HEPATITIS

Dr.LeonardoBDairiSpPDKGEH

Manycausesofhepatitis
Infectious

Bacterial

Parasitic

Viral

Noninfectious

Leptospirosis
Syphillis
Tuberculosis
Toxoplasmosis
Amebiasis
EpsteinBarr
HerpesSimplex
VaricellaZoster
Coxsackievirus
Rubella
YellowFever
Alcohol
Drugs

Viralagentsthatprimarilyor
exclusivelyinfecttheliver
HepatitisAvirus

Infectioushepatitis

HepatitisBvirus

Serumhepatitis

HepatitisCvirus

Parenterallytransmitted

HepatitisEvirus

Entericallytransmitted

HepatitisDvirus

CoinfectionwithHBV

HepatitisGvirus

Parenterallytransmitted

ViralHepatitisHistoricalPerspective
Enterically
E
transmitted

Infectious A
Viral
hepatitis

NANB

Serum B D

Parenterally
C transmitted

F, G,
? other

ViralHepatitisOverview
Type of Hepatitis

A
Source of
virus
Route of
transmission
Chronic
infection
Prevention

feces

fecal-oral
no

blood/
blood/
blood/
blood-derivedblood-derived blood-derived
body fluids body fluids body fluids

E
feces

percutaneouspercutaneous percutaneous fecal-oral

permucosal permucosal permucosal
yes

yes

yes

no

pre/postpre/post- blood donor

pre/post- ensure safe
exposure
exposure
screening;
exposure
drinking
immunization immunization risk behavior immunization;
water
modification risk behavior
modification

Initiallaboratoryevaluationof
jaundicedpatient
TEST PERFORMED

MEASUREMENT

Urine bilirubin

Conjugated bilirubin

Serum bilirubin

Conjugated and
unconjugated bilirubin

Alanine aminotransferase (ALT) Hepatocellular damage

Aspartate aminotransferase
(AST)

Hepatocellular damage

Alkaline phosphatase

Intrahepatic or extrahepatic
obstruction

Prothrombin time, partial

thromboplastin time, platelet
count, bleeding

Clotting mechanism

Blood count with blood smear

exam

Red blood cell morphology,

parasites, atypical
lymphocytes

HEPATITIS
A

 RNA Picornavirus

Single serotype worldwide

Acute disease and asymptomatic
infection

No chronic infection

Protective antibodies develop in

response to infection - confers lifelong
immunity

ACUTE HEPATITIS A CASE

DEFINITION FOR SURVEILLANCE
Clinical criteria

An acute :
discrete onset of symptoms (e.g. fatigue, abdominal
pain, loss of appetite, nausea, vomiting),
jaundice or elevated serum aminotransferase levels
Never chronic
Adults often feel unwell for 6 weeks
Laboratory criteria

IgM antibody to hepatitis A virus (anti-HAV) positive

HAVCLINICALSYNDROMES
Incubation phase: long (6weeks-6month)
Prodromal phase: insidious
Flu-like: malaise, fatigue, anorexia, nausea,
abdominal discomfort, chills
Icteric phase: liver damage: jaundice, dark
urine, pale stools
Recovery: decline in fever; renewed appetite

HEPATITISACLINICALFEATURES
Jaundice by

<6 yrs
6-14 yrs
>14 yrs

Rare complications:

Fulminant hepatitis
Cholestatic hepatitis
Relapsing hepatitis

Incubation period:

Average 30 days
Range 15-50 days

Chronic sequelae:

None

age group:

<10%
40%-50%
70%-80%

EVENTSINHEPATITISAVIRUSINFECTION
Clinical illness

Infection

ALT

Response

IgM

IgG

Viremia

HAV in stool

Week

10

11

12

13

CONCENTRATIONOFHEPATITISAVIRUS
INVARIOUSBODYFLUIDS
Body Fluids

Feces
Serum
Saliva
Urine

100

102

104

106

Infectious Doses per mL

Source:

Viral Hepatitis and Liver Disease 1984;9-22

J Infect Dis 1989;160:887-890

108

1010

GLOBALPATTERNSOF
HEPATITISAVIRUSTRANSMISSION

Hi

Rate
Diseas
es
Low to high

Peak Age
of
Infection
Early childhood

Moderate

High

Late childhood/
young adults

Person to person;
food and waterborne
outbreaks

Low

Young adults

Very low

Adult

Person to person;
food and waterborne
outbreaks
Travelers; outbreaks
uncommon

Endemiciy

Low
Very low

Transmission
Patterns
Person to person;
outbreaks uncommon

GEOGRAPHIC DISTRIBUTION OF
HEPATITIS A VIRUS INFECTION

HEPATITIS A VIRUS TRANSMISSION

Close personal contact
(e.g., household contact, sex
contact, child day-care centers)
Contaminated food, water
(e.g., infected food handlers)
Blood exposure (rare)
(e.g., injection drug use, rarely by
transfusion)

MANAGEMENT HEPATITIS A
Nospecifictreatment
Symptomatis
Prednisolone40mgPOdaily,taperingoff(2
4)weeks
Preventionisbetterthancure

PREVENTING HEPATITIS A
Hygiene(e.g.,handwashing)
Sanitation(e.g.,cleanwatersources)
HepatitisAvaccine(preexposure)
Immuneglobulin(preandpostexposure)

HEPATITIS A VACCINES
Highly immunogenic
97%-100% of children, adolescents, and adults have

protective levels of antibody within 1 month of

receiving first dose; essentially 100% have protective
levels after second dose

Highly efficacious
In published studies, 94%-100% of children protected

against clinical hepatitis A after equivalent of one

dose

HEPATITIS A VACCINE EFFICACY STUDIES

Site/
Age Group

HAVRIX
(GSK)
2 doses
360 EL.U.

Thailand

38,157

VAQTA
(Merck)
1 dose
25 units

New York

Vaccine

1-16 yrs

2-16 yrs

JAMA 1994;271:1363-4; N Engl J Med 1992;327:453-7

Vaccine Efficacy
(95 % Cl)

94%
(79%-99%)

1,037

100%
(85%-100%)

DURATION OF PROTECTION AFTER

HEPATITIS A VACCINATION
Persistence of antibody

At least 5-8 years among adults and children

Efficacy

No cases in vaccinated children at 5-6 years

of follow-up

Mathematical models of antibody decline

suggest protective antibody levels persist
for at least 20 years
Other mechanisms, such as cellular
memory, may contribute

COMBINED HEPATITIS A HEPATITIS B

VACCINE
Twinrix, Approved by the FDA in United States for
persons >18 years old, contains 720 EL.U. hepatitis A
antigen and 20 g. HBsAg
Vaccination schedule: 0,1,6 months
Immunogenicity similar to single-antigen vaccines given
separately
Can be used in persons > 18 years old who need
vaccination against both hepatitis A and B
Formulation for children available in many other
countries

HEPATITIS A PREVENTION
IMMUNE GLOBULIN
Pre-exposure

travelers to intermediate and high

HAV-endemic regions

Post-exposure (within 14 days)

Routine
household and other intimate contacts
Selected situations
institutions (e.g., day-care centers)
common source exposure (e.g.,
food prepared by infected food handler)

SAFETY OF HEPATITIS A VACCINE

Most common side effects
Soreness/tenderness at injection site - 50%
Headache - 15%
Malaise - 7%
No severe adverse reactions attributed to vaccine
Safety in pregnancy not determined risk likely low
Contraindications - severe adverse reaction to previous
dose or allergy to a vaccine component
No special precautions for immunocompromised
persons

HEPATITISB

HBV

HBV

1/3worldspopulation
infected
350millionchronic
infected.

Acute/fulminant
Inactivecarrierstate
ChronicHepatits
Livercirrhosis
HepatocellularCarcinoma.

