Hepatitis Viral

Assoc Prof Dr. dr. Shahrul Rahman, Sp.PD, FINASIM

Departemen Ilmu Penyakit Dalam

Fakultas Kedokteran
Universitas Muhammadiyah Sumatera Utara
 DEFENISI
Hepatitis : Radang sistemik difus disertai pembengkakan
dari hati dilanjuti dengan nekro inflamasi hati dan
peningkatan serum enzim transaminase (AST/ SGOT)
dan ( ALT / SGPT), bilirubin bisa normal / anikterik dan
meningkat tinggi/ ikterik. Gangguan kelainan nekro
inflamasi menimbulkan gejala klinik, kelainan serologis
dan imunologik hati dari mana kita dapat menegakkan
diagnosis.
Hepatitis : penyakit umum dapat menyerang host/manusia walaupun
sistem imunnya baik, bisa sembuh self limited dan kronik
(BCD) dan berlanjut menjadi sirosis hati dan KHP (fatal).
 HEPATITIS VIRAL AKUT

DEFENISI :
PERADANGAN JARINGAN HATI YANG
DISEBABKAN OLEH VIRUS HEPATITIS.

JENIS - JENIS HEPATITIS:

- ACDE DAN G ( RNA VIRUS )
-- B ( DNA VIRUS )
 Introduction:
 Inflammation of Liver
 Viral, immune, drugs, toxins & other.
 Acute, Chronic & Fulminant - types
 Viral Hepatitis –
 Specific
– Hepatitis A, B, C, D, E, & other
 Systemic - CMV, EBV, other.
Hepatitis-5

HEPATITIS AKUT

ETIO: - VIRUS ( A,B,C,D,E,G,EBV & CMV )

- TOKSIN
- ALKOHOL
- WILSON DISEASE
- LEUKEMIA

GEJALA KLINIS : - ASIMPTOMATIK

- SIMPTOMATIK

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 Hepatitis-6
Hepatitis Kronis
 Defenisi :
Terjadinya peradangan dan nekrosis hati yang
berlangsung minimal selama 6 bulan.
 Etiologi :
- Infeksi virus :
 Hepatitis B, B plus D, C dan virus - virus lain

- Penyakit auto imun

- Obat-obatan : metil dopa, INH, aspirin
- Genetik : Wilson, defisiensi 1 anti
tripsin.
 Penyebab paling sering pada orang dewasa.

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Hepatitis-7

HEPATITIS - causes
 ACUTE:  CHRONIC:
 Viralhepatitis  Viralhepatitis
 Non-viral infection  Alcohol
 Alcohol  Drugs
 Toxins  Non-alcoholic
 Drugs steatohepatitis
 Ischemic hepatits  Autoimmune

 Autoimmune  Heredity

 Metabolic diseases

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Hepatitis-8

HEPATITIS - symptoms
 CHRONIC:
 ACUTE:
 Malaise, tiredness,
 Malaise
weakness
 Muscle and join
 Weight loss
ache
 Peripheral oedema
 Fever
 Ascites
 Nausea or vomiting
 Loss of apetite
 Abdominal pain
 Dark urine
 Jaundice
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 Hepatitis-9

VIRUS PENYEBAB HEPATITIS

= VIRUS (5 yang paling sering sebagai penyebab):
HAV – HBV – HCV – HDV – HEV
= Virus virus lainnya : (bukan primer hepatitis)
 VIRUS YELLOW FEVER

 CYTOMEGALOVIRUS

 VIRUS EPSTEIN BARR (EBV)

 VIRUS HERPES SIMPLEX

 VIRUS RUBELLA

 VIRUS ENTEROVIRUS

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 Hepatitis-10

PENEMUAN VIRUS HEPATITIS

 HAV : Perang Dunia ke II
 HBV : Perang Dunia ke II
 HCV : 1989 di USA
 HEV : 1990 di USA
 HDV : 1977 di Italia (disebut juga Delta Agent)
 HGV : awal 1996

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Hepatitis-11

Hepatitis viruses:(A,B,C,D,E,G & other)

