CURRICULUM VITAE

Nama : dr. Firhat Esfandiari, SpPD.

Tempat/ Tgl Lahir : Teluk Betung / 29 Januari 1959
Pendidikan :
- SD – SMP Teluk Betung, s/d 1974
- SMA Surakarta (Solo), s/d 1977
- SI – FKUNS Surakarta, s/d 1985
- PPDS Penyakit Dalam FKUGM, s/d 1999
- Pelatihan Pemeriksaan HLA dan biopsi ginjal, Sydney 1996
- Pelatihan Program VCT-CST, Bangkok 2003
- Pelatihan Program PMTCT, Ko-infeksi TB-HIV, dan MDR-TB, Jerman 2006
Pekerjaan :
- Dokter inpres Pks Palas, Kemiling, P. Panggung, Prop. Lampung, s/d 1992
- Staff Medik Unit Dialisis, RSUP DR. Sardjito, Yogyakarta s/d 1999
- RSU Majene, Kabupaten Majene, Sulbar, s/d 2001
- RSU Raha, Kabupaten Muna, Sultra s/d 2002
- RSU Kota Sorong, Irian Jaya Barat s/d 2007
- RSUD Karimun, Tanjung Balai Karimun, Kepri s/d 2010
- RSD Liwa, Lampung Barat 2010 s/d 2012
- RS Pertamina Bintang Amin Lampung s/d Sep. 2013
- RS Natar Medika, Natar, Lampung Selatan sejak Oktober 2013 s/d sekarang
 Natural History of
Hepatitis B Virus Infection
Prevalence of Chronic Hepatitis B

~ 2 million Asians

~ 930, 000
Europeans
~ 400,000
South Americans

HBsAg Prevalence
> 8% - High ~ 350,000
2-8% - Intermediate Africans
< 2% - Low
Immigration numbers summed by continent from 1996-2002

Centers for Disease Control. Hepatitis B fact sheet. Available at:

http://www.cdc.gov/hepatitis. Accessed January 31, 2006. Mahoney FJ. Clin Microbiol
Rev. 1999;12:351-366. Hepatitis B Foundation. Hepatitis B statistics. Available at:
http://www.hepb.org/hepb/statistics.org. Accessed January 31, 2006.
Clinical options.com
Epidemiologi Hepatitis B

A Public health Problem

Worldwide :
 400 million cases of chronic
hepatitis B, risk to develop liver
cirrhosis and HCC
(second only to tobacco as a
recognized cause of a major
cancer in humans - WHO
2003)
 500,000 deaths/year
 75% lives in Southeast-East Asia

Indonesia :
 10% (3.4-20.3%) of the population
are HBV carriers
Prevalensi Hepatitis B di Asia Pasifik

Country Long-Term
carriers (Millions)

China 120.0
India 48.0
Indonesia 11.6
The Philippines 7.6
Korea 2.5
Japan 1.3
Hong Kong 0.7
Singapore 0.03
Australia 0.2
Taiwan 3.0

Various local sources

 Prevalensi di Indonesia
Penduduk Koja (Jakarta) 4.8 Budihusodo, 1990
Penduduk daerah Irian Jaya 10.5 Mulyanto, 1991
Penduduk Desa Sokong Lombok 11.3 Gunawan, 1985
Anggota TNI AD Mataram 8.5 Sumarsidi, 1982
Donor Darah Mataram 7.3 Nuryandari, 1987
Penduduk Gili Air, Selat Lombok 10.9 Suwignyo, 1987
Penduduk Segenter Lombok 20.3 Gunawan, 1987

Penduduk Gili Gede Selat 13.4 Darmono, 1990

Lombok
Murid-murid Sumbawa besar 11.7 Mulyanto, 1982
Murid-murid Bima 11.3 Effendi, 1982
Tahuna (Sulawesi Utara) 0.96 Wenny, 2005
Virus dan Patogenesis
 Hepatitis B Virus : a DNA virus
(Dane particle)

Circular, Double-stranded DNA

Protein Products:

 HBsAg
 HBeAg
 HBcAg*
 Polymerase
 X Protein
VHB tidak bersifat sitopatik
Sistem kekebalan
Tubuh mendeteksi
Keberadaan virus

Virus
masuk ke
sel hati
Membunuh virus dengan
menyerang sel hati yang
terinfeksi

Berkembang biak

Sel Hati
VHB tidak bersifat sitopatik

Membunuh virus dengan

menyerang sel hati yang
terinfeksi

Sel hati hancur

SGPT/ALT
meningkat

Sel Hati
 Progresi infeksi hepatitis B
5%-10% of
chronic HBV- Liver
infected Cancer
individuals1 (HCC)

>30% of CHB
Acute Chronic individuals1
Infection Infection Cirrhosis Death

• >90% of infected
children progress to
chronic disease

• <5% of infected Liver Failure

immunocompetent (Decompensation)
adults progress to
chronic disease1

1. Torresi J, Locarnini. Gastroenterology 2000.

2. Fattovich G et al. Hepatology 1995
 Siklus Replikasi HBV

2. Viral uncoating Nucleus

3. DNA repair

cccDNA
4. Transcription
1. HBV binds to
membrane receptors
and enters the cell 5. mRNA
molecules leave
6. Translation to the nucleus
Extracellular Space produce viral
proteins
Hepatocyte 7. Core assembly
and RNA
packaging 8. (-) strand synthesis
(reverse transcriptase)
11. Complete Viron Antiviral Drugs
buds from cell
10. Assembly of
membrane 9. (+) strand synthesis
nucleocapsid and
envelope proteins (DNA polymerase)
 Ibu HBsAg (+) HBeAg (+) 90%
menularkan pada janin
VHB
Penularan vertikal

4-5 % virus hilang

95% Infeksi menetap

 FASE IMMUNE TOLERANCE

Respon immun (-)
Inflamasi (-)/ minimal
SGPT N
HBeAg (+)
(Serokonversi spontan jarang < 5%)
HBV DNA tinggi
Infeksius
 Penularan Horisontal VHB

Fase Immune 95% virus hilang

Tolerance
 5% Infeksi Menetap

FASE IMMUNE CLEARANCE

Respon imun (+)

Hepatitis B akut
pada umumnya asimtomