaseDrug induced chr. Liver Disease
Idiosyncratic reactionsIdiosyncratic reactions- - Isoniazid, sodium Isoniazid, sodium
valproate, phenytoinvalproate, phenytoin
Cholestatic reactionsCholestatic reactions- - Erythromycin, Erythromycin, phenothiazinesphenothiazines
Acute and chronic hepatitisAcute and chronic hepatitis – – Amiodarone, HIV drugs, Amiodarone, HIV drugs, àà methyl dopa methyl dopa
Discontinuation of the offending drug is the main line of therapy
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Metabolic and genetic disorders:Metabolic and genetic disorders: (a) Haemochromatosis(a) Haemochromatosis (b) Wilson’s disease(b) Wilson’s disease (c) (c) αα- antitrypsin deficiency- antitrypsin deficiency (d) Glycogen storage disease type IV(d) Glycogen storage disease type IV
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Thank youThank you