HEPATITIS

Dr. Leonardo B Dairi SpPD KGEH

 Many causes of hepatitis
Leptospirosis
Infectious Bacterial Syphillis
Tuberculosis
Toxoplasmosis
Parasitic Amebiasis
Epstein Barr
Herpes Simplex
Viral Varicella Zoster
Coxsackievirus
Rubella
Yellow Fever
Alcohol
Noninfectious Drugs
 Viral agents that primarily or
exclusively infect the liver
Hepatitis A virus Infectious hepatitis
Hepatitis B virus Serum hepatitis
Hepatitis C virus Parenterally transmitted
Hepatitis E virus Enterically transmitted
Hepatitis D virus Coinfection with HBV
Hepatitis G virus Parenterally transmitted
 Viral Hepatitis - Historical
Perspective
“Infectious” A Enterically
E
transmitted

Viral hepatitis NANB

Parenterally
“Serum” B D C transmitted
F, G,
? other
 Viral Hepatitis - Overview
Type of Hepatitis

A
A B C
C D E
E
Source of feces blood/ blood/ blood/ feces
virus blood-derivedblood-derived blood-derived
body fluids body fluids body fluids
Route of fecal-oral percutaneouspercutaneous percutaneous fecal-oral
transmission permucosal permucosal permucosal

Chronic no yes yes yes no

infection

Prevention pre/post- pre/post- blood donor pre/post- ensure safe

exposure exposure screening; exposure drinking
immunization immunization risk behavior immunization; water
modification risk behavior
modification
 Initial laboratory evaluation of jaundiced
patient
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 Clotting mechanism
thromboplastin time, platelet
count, bleeding
Blood count with blood smear Red blood cell morphology,
exam 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), and
• jaundice or elevated serum aminotransferase levels

– Laboratory criteria
• IgM antibody to hepatitis A virus (anti-HAV) positive
 HEPATITIS A - CLINICAL FEATURES

•Jaundice by <6 yrs <10%

age group: 6-14 yrs 40%-50%
>14 yrs 70%-80%
•Rare complications: Fulminant hepatitis
Cholestatic hepatitis
Relapsing hepatitis

•Incubation period: Average 30 days

Range 15-50 days

•Chronic sequelae: None

EVENTS IN HEPATITIS A VIRUS INFECTION
Clinical illness

Infection ALT

IgM IgG
Response

Viremia

HAV in stool

0 1 2 3 4 5 6 7 8 9 10 11 12 13
Week
 CONCENTRATION OF HEPATITIS A VIRUS
IN VARIOUS BODY FLUIDS
Feces
Body Fluids

Serum

Saliva

Urine

100 102 104 106 108 1010

Infectious Doses per mL
Source: Viral Hepatitis and Liver Disease 1984;9-22
J Infect Dis 1989;160:887-890
 GLOBAL PATTERNS OF
HEPATITIS A VIRUS TRANSMISSION
Rate Peak Age Transmission
Endemiciy
Diseas of Patterns
es Infection
Hi Low to high Early childhood Person to person;
outbreaks uncommon
Moderate High Late childhood/ Person to person;
young adults food and waterborne
outbreaks
Low Low Young adults Person to person;
food and waterborne
outbreaks
Very Very Adult Travelers; outbreaks
low low 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)
 PREVENTING HEPATITIS A

• Hygiene (e.g., hand washing)

• Sanitation (e.g., clean water sources)
• Hepatitis A vaccine (pre-exposure)
• Immune globulin (pre- and post-exposure)
 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/ Vaccine Efficacy

Age Group (95 % Cl)
Vaccine N

HAVRIX  Thailand 38,157 94%

(GSK) 1-16 yrs (79%-99%)
2 doses
360 EL.U.

VAQTA  New York 1,037 100%

(Merck) 2-16 yrs (85%-100%)
1 dose
25 units

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

 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

 Approved by the FDA in United States for persons >18

years old Contains 720 EL.U. hepatitis A antigen and
20 μg. 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
HEPATITIS B
HBV •
•
1/3 world’s population infected
350 million chronic infected.

•Acute / fulminant
HBV •Inactive carrier state
•Chronic Hepatits
•Liver cirrhosis
•Hepatocellular Carcinoma.
 HBV
A Global Health Problem

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
Prevalensi HBsAg
India 2.4-4.7
High (≥ 8%)
Russia 1.4-8.0
Intermediate (2% to 8%)
US 0.2-0.5
Low (< 2%)

Mast EE, et al. MMWR Recomm Rep. 2006;55:1-33.