Virus Hep-A Hep-B Hep-C

Agent ssRNA dsDNA ssRNA

Transm. Feco-oral Parenteral Parenteral

Carrier None 0.1-1.0% 0.2-1.0%

state
Chronic None 5-10% >50%
Hepatitis
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Clinical Features Of Hepatitis Agents
Hepatitis-12
Feature HAV/RNA HBV/DNA HCV/RNA HDV/RNA HEV/DNA
Transmission
Oral Common Not likely No No Common
Percutaneous Rare Common Common Common Unknown
Sexual No Common Yes, rare Yes, rare No
Perinatal No Common yes, low frequency No Yes, unknown freq.
Incubation period 15-49 60-180 14-160 21-45 15-60
(days) (avg=25)
Clinic. Illness at 5% pediatric 10-15% 5-10% 10%,higher 70-80% in adults
presentation 70-80% adults with superinfection
Jaundise Adults 30% 5-20% 5-10% Unknown Common
Fulminant < 1% <1% Rare 2-7,5% <1%, up to 30%
in pregnancy 3rd
tri semester
Diag. test
Acute infection IgM anti HAV HBsAg, HCV RNA (anti HCV) IgM anti HDV IgG anti HEV
IgM anti HBe (sero conversion)
Chronic infec. Not applicable HBsAg, IgG anti HCV (EIA) IgG anti HDV Not applicable
anti HBc RIBA,HCV RNA
Immunity IgG anti HAV IgG anti HBs Unknown Not applicable Not applicable
Case-fatality rate 0,1-2,7% 1-3% 1-2% <1% coinfection 0.5-4%
>5% superinfect 1,5-21% in
pregnant woman
Chronic infec. None <5% adults 80-90% superinfec ~80% None
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Hepatitis-13
TRANSMISI & JENIS VIRUS
TRANSMISI MELALUI :
 MAKANAN DAN MINUMAN
 HAV DAN HEV
 SUNTIKAN / INFUS / TRANSFUSI :
 HBV, HCV, HDV, HGV

JENIS MENURUT ASAM NUKLEAT

VIRUS RNA :
 HAV, HCV, HDV, HEV & HGV

VIRUS DNA :
 HBV

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 Phases of Hepatitis :
 Carrierstate / Asymptomatic phase
 Acute hepatitis
 Chronic Hepatitis
 Chronic Persistent Hepatitis
 Chronic Active Hepatitis

 Fulminant hepatitis
 Cirrhosis
 Acute Hepatitis:
1. Incubation phase.
2. Symptomatic pre-icteric / prodromal phase.
3. Symptomatic icteric phase.
4. Convalescence.
Fase Prodromal 2- Fase Ikterik 2-3 minggu Fase
7 hari penyembuhan
Hepatitis-16

PRODROMAL :
3-4 HARI S/D 2-3 MGG,LELAH, ANOREKSIA,
MUAL, HIPERPIREKSIA RINGAN,NYERI PERUT
KANAN ATAS, SAKIT KEPALA, NYERI OTOT

IKTERIK :
1-4 MGG URIN GELAP, HEPATOMEGALI,
SPLENOMEGALI.

KONVASELEN :
MULAI MENGHILANGNYA IKTERUS,NAFSU
MAKAN BAIK.
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Hepatitis-17

Acute Chronic
1. Ballooning deg.  Ground glass (B)
2. Cholestasis  Apoptosis
3. Apoptosis  Periportal Necrosis
4. Periportal Necrosis  Macrophages
5. Macrophages  Portal Lymphoid
6. Inflammation infiltrate
7. Portal inflammation  Bridging fibrosis

8. Fatty change(C)  Fatty change(C)

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Hepatitis-18

HEPATITIS AKUT - A

. 1912 COCKAYNE = “ HEPATITIS INFEKSIOSA”.

. 1923 BLUMMER MENDESKRIPSI SEMPURNA.
. DIGOLONGKAN ENTERO VIRUS TIPE 72
( PICORNAVIRIDAE VIRUS FAMILY ).
. 27-28 nm.
. STABIL PADA 60 0C.
. INAKTIF PADA 85 0C DALAM 1 MENIT.
. HANYA 1 ( SATU ) JENIS SERO TIPE

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Hepatitis-19
HAV
 Dulu dikenal penyebab Hepatitis Infectiosa
 Masa inkubasi : 30 hari (15-50 hari)
 Virus di jumpai dalam FECES 2 minggu sebelum
dan 2 minggu setelah icterus (pada anak anak
bisa sampai beberapa minggu setelah infeksi).
 Bisa juga dijumpai di dalam serum dan saliva, tapi
transmisi melalui saliva belum pernah dilaporkan
(di dalam urine tidak dijumpai HAV)
 Post Infeksi terjadi kekebalan seumur hidup
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Hepatitis-20

PATOGENESE :

. ORAL FECAL ROUTE INOKULASI

VIRUS HEPATOCYTE REPLIKASI
JUMLAH VIRUS AKAN MENURUN SETELAH
TIMBUL MANIFESTASI KLINIS MUNCUL
IgM ANTI HAV YANG SPESIFIK.
. KERUSAKAN SEL HATI OLEH KARENA VIREMIA
YANG SANGAT PENDEK.
. KERUSAKAN SEL HATI DISEBABKAN OLEH
AKTIFASI SEL T LIMFOSIT.

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Hepatitis-21

. HISTOLOGIS :
NEKROSIS SEL HATI
DIIKUTI INFILTRASI LIMFOSIT, MAKROFAG,
SEL PLASMA, EOSINOFIL DAN NEUTROFIL.

. IKTERUS AKIBAT GANGGUAN ALIRAN EMPEDU

. KERUSAKAN SEL HATI MENYEBABKAN

PELEPASAN ENZIM TRANSAMINASE (SGPT)

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Hepatitis-22

GEJALA KLINIS
-ASYMPTOMATIS
-SYMPTOMATIS  JAUNDICE SELF LIMITED
SEMBUH DALAM 8 MINGGU
-CHOLESTASIS JAUNDICE DALAM 10 MINGGU
ATAU LEBIH
-RELAPSE
-FULMINANT HEPATITIS (JARANG HIDUP)
-PENINGGIAN TRANSAMINASE > 10-20 KALI
-GEJALA KLINIS KLASIK TDD :
PRODROMAL (FLU LIKE SYNDROME)
FASE IKTERIK
FASE PENYEMBUHAN

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Hepatitis-23

DIAGNOSTIK :
Gejala klinis, pemeriksaan fisik dan laboratorium.
Berdasarkan ditemuinya Ig M anti HAV

PENATALAKSANAAN :
- Tidak ada yang spesifik, bersifat :
- Suportif
- Simptomatis

Prognosis
- Prognosis baik, angka kematian akibat hepatitis
fulminan 0,1 - 0,2%.
- Dilaporkan terjadi 0,13 - 0,35% kasus hospitalisasi.
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Hepatitis-24

2 minggu sebelum dan 2 minggu sesudah gejala icterus

Menunjukkan
Transmisi imunitas
Fecal – oral route
Bisa juga dijumpai di dalam
serum dan saliva, tapi
transmisi melalui saliva belum
pernah dilaporkan
Tidak dijumpai HAV di urine

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Hepatitis-25

PENCEGAHAN :
POLA HIDUP YANG BAIK DAN BERSIH.

• SECARA UMUM :
HIGIENE PERORANGAN, LINGKUNGAN
SANITASI YANG BAIK,PEMAKAIAN AIR BERSIH,
PEMBUANGAN EKSKRETA, PEMBUATAN
SUMUR YANG MEMENUHI STANDAR.

• MENCEGAH KONTAMINASI MAKANAN,

MEMASAK DENGAN BAIK.

VAKSINASI
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Hepatitis-26

IMUNISASI PASIF :
a. PENCEGAHAN SEGERA SETELAH KONTAK.
(KELUARGA SERUMAH).

b. PENCEGAHAN SEBELUM KONTAK (BERPERGIAN KE

DAERAH ENDEMIS).

HBIG( HUMAN NORMAL IMUNO GLOBULIN ), 0,02 ml / kg

BB, TIDAK LEBIH SATU MINGGU SETELAH KONTAK.

SEBELUM KONTAK 0,02ml/kg BB UNTUK PERJALANAN <

2 BULAN, 0,08ml/kg BB > 4 BULAN.

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Hepatitis-27

IMUNISASI AKTIF :

VAKSIN LIVE ATTENUATED YANG BERASAL

DARI GINJAL MONYET HIJAU AFRIKA
STRAIN HM -175

1993 DIIJINKAN PENGGUNAANNYA OLEH

REPORT OF COMMITTEE ON INFECTIOUS
DISEASE.

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Hepatitis-28

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 Hepatitis-29

Hepatitis B - Clinical Features

• Incubation period: Average 60-90 days
Range 45-180 days
• Clinical illness (jaundice): <5 yrs, <10%
5 yrs, 30%-50%
• Acute case-fatality rate: 0.5%-1%
• Chronic infection: <5 yrs, 30%-90%
5 yrs, 2%-10%
• Premature mortality from
chronic liver disease: 15%-25%

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 Hepatitis-30

HBV CHRONIC INFECTION OCCURS IN :

 90% infected at birth
 30% of children infected at age 1 – 5
years
 6% of persons infected after age 5
years
 Death from chronic liver disease
occurs in 15 – 25% of chronically
infected persons
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Hepatitis-31

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Hepatitis-32

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 Hepatitis-33

Typical Serologic HepB Course

Symptoms

HBeAg anti-HBe

Total anti-HBc
Titer

HBsAg IgM anti-HBc anti-HBs

0 4 8 12 16 20 24 28 32 36 52 100
Weeks after Exposure
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 Hepatitis-34
Outcome of Hepatitis B Virus Infection
100 by Age at Infection 100

Symptomatic Infection (%)

Chronic Infection (%)

80 80

60 60
Chronic Infection

40 40

20 20

Symptomatic Infection
0 0
Birth 1-6 months 7-12 months 1-4 years Older Children
and Adults
Age at Infection
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Hepatitis-35

Hepatitis B Virus
Modes of Transmission

• Sexual
• Parenteral
• Perinatal

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Hepatitis-36

Risk Factors for Acute Hepatitis B

United States, 1992-1993
Heterosexual*
(41%)

Injecting
Drug Use
(15%)

Homosexual Activity (9%)

Household Contact (2%)
Health Care Employment (1%)

Unknown (31%)
Other (1%)
* Includes sexual contact with acute cases, carriers, and multiple partners.
Source: CDC Sentinel Counties Study of Viral Hepatitis
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Hepatitis-37
RESIKO TINGGI TERINFEKSI HBV

 Persons with multiple sex partners

 Homosexual
 Sexual contact with infected persons
 Injection drug users (narcotic users)
 Live in the same house with someone who
has lifelong HBV infection
 Have a job that contact with human blood
 Shoot drugs (health care workers)
 Hemodialysis patients
 Infants born & children of infected mothers
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Hepatitis-38
Elimination of Hepatitis B Virus
Transmission United States
Strategy
• Prevent perinatal HBV transmission
• Routine vaccination of all infants
• Vaccination of children in high-risk groups
• Vaccination of adolescents
– all unvaccinated children at age 11-12
– “high-risk” adolescents at all ages
• Vaccination of adults in high-risk groups
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Hepatitis-39

Concentration of Hep B Virus

in Various Body Fluids

Low/Not
High Moderate Detectable

blood semen urine

serum vaginal fluid feces
wound exudates saliva sweat
tears
breastmilk

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 Hepatitis-40

Patients who become persistently infected are at risk

of developing hepatocellular carcinoma (HCC)..

 HBV is thought to play a

role in the development of
this malignancy because:
 a) 80% of patients with
HCC are carriers of
hepatitis B.
 b) Virus DNA can be
identified in hepatocellular
carcinoma cells.
 c) Virus DNA can integrate
into the host chromosome.

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Hepatitis-41

Fulminant Hepatitis:
 Hepatic failure with in 2-3 weeks.
 Reactivation of chronic or acute hepatitis
 Massive necrosis, shrinkage, wrinkled
 Collapsed reticulin network
 Only portal tracts visible

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Hepatitis-42

GAMBARAN KLINIS
IKTERUS PROGRESIF

BILIRUBIN > 20MG%

GANGGUAN KESADARAN PROGRESIF,

MUAL DAN MUNTAH, HATI MENGECIL,
MASA PROTROMBIN MEMANJANG,
TRANSAMINASE NAIK CEPAT DAN SANGAT
MENINGGI SERTA ALBUMIN MENURUN.

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Hepatitis-43

TATALAKSANA
N-ASETIL SISTEIN
PENDEKATAN
FARMAKOLOGI PROSTAGLANDIN

HAEMOPERFUSI ARANG
KOLOUMN HEPATOSIT
PENDEKATAN REGULASI SITOKIN
MOLEKULER
REGULASI KASKADE KOAGULASI

INHIBISI APOPTOSIS
HEPATOSIT GROWTH FACTOR

HEPATOSIT TRANSPLANT
TRANSPLANTASI
LIVER TRANSPLANT

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Hepatitis-44

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Hepatitis-45

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Hepatitis-46

46
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Hepatitis-47

Konsensus
PPHI
2006

47
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 AASLD 2007 Guidelines: Treatment
Hepatitis-48

algorithm for CHB patients

HBeAg-positive HBeAg-negative

ALT <1 x ULN ALT >2 x ULN ALT <1 x ULN ALT  2 x ULN

No treatment (HBV DNA (HBV DNA <2,000 (HBV DNA

>20,000 IU/mL) IU/mL)  20,000 IU/mL)