HBV,GlobalHealthProblem
HBsAg
Positif, %
Taiwan

10.0-13.8

Vietnam

5.7-10.0

China

5.3-12.0

Africa

5.0-19.0

Philippines

5.0-16.0

Thailand

4.6-8.0

Japan

4.4-13.0

Indonesia

4.0

South Korea

2.6-5.1

India

2.4-4.7

High ( 8%)

Russia

1.4-8.0

Intermediate (2% to 8%)

US

0.2-0.5

Prevalensi HBsAg

Low (< 2%)

Mast EE, et al. MMWR Recomm Rep. 2006;55:1-33.
Custer B, et al. J Clin Gastroenterol. 2004;38(10 suppl):S158S168.

8genotypes(AH):

and

Moreadvancedliverdisease
Lowerresponseratetointerferon
GreaterriskofHCCdevelopment.

HBVnomenclature
HBV:hepatitisBvirus
HBsAg:hepatitisBvirussurfaceantigen
HBcAg:hepatitisBviruscoreantigen

HepatitisBVirus(HBV)
3213

S1
pre polymerase

157

Domain Reverse
transcriptase/ DNA
polymerase mengalami
overlap dengan gen
permukaan

56
8
2

preS2

4 overlapping open
reading frames

2458

D
YM

EcoRI
3221, 1

DR1

(-)

re
co

19
03

pre
co

183
7

re

834

230

(+)

A er
RN im
DR2 pr

1622
1816

7
13

Ditemukan dalam darah

dan cairan tubuh
cccDNA

MMWR.2003;52:133.OttMJandArudaM.JPediatrHealthCare.1999;13:211216.
RibeiroRM,etal.MicrobesandInfection.2002;4:829835.

NATURALCOURSEOFCHRONICHBV
INFECTIONS
The HBV three detectable antigens :
1. HBsAg Surface antigen
2. HbcAg Core antigen
3. HBeAg e antigen
Chronic infection HBsag persistence for more than 6
months
HBsAg non infectious
HBcAg represents the nucleocapsid of the virus
presence indicates infectivity, found in the liver not in
the serum.
HBeAg found in the serum
a. Viral replication
b. Infectivity

Modes of Transmission
Transfusion
(blood, blood
products)

Fluids
(blood, semen)

Tattoos; Body Mother to infant

piercing

Hepatitis B

Organs &
tissue
transplantation

Shared needles
& syringes

Child to child

HBVCLINICALSYNDROMES
ACUTE INFECTION
Incubation phase: long (6weeks-6month)
Prodromal phase: insidious
Flu-like: malaise, fatigue, anorexia, nausea, abdominal
discomfort, chills

Icteric phase: liver damage: jaundice, dark urine, pale

stools
Recovery: decline in fever; renewed appetite

FaseInfeksiKronikHepatitisB
Increasing age
HBeAg+/antiHBe

HBeAg - / anti-HBe +

HBV DNA
ALT
FASE IMMUNE
TOLERANCE

FASE IMMUNE
CLEARANCE

FASE INACTIVE
CARRIER HBsAg

Fattovich G. J Hepatol 2003;39(suppl 1):S50-S58.

FASE REACTIVATION

Monitor HBV DNA and ALT/ 3-6 month

No to treat

FaseInfeksiKronikHepatitisB
Increasing age
HBeAg+/antiHBe

HBeAg - / anti-HBe +

HBV DNA
ALT
FASE IMMUNE
TOLERANCE

FASE IMMUNE
CLEARANCE

FASE INACTIVE
CARRIER HBsAg

FASE REACTIVATION

Rekomendation to
treat

Fattovich G. J Hepatol 2003;39(suppl 1):S50-S58.

FaseInfeksiKronikHepatitisB
Increasing age
HBeAg+/antiHBe

HBeAg - / anti-HBe +

HBV DNA
ALT
FASE IMMUNE
TOLERANCE

FASE IMMUNE
CLEARANCE

Monitor HBV DNA and ALT/3-6 month

No to treat

Fattovich G. J Hepatol 2003;39(suppl 1):S50-S58.