Custer B, et al. J Clin Gastroenterol. 2004;38(10 suppl):S158-S168.
8 genotypes (A-H) :
C and
B
•More advanced liver disease
•Lower response rate to interferon
•Greater risk of HCC development.
 HBV nomenclature

• HBV: hepatitis B virus

• HBsAg: hepatitis B virus surface antigen
• HBcAg: hepatitis B virus core antigen
 Hepatitis B Virus (HBV)

 4 overlapping open reading

3213 157 frames
preS2
S1
pre polymerase
56  Domain Reverse transcriptase/
28
DNA polymerase mengalami
S
EcoRI
3221, 1 overlap dengan gen
2 458

YM

permukaan
DDD

 Ditemukan dalam darah dan

834

(+) cairan tubuh

230 cor

r
R NAAme
R i
(-) DR1 R22 p
DR r
9

19  cccDNA
03
e

p
pre 1622 76
co r
e 13
183 181 6
7
X

MMWR. 2003;52:1-33. Ott MJ and Aruda M. J Pediatr Health Care. 1999;13:211-216.

Ribeiro RM, et al. Microbes and Infection. 2002;4:829-835.
 NATURAL COURSE OF CHRONIC HBV
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 Tattoos; Body Mother to infant
(blood, blood piercing
products)

Shared needles
Fluids Hepatitis B & syringes
(blood, semen)

Organs & Child to child

tissue transplantation
 HBV CLINICAL SYNDROMES

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
 Fase Infeksi Kronik Hepatitis B

Increasing age

HBeAg+/antiHBe – HBeAg - / anti-HBe +

HBV DNA

ALT

FASE IMMUNE FASE IMMUNE FASE INACTIVE FASE

TOLERANCE CLEARANCE CARRIER HBsAg REACTIVATION

• Monitor HBV DNA and ALT/ 3-6 month

• No to treat

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

 Fase Infeksi Kronik Hepatitis B

Increasing age

HBeAg+/antiHBe – HBeAg - / anti-HBe +

HBV DNA

ALT

FASE IMMUNE FASE IMMUNE FASE INACTIVE FASE

TOLERANCE CLEARANCE CARRIER HBsAg REACTIVATION

Rekomendation
to treat

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

 Fase Infeksi Kronik Hepatitis B

Increasing age

HBeAg+/antiHBe – HBeAg - / anti-HBe +

HBV DNA

ALT

FASE IMMUNE FASE IMMUNE FASE INACTIVE FASE

TOLERANCE CLEARANCE CARRIER HBsAg REACTIVATION

•Monitor HBV DNA and ALT/3-6 month

•No to treat

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

 Fase Infeksi Kronik Hepatitis B

Increasing age

HBeAg+/antiHBe – HBeAg - / anti-HBe +

HBV DNA

ALT

FASE IMMUNE FASE IMMUNE FASE INACTIVE FASE

TOLERANCE CLEARANCE CARRIER HBsAg REACTIVATION

Rekomendation to
treat

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

39
 HBV DIAGNOSIS

• CLINICALL
• LABORATORY
– Liver enzymes
– Serology
• HBeAg, HBcAg, virus: active infection
• Anti-HBc IgM: acute active infection
• Anti-HBe IgG: acute infection
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.
Suggested management of chronic HBV
infection
54
 Phases of Chronic HBV Infection:
Candidates for Therapy
Phases of Chronic HBV Infection
Immune Clearance/ Reactivation/
Immune Nonreplicative
HBeAg-Positive HBeAg-Negative
Tolerance (Inactive Carrier)
CHB CHB
HBV DNA,
105 - 1010 104 - 1010 < 104 103 - 108
IU/mL
HBeAg HBeAg+ HBeAg+ HBeAg- HBeAg-
ALT Normal High or fluctuating Normal High or fluctuating
HBsAg may
Active inflammation Active inflammation
Other -- become
on liver biopsy on liver biopsy
undetectable
Candidates
No Yes No Yes
for therapy?

Yim HJ, et al. Hepatology. 2006;43:S173-S181.

 Treatment of Chronic Hepatitis B
Drugs for Chronic HBV inf
1. Interferon Alfa 2b ( 1992)
2. Peginterferon Alfa 2a ( 5/2005 )
3. Lamivudin ( 1998 )
4. Adifovir – dipivoxil ( 2002 )
5. Entecavir ( 3/ 2005 )
6. Tenofovir
7. Telbivudine ( 2/2007)
8. Emtricitabine
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
Rekomendation treatment patient with HBeAg (+) /(APASL 2008)
Rekomendation Treatment Patient With HBeAg (-) / (APASL 2008)
 Rekomendation Treatment Pasient Cirrhosis (APASL 2008)

Yun FL et al Liver Int 2005;25:472

Yun FL.et al Guidelines for HBV management, APASL 2008
60
 Rekomendasi terapi dari EASL (European
Association for the Study of the Liver) 2009

• Indikasi terapi sama untuk pasien HBeAg (+) dan HBeAg

(-). Memenuhi 3 kriteria : kadar serum HBV DNA, kadar
serum aminotransferase & grade/tingkat histologi.

• Pasien dapat diterapi bila kadar HBV DNA > 2000 IU/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
skor METAVIR.

61
ALGORITMA PENATALAKSANAAN HBV KRONIK
( PPHI )
HBsAg (+)

Periksa HBeAg dan ALT

HBe Ag (+) HBe Ag (-)

ALT <BANN ALT >BANN

<2X >2X ALT > BANN ALT < BANN

Monitor/3 bulan

Monitor/1-2 bulan Dekompensasi hati Monitoring/ 6 bln

HBV DNA
\ Ya Tidak ada
Pos Neg

AN AN atau IFN

AntiVirus -
Respoms Tidak Respons

MONITORING Strategi lain???

Kombinasi IFN dan AN
Kombinasi AN
Terapi alternatif
 HBV Prevention

• Screen blood products

• Sterilization of needles, etc.
• Avoiding intimate contact, e.g.,
household or sexual contacts
• Vaccination
HEPATITIS C
Progression of liver disease in chronic hepatitis C

Chronic hepatitis
mild
moderate
severe fibrosis

Liver cirrhosis

End-stage liver
disease

HCC
0 10 20 30 40
Time after infection
 HCV Risk Factors
• received blood, blood products,
or an organ transplant prior to
1992
• ever, even once, shared drug
paraphernalia
• ever been stuck by a used blood
needle
• been on kidney dialysis
• had a tattoo or body piercing
• had multiple sex partners, or
sexual activity that involved
contact with blood
• shared personal care items
(razors, tooth brushes, etc.) with
other people
• combat veteran
Chronic hepatitis C infection

• HCV affects about 2 % of the world population and

approximately 300 million people are infected.
• The majority transmitted parenterally
• Up to 80 % will develop chronic infection
• Patients with chronic disease will develop cirrhosis over
20 to 30 years  proportion of them will develop PHC.
• Co infection with HBV and HCV increases the risk of
developing PHC.
Factors Promoting Progression of severity
CHC
• Increased alcohol intake

• Age > 40 years at time of infection

• HIV co-infection

• Other
– Male gender
– Chronic HBV co-infection
Serologic Pattern of Acute HCV Infection
with Recovery
anti-
HCV
Symptoms +/-

HCV RNA
Titer

ALT

Normal
0 1 2 3 4 5 6 1 2 3 4
Months Years
Time after exposure
 HCV Prevention and Control

Reduce or Eliminate Risks for

Acquiring HCV Infection
• Screen and test donors
• Virus inactivation of plasma-derived products
• Risk-reduction counseling and services
– Obtain history of high-risk drug & sex behaviors
– Provide information on minimizing risky behavior, including
referral to other services
– Vaccinate against hepatitis A and/or hepatitis B
• Safe injection and infection control practices
 HCV Counseling

Preventing HCV Transmission to Others

Avoid Direct Exposure to Blood

• Do not donate blood, body organs, other

tissue or semen
• Do not share items that might have blood
on them
– personal care (e.g., razor, toothbrush)
– home therapy (e.g., needles)
• Cover cuts and sores on the skin
 HCV Counseling