Treat if persistent ALT 1–2 x ULN Treat

No treatment
ALT 1–2 x ULN

(HBV DNA >20,000 IU/mL) (HBV DNA

Bx if persistent 2,000–20,000 IU/mL)
Bx; treat if needed
or >40 yrs; treat if needed

48
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Lok ASF & McMahon B. Hepatology 2007; 45:507-539.
Hepatitis-49

Features of Hepatitis C Virus

Infection

Incubation period Average 6-7

weeks
Range 2-26
weeks
Acute illness (jaundice) Mild (<20%)
Chronic infection 60%-85%

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Hepatitis-50

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Hepatitis-51

Chronic Hepatitis C
Factors Promoting Progression
or Severity
 Increased alcohol intake
 Age > 40 years at time of infection
 HIV co-infection
 Other
 Malegender
 Chronic HBV co-infection

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 Hepatitis-52
HCV
 TRANSMISI PARENTERAL
Sebelum 1990 paling sering karena transfusi darah
(90% of cases), hemodialysis & renal transplantation
(20% of cases).
 PENYAKIT KHRONIS (Chronic infection occurs in
>85% of persons infected with HCV)
 20% kasus HCV khronis jadi Cirrhosis hepatis (HBV
and HCV play some role in 64% of patients with
chonic liver disease)

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Hepatitis-53

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
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 Hepatitis-54

Estimated Incidence of Acute HCV

Infection
United States, 1960-2001
140
120
New Infections/100,000

100 Decline in injection

80 drug users
60
40 Decline in
transfusion recipients
20
0
1960 1965 1970 1975 1980 1985 1989 1992 1995 1998 2001
Year
Source: Hepatology 2000;31:777-82; Hepatology 1997;26:62S-65S;
CDC, unpublished data
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Hepatitis-55

Exposures Known to Be Associated With

HCV Infection in the United States

 Injecting
drug use
 Transfusion, transplant from infected donor
 Occupational exposure to blood
 Mostly needle sticks
 Iatrogenic (unsafe injections)
 Birth to HCV-infected mother
 Sex with infected partner
 Multiple sex partners

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Hepatitis-56 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

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Hepatitis-57

TRANSMISI HCV
 Bila darah atau cairan tubuh pasien HCV
masuk ke tubuh orang lain.
 Transmisi HCV melalui penggunaan
jarum suntik atau alat bedah, bor gigi
yang ter-cemar atau infeksi ke petugas
kesehatan.
 Bayi terinfeksi sewaktu dilahirkan oleh
ibu yang hepatitis

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 Hepatitis-58

HCV Testing Routinely

Recommended
Based on increased risk for infection
 Ever injected illegal drugs
 Received clotting factors made before 1987
 Received blood/organs before July 1992
 Ever on chronic hemodialysis
 Evidence of liver disease

Based on need for exposure management

 Healthcare, emergency, public safety workers
after needle stick/mucosal exposures to HCV-
positive blood
 Children born to HCV-positive women
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Hepatitis-59

Postexposure Management for HCV

 IG, antivirals not recommended for prophylaxis
 Follow-up after needlesticks, sharps, or
mucosal exposures to HCV-positive blood
 Test source for anti-HCV
 Test worker if source anti-HCV positive
 Anti-HCV and ALT at baseline and 4-6 months later
 For earlier diagnosis, HCV RNA at 4-6 weeks

 Confirm all anti-HCV

 Refer infected worker to specialist for medical
evaluation and management

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Hepatitis-60 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
 personalcare (e.g., razor, toothbrush)
 home therapy (e.g., needles)

 Cover cuts and sores on the skin

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Hepatitis-61 HCV Counseling
Mother-to-Infant Transmission of HCV
 Postexposure prophylaxis not available
 No need to avoid pregnancy or breastfeeding
 Consider bottle feeding if nipple cracked/ bleeding
 No need to determine mode of delivery based
on HCV infection status
 Test infants born to HCV-positive women
 >15-18 months old
 Tests any children born since mom infected
 Evaluate infected children for CLD

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Hepatitis-62 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

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Hepatitis-63

Diagnostik :
• Ditemuinya anti HCV. (minggu 5-6 setelah terpapar)
• Peninggian transaminase pada minggu ke-2 s/d 26,
puncaknya minggu ke-5 s/d 12.
• Kadar ALT biasanya meninggi pada ¾ pasien lebih
dari 15 kali dari batas atas normal.
• RNA HCV (+) menetap pada yang terinfeksi.

Gejala :
• Banyak kasus asimtomatik
• Flu-like sindrome, anoreksia, BB menurun, nyeri
abdominal, mialgia, atralgia dan fatigue.
• Simptom yang jarang : demam dan rash.
• Jaundice < 1/3 pasien.

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Hepatitis-64

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Hepatitis-65

HEPATITIS AKUT - D
• Terdeteksi bersamaan dengan virus Hepatitis B.
• HDV (+) diseluruh dunia berhubungan dengan
prevalensi infeksi HBV (+).
• Lebih dominan didaerah tropikal dan subtropikal.
• Infeksi HDV di negara berkembang lebih besar dari
pada di negara maju (Barat).
• Manifestasi klinis dari coinfeksi atau super infeksi
bervariasi dari asimptomatis sampai yang berat
• 80% kasus kronik hepatitis D  menjadi sirosis dalam
5-10 tahun.
• Gold standard diagnosis : HDV RNA (+) atau HDAg (+)
liver.
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Hepatitis-66

Transmisisi :
• Melalui parenteral, seksual, transfusi, jarum suntik,
haemodialisis.
• Infeksi HDV dapat berupa koinfeksi atau superinfeksi
dengan HBV.

Prevalensi Geografis :
+ 5% carier HbsAg terinfeksi dengan HDV

Diagnosa :
HDV (+) di serum dan liver, HDV RNA dan HDAg (+)
Diagnosa dini dengan IgM anti HD

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Hepatitis-67

Gambaran Klinis :
Biasanya berat dan ikterus
Amino transferase meningkat

Pencegahan :
Dengan cara vaksinasi HBV

Therapi :
Tidak banyak bermanfaat dengan pemberian
antivirus dan immunodulator

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Hepatitis-68

HEPATITIS AKUT –E
• Tidak berkapsul, sporadis , bersifat akut.
• Terdistribusi di Asia, Timur Tengah, sebagian Afrika, dan
Meksiko.
• Transmisi fecal – oral route.
• Paling sering pada dewasa muda.
• Masa inkubasi 2 - 10 minggu.
• Mortalitas : 25 %.
• Bersifat asimptomatis dan anikterik

Diagnosa :
HEV (+) , anti HEV (+) dan HEV RNA (+)
Tidak ada yang spesifik untuk terapi hepatitis E

Shashi-12/20/23
Hepatitis-69
HEV
 Outbreak di India tahun 1955 dengan 29.000
kasus akibat pencemaran air minum oleh tinja
(tinja manusia & hewan) dan wabah sporadis
karena makan kerang (shellfish)
 Wanita hamil mortalitas 20% (Fulminant hepatitis
in pregnant women up to 40%)
 Menjangkiti hewan akibat pencemaran faeces
(fecal–oral route).
 Acute, self limiting hepatitis, no chronic carrier
state
Age: predominantly young adults, 15-40 years
Shashi-12/20/23
Hepatitis-70

HEPATITIS AKUT – 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.

Shashi-12/20/23
 Hepatitis-71 Acute Hepatitis

History and LFTs

HBsAg, Anti-HBc (IgM), anti HAV (IgM)

HBsAg – ve HBsAg + ve HBsAg + ve HBs – ve

Anti-HBc IgM – ve Anti-HBc IgM + ve Anti-HBc IgM – ve
Anti-HBc IgM – ve
Anti HAV IgM +ve Anti HAV IgM -ve Anti HAV IgM -ve
Acute Hepatitis in
Anti HAV IgM -ve
Acute Hepatitis A Acute Hepatitis B
a HBs carrier Acute Hepatitis
Non A non B
Or Or
Exclude
HBsAg + ve HBsAg - ve Exclude
HCV, HDV, HEV,
Anti-HBc IgM – ve Anti-HBc IgM + ve CMV, EBV HCV, HEV, CMV,
Anti HAV IgM +ve Anti HAV IgM -ve Alcohol, Drugs, EBV
Acute Hepatitis A Acute Hepatitis B Wilson’s disease HBs
Alcohol, Drugs,
carrier with sero-
pada B kronik conversion from HBe Wilson’s disease
to anti –HBe, or
reactivation from
HBe –ve to HBe +ve

Shashi-12/20/23
Thank You…