FASE INACTIVE
CARRIER HBsAg

FASE REACTIVATION

FaseInfeksiKronikHepatitisB
Increasing age
HBeAg+/antiHBe

HBeAg - / anti-HBe +

HBV DNA
ALT
FASE IMMUNE
TOLERANCE

FASE IMMUNE
CLEARANCE

FASE INACTIVE
CARRIER HBsAg

Rekomendation to
treat

Fattovich G. J Hepatol 2003;39(suppl 1):S50-S58.

FASE REACTIVATION

41

HBVDIAGNOSIS
CLINICALL
LABORATORY
Liverenzymes
Serology
HBeAg,HBcAg,virus:activeinfection
AntiHBcIgM:acuteactiveinfection
AntiHBeIgG:acuteinfection

Healthy Liver

Hepatic Fibrosis

Cirrhosis

Liver Cancer

Healthy Liver

Hepatic Fibrosis

Cirrhosis

Liver Cancer

HBV Complications
Chronic HBsAg antigenemia
Chronic persistent hepatitis (CPH)
Chronic active hepatitis (CAH)
Chronic lobular hepatitis (CLH)
Liver cirrhosis
Hepatocellular carcinoma

MANAGEMENT HBV
PREVENTION OF LIVER
CIRRHOSIS,HEPATOMA
AND MORTALITY

Supretion
replikation of
HBV

MANAGEMENT
1. Evaluation of the disease
2. Non-specific/specific therapy
3. Monitoring and surveillance
The diagnosis of CHB infection HBsAg at least 6
month
HBeAg and Anti-HBe Viral replication and thus
infectivity.
ALT/AST measured inflammation
Liver Biopsy is more accurate
USG/Fibro Scan parenchymal impairment, fibrosis
Early cirrhosis ussually not detected by ultrasound

MANAGEMENT
Non-spesific advice
General advice
CHB infection potentially infectious should not share
toothbrushes or shaving equipment
Household contacts and sexual partners should have their hepatitis
serology determined and should be immunized if found negative
for HBsAg, anti-HBs and anti HBc
When a woman becomes pregnant inform her gynecologist
about her HBV status appropriate steps can be taken to
immunize her baby at birth
A Baby born to HBeAg-positive mother should be given hepatitis B
immune-globulin at the same time

MANAGEMENT
Diet
Nutritious diet to maintain normal body weight
May be needed protein, salt and water restriction
Exercise
Subjects with asymptomatic infection should
continue their regular form of exercise
With cirrhosis should avoid strenuous jogging and
heavy weight lifting

MANAGEMENT
Alcohol and Drugs
Should be avoided Potentially hepatotoxic
agents or regular alcohol intake, steroids and
immunosuppressive agents
In Endemic countries patients need steroids or
immunosuppressive drugs,HBV status checked to
prevent HBV flares.

55

TreatmentofChronicHepatitisB
Drugs for Chronic HBV inf
1.
2.
3.
4.
5.
6.
7.
8.
9.

Interferon Alfa 2b ( 1992)

Peginterferon Alfa 2a ( 5/2005 )
Lamivudin ( 1998 )
Adifovir dipivoxil ( 2002 )
Entecavir ( 3/ 2005 )
Tenofovir
Telbivudine ( 2/2007)
Emtricitabine
Cleovudine

Pemberian terapi imunomodulator atau nucleoside analog b

ergantung kepada :
1. Genotipe HBV
2. Kadar ALT
3. Kadar serum HBV DNA
4. Sirosis kompensasi atau dekompensasi
5. Resistensi Obat
6. Cost effective

PhasesofChronicHBVInfection:
CandidatesforTherapy
Phases of Chronic HBV Infection
Immune
Tolerance

Immune Clearance/
HBeAg-Positive
CHB

Nonreplicative
(Inactive Carrier)

Reactivation/
HBeAg-Negative
CHB

HBV DNA,
IU/mL

105 - 1010

104 - 1010

< 104

103 - 108

HBeAg

HBeAg+

HBeAg+

HBeAg-

HBeAg-

ALT

Normal

High or fluctuating

Normal

High or fluctuating

--

Active inflammation
on liver biopsy

HBsAg may
become
undetectable

Active inflammation
on liver biopsy

No

Yes

No

Yes

Other
Candidates
for therapy?