Other Transmission Issues

• HCV not spread by kissing, hugging, sneezing,
coughing, food or water, sharing eating utensils
or drinking glasses, or casual contact
• Do not exclude from work, school, play, child-
care or other settings based on HCV infection
status
Chronic hepatitis C infection
• Recent studies indicate a slow disease progression in
patients with persistently normal ALT levels  show
minimal inflammation and low fibrosis scores in their liver
histology.
• To diagnose  anti-HCV
• HCV-RNA by PCR  highly sensitive molecular
• Six genotypes (strains) of HCV
 Genotypes does not seem to influence the progression
of the disiase  sensitivities to therapeutic.
 HCV Diagnosis
• Most patients asymptomatic
• Abnormal liver function tests; AST/ALT
• Hepatitis C antibody (EIA)
• RIBA
• HCV RNA levels
• Liver biopsy: grade and stage damage
 Diagnosis of Chronic Viral Hepatitis:
Serologic Testing
• Patients should be tested for HCV and HBV
if they:
– have known risk factors for viral hepatitis
– indicate possible risk factors for hepatitis
– have elevated liver enzymes
– express a desire to know their HCV and/or HBV
status

Management of Hepatitis C NH Consensus Statement, 1997.

 Diagnosing Chronic HCV
Elevated ALT
All persons with chronic ALT elevation should undergo HCV testing.

elevated ALT level + risk factor(s) for hepatitis

C

anti-HCV (EIA) testing

- +
<5% chance of diagnosis of hepatitis C
hepatitis C >95% certain

Confirm with HCV RNA testing.

Refer to specialist for evaluation and treatment.
Chronic HCV Infection : Recommended pretreatment
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 .

 HCV TESTING

EIA
Negative Positive

Measure HCV RNA by PCR

Negative Positive

Low risk High risk

RIBA Consider treatment

for HCV infection

Negative Positive

No further workup Previous infection and clearance

 Chronic hepatitis C infection
• The progression of fibrosis determines the ultimate
prognosis and urgency therapy.
• Liver biopsy remains the gold standard to access fibrosis.
• The major factors known to be associated with fibrosis
progression :
1. Older age at infection
2. Male gender
3. Excessive alcohol consumption
• Alcohol  to enhance the risk of developing PHC
• Co-infection with the HIV  shown to worsen the course
of chronic HCV infection
• Cirrhosis develops more frequently in those infected
through blood transfusion than intravenous drug usage.
 Chronic hepatitis C infection

• The general management of patients with chronic hepatitis

C is similar to that for chronic hepatitis B infection.
• Alcohol should be avoided as this has been shown to
accelerate liver damage.
• Reducing the number of patients with HCV viraemia :
1. Screening of blood donors for anti-HCV
2. Active treatment of viraemic patients with Interferon
and/or Ribavirin
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
Management of chronic HCV Infection
 HCV Therapy
Pegylated Interferon injections weekly
AND
Ribavirin pills (or liquid) twice daily
 HEPATITIS
FULMINANT
HEPATITIS FULMINANT
• Hepatic failure with in 2-3 weeks.
• Reactivation of chronic or acute hepatitis
• Massive necrosis, shrinkage, wrinkled
• Collapsed reticulin network
• Only portal tracts visible
• Little or massive inflammation
• More than a week – regenerative activity
• Complete recovery – or - cirrhosis.
ACUTE LIVER FAILURE acute liver disease with
prothrombin time less than 50% of normal
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
O”GRADY and colleagus/:
Based liver failure,onset of jaundice,encepalopathy
• HYPERACUTE LIVER FAILURE,interval less than 7
days
• ACUTE LIVER FAILURE,interval 8 and 28 days
• SUBACUTE LIVER FAILURE,interval between 5 and
12 weeks
 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
 E
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
N-ASETIL SISTEIN
FARMAKOLOGI
PROSTAGLANDIN

HAEMOPERFUSI ARANG
KOLOUMN HEPATOSIT
MOLEKULER REGULASI SITOKIN

REGULASI KASKADE KOAGULASI

INHIBISI APOPTOSIS
HEPATOSIT GROWTH FACTOR

HEPATOSIT TRANSPLANT
TRANSPLANTASI
LIVER TRANSPLANT
HEPATITIS D
 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
Prevention,dvaccination with Hepatitis B Vaccine
HEPATITIS E
 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

•
HEPATITIS G
 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.
 Wilson’s disease
• It is important to exclude wilson’s 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 Kayser-Fleischer 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 of autoimmune hepatitis 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 :
1. Amenorhea 4. Acne
2. Striae 5. Hirsutism
3. Obesity 6. Cushingoid facies