YimHJ,etal.Hepatology.2006;43:S173S181.

RekomendationtreatmentpatientHBeAg(+)/(APASL2008)

RekomendationTreatmentPatientHBeAg()/(APASL2008)

RekomendationTreatmentPasientCirrhosis(APASL2008)

Yun FL et al Liver Int 2005;25:472

Yun FL.et al Guidelines for HBV management, APASL

61

RekomendasiterapidariEASL(European
AssociationfortheStudyoftheLiver)2009
IndikasiterapisamauntukpasienHBeAg(+)danHBeAg
().Memenuhi3kriteria:kadarserumHBVDNA,kadar
serumaminotransferase&grade/tingkathistologi.
PasiendapatditerapibilakadarHBVDNA>2000IU/ml
(10.000 kopi/ml) dan atau kadar ALT diatas BANN, dan
biopsi hati menunjukkan moderate sampai severe necro
inflammation dan atau fibrosis memakai sistim skor
standar (contoh paling sedikit grade A2 atau tingkat F2
skorMETAVIR.
62

HBV Prevention
Screenbloodproducts
Sterilizationofneedles,etc.
Avoidingintimatecontact,e.g.,
householdorsexualcontacts
Vaccination

HEPATITIS
FULMINANT

HEPATITIS FULMINANT

Hepaticfailurewithin23weeks.
Reactivationofchronicoracutehepatitis
Massivenecrosis,shrinkage,wrinkled
Collapsedreticulinnetwork
Onlyportaltractsvisible
Littleormassiveinflammation
Morethanaweekregenerativeactivity
Completerecoveryorcirrhosis.

ACUTE LIVER FAILURE, acute liver disease

with clinically jaundice to encephalopathy
progresive rapidly
FULMINANT HEPATIC FAILURE, acute liver
failure with hepatic encephalopathy,develoving
less than 2 weeks or 8 weeks after onset
jaundice
SUBFULMINANT HEPATIC FAILURE, acute
liver disease with hepatic
encepalopathy,develoving from 2/8 weeks to 3/6
month onset jaundice

OGRADY dkk :
Basedliverfailure,onsetofjaundice,encepalopathy
HYPERACUTE LIVER FAILURE,intervalless
than7days
ACUTE LIVER FAILURE,interval8and28days
SUBACUTE LIVER FAILURE,intervalbetween
5and12weeks

Clinical features
ICKTERUS PROGRESIF
BILIRUBIN > 20mg %
NAUSEA,MALAISE,VOMITING,FEVER.LIVER
SIZE SMALL.COMA MAY RAPIDLY (FEWDAYS).
TACHYCARDIA,HYPOTENSION,HYPERVENTILAT
ION ,CEREBERAL OEDEME ARE LATER
FEATURES
PROLONG PROTROMBIN TIME,ALT/AST
INCREASE

IMUNOPATOGENESE DARI FULMINAN HEPATITIS

ETIOLOGI
VIRAL HEMORAGIC FEVER VIRUS
HEPATITIS VIRUS
SITOMEGALOVIRUS
HEPATITIS A
HERPES SIMPLEX VIRUS
HEPATITIS B
EPSTEIN BARR VIRUS
HEPATITIS C
PARAMIXOVIRUS
HEPATITS E
ADENOVIRUS
HEPATITIS G
DRUG/ TOXIN,
HALOTHANE
ISCHEMIC
ACETAMINOFEN
ISCHEMIC HEPATITIS
ISONIAZID-RIFAMPICIN
SURGICAL SHOCK
ANTIDEPRESANT
ACUTE BUCCHIARY SYNDROME
NSAID
VALPROIC ACID
MISCELLANEUS (RARE)
MUSHROOM POISONING
HEAT STROKR
HERBAL REMEDIES
SEVERE BACTERIAL INFECTION
AMANITA POISONING
MASSIVE MALIGNANT INFILT.
YELLOW PHOSPORUS
BACILLUS CEREUS EMETIC TOXIN
PREGNANCY RELATED
ACUTE FATTY LIVER OF PREGNANCY
HELLP SINDROME

MANAGEMENT
FARMAKOLOGI

N-ASETIL SISTEIN
PROSTAGLANDIN
HAEMOPERFUSI ARANG
KOLOUMN HEPATOSIT

MOLEKULER

REGULASI SITOKIN
REGULASI KASKADE KOAGULASI
INHIBISI APOPTOSIS
HEPATOSIT GROWTH FACTOR
HEPATOSIT TRANSPLANT

TRANSPLANTASI
LIVER TRANSPLANT

HEPATITISC

Introduction
Hepatitis C virus (HCV) infection is one of the main
causes of chronic liver disease worldwide
The long-term hepatic impact of HCV infection is
highly variable, from minimal changes to chronic
hepatitis, extensive fibrosis, and cirrhosis with or
without hepatocellular carcinoma (HCC)

Introduction
Prior to the 1990s, the principal routes of HCV infection
were via blood transfusion, unsafe injection procedures,
and intravenous drug use.

Currently, new HCV infections are primarily due to

intravenous or nasal drug use, and to a lesser degree to
unsafe medical or surgical procedures. Parenteral
transmission via tattooing or acupuncture with unsafe
materials is also implicated in occasional transmissions.

Natural History of HCV Infection

Acute HCV

Chronic HCV
60% to 85%

Resolved
15% to
40%

Cirrhosis
10% to 15%
After 20
yrs

Stable
25%
Slowly
progressiv
e
75%

NIH Management of Hepatitis C Consensus

Conference Statement. June 10-12, 2002. Available
at:
http://consensus.nih.gov/2002/2002HepatitisC2002
116html. Accessed April 10, 2007.

HCC, liver failure

25% of cirrhotics
(2% to 4% overall
3%pa after 2025yrs)

Progression of liver disease in chronic

hepatitis C
Chronic hepatitis
mild
moderate
severe fibrosis
Liver
cirrhosis
Endstage liver disease
0

HCC

10

20
Time after infection

HepatitisCVirusInfection
PopulationatRisk
Transfusionofbloodproductsbefore1992
Intravenousdruguse
Nasalinhalationofcocaine
Chronicrenalfailureondialysis
Incarceration
Occupationalexposuretobloodproducts
Transplantationofanorgan/tissuegraftfromanHCV
positivedonor

Bodypiercingandpotentiallytattoo

Centers for Disease Control and Prevention. Hepatitis C fact sheet. Available at:
http://www.cdc.gov/ncidod/diseases/hepatitis/c/fact.htm. Accessed February 1,
2006.

HCVRiskFactors

receivedblood,bloodproducts,or
anorgantransplantpriorto1992
ever,evenonce,shareddrug
paraphernalia
everbeenstuckbyausedblood
needle
beenonkidneydialysis
hadatattooorbodypiercing
hadmultiplesexpartners,or
sexualactivitythatinvolved
contactwithblood
sharedpersonalcareitems(razors,
toothbrushes,etc.)withother
people
combatveteran

Chronic hepatitis C infection

HCVaffectsabout2%oftheworldpopulationand
approximately300millionpeopleareinfected.
Themajoritytransmittedparenterally
Upto80%willdevelopchronicinfection
Patientswithchronicdiseasewilldevelopcirrhosisover
20to30yearsproportionofthemwilldevelopPHC.
CoinfectionwithHBVandHCVincreasestheriskof
developingPHC.

Factors Promoting Progression of

severity CHC
Increasedalcoholintake
Age>40yearsattimeofinfection
HIVcoinfection
Other

Malegender
ChronicHBVcoinfection

Serologic Pattern of Acute HCV Infection

with Recovery
antiHCV

Symptoms +/-

Titer

HCV RNA

ALT

Normal
0

3
4
Months

2
3
Years

Time after exposure

HCV Prevention and Control

Reduce or Eliminate Risks for

Acquiring HCV Infection
Screenandtestdonors
Virusinactivationofplasmaderivedproducts
Riskreductioncounselingandservices
Obtainhistoryofhighriskdrug&sexbehaviors
Provideinformationonminimizingriskybehavior,including
referraltootherservices
VaccinateagainsthepatitisAand/orhepatitisB
Safeinjectionandinfectioncontrolpractices

HCV Counseling

Preventing HCV Transmission to

Others
Avoid Direct Exposure to Blood

Donotdonateblood,bodyorgans,other
tissueorsemen
Donotshareitemsthatmighthaveblood
onthem
personalcare(e.g.,razor,toothbrush)
hometherapy(e.g.,needles)

Covercutsandsoresontheskin

HCV Counseling

Other Transmission Issues

HCVnotspreadbykissing,hugging,sneezing,
coughing,foodorwater,sharingeatingutensils
ordrinkingglasses,orcasualcontact
Donotexcludefromwork,school,play,child
careorothersettingsbasedonHCVinfection
status

HCV Diagnosis

Mostpatientsasymptomatic
Abnormalliverfunctiontests;AST/ALT
HepatitisCantibody(EIA)
RIBA
HCVRNAlevels
Liverbiopsy:gradeandstagedamage

Diagnosis Hepatitis C
Kelompok resiko tinggi / terpapar darah yang diduga
terkontaminasi HCV: skrining Anti-HCV

Quantitative assays

Anti-HCV positif

Qualitative assays
High sensitivity
( 50 IU/mL)

Detection cutoff >

qualitative

Berapa banyak HCV yang

Jika positif

Apakah ada HCV?

Genoty
pe
assays
Apa tipe HCV yang ada?

Kriteria Diagnostik Infeksi HCV:

Hepatitis C Akut

Hepatitis C Kronik

1. Diketahui paparan < 6

bulan*
2. Anti-HCV positif / negatif
3. HCV RNA positif
4. ALT meningkat

1. Anti-HCV positif > 6 bulan

2. HCV RNA positif
3. ALT meningkat / normal

* Operasi / transfusi / trauma

dll.

Gejala & tanda biasanya ringan / tidak khas

(asimtomatik)
Singkirkan penyebab lain (virus, obat,
autoimunitas)

DiagnosisofChronicViralHepatitis:
SerologicTesting
PatientsshouldbetestedforHCVandHBV
ifthey:

haveknownriskfactorsforviralhepatitis
indicatepossibleriskfactorsforhepatitis
haveelevatedliverenzymes
expressadesiretoknowtheirHCVand/orHBV
status

Management of Hepatitis C NH Consensus Statement, 1997.

ChronicHCVInfection:Recommendedpretreatment
evaluation
Test

Purpose

HCV-RNA by PCR

Confirm viremia.

Serum albumin, bilirubin, PT

Assess liver function.

Iron, transferrin, ferritin

Assess for iron overload.

Antinuclear antibody

Detect autoimmune hepatitis.

1- Antitrypsin phenotype

Detect 1- antitrypsin deficiency.

Ceruloplasmin (age<45 years)

Detect Wilson disease.

HBsAg, HIV antibody test

Detect viral coinfection.

Hepatitis C genotype

Assess likelihood of response to

therapy.

Liver biopsy

Determine severity of disease

and urgency for therapy.

Hepatitis B surface antibody

Determine need for hepatitis B

vaccination.

Hepatitis A antibody (total)

Determine need for hepatitis A

vaccination.

Peter R.McNally:GI/Liver Secret plus 4th ed.2010

Therapeutic goals in CHC

Eradication of the viral infection
Diminution of viremia and infectivity
Diminution of the severity of hepatitis
Diminution of fibrogenesis and
progression
Prevention of complications of cirrhosis
Delay in development of HCC

HCV Therapy
Pegylated Interferon injections weekly
AND
Ribavirin pills (or liquid) twice daily

HEPATITISD

HEPATITIS AKUT - D
Terdeteksi bersamaan dengan virus Hepatitis B.
Prevalensi HDV (+) berhubungan dengan
prevalensi infeksi HBV (+).
HDV lebih dominan didaerah tropikal dan
subtropik,di
negara berkembang drpd negara
maju (Barat).
Klinis bervariasi dr asimptomatis sampai berat
80% kasus kronik hepatitis D menjadi sirosis
dalam
5-10 tahun.
Gold standard d/: HDV RNA (+) atau HDAg (+)
liver.

Transmisisi ,Parenteral contant, seksual,

transfusi,needle,Hemodyalisa
Prevalence, less than 5% carier HbsAg
Clinical finding, acute HBV-HDV coinfection, severe
hepatitis withhepatocelluler necrosis and
inflammation,Chronic.
Chronic HBV-HDV infection,initial severe liver
disesase,may be chronic healthy carrier state similar
with HBV chronic
Diagnosa , Anti HDV (+) IgM /IgG,in the presence
Hepatitis B patient
Therapi ,is problematic, initial Interferron alpha result in
clinical and biochemical respons,but relaps are common

HEPATITISE

HEPATITIS E
Nonenveloped spherical RNA virus
Transmission fecal oral,main target
hepatocyte
Endemic in India,Southeast and Central Asia
The largest affected in young adult (15-40 years)
Incubation period 2 10 weeks
Clinical same with HepatitisA,but generrally
more severe
Diagnosed presence anti HEV (+) / IgG or IgM,
HEV RNA (+)
TREAEMENT,supportive and no effective vaccine
available
Prvention,improved sanitation,sanitary
handling,food,water, boil of water

HEPATITISG

HEPATITIS G

Termasuk Flava virus.

Terdistribusi secara luas.

Ditularkan melalui parenteral, seksual
dan perinatal.
HGV RNA dideteksi dengan PCR.
HGV tidak mempengaruhi respon untuk terapi
antiviral.

DILD

Drug-induced chronic hepatitis

Many drugs including herbal products
can cause acute hepatotoxicity will induce
chronic hepatitis with prolonged
administration.
These include gold, isoniazid,
ketoconazole, methyldopa, nitrofuratoin,
phenylbutazone and silfonamides.
Oxyphenisatin the first agent known to
be associated with chronic hepatitis.
Older females are affected more frequently.

Wilsons disease
It is important to exclude wilsons disease
as a cause of chronic hepatitis when it
apprears in patients younger than 35 years.
Liver disease often precedes symptoms
attributed to central nervous system
involvement and the appearance of KayserFleischer rings and may be the initial
presentation in 50 % of cases.
Elevated urinary and hepatic copper levels
are diagnostic.
Improvement may be achieved by early
treatment with D-penicillamine.

Autoimmune chronic
hepatitis

This condition is relatively rare locally and

usually affects young woman.
Lipoid hepatitis positive lupus
erythematosus (LE) cell test 15 %
This is not the same as classical systemic
lupus erythematosus (SLE) as the liver is
typically not involved in SLE.
The etiology is not fully understood but
genetic factors influence susceptibility and
multiple viruses (including hepatitis C) and
drugs can trigger the disease.
Extrahepatic manifestations are prominent :
amenorhea, acne, striae,hirsutis,obesity,
cushingoid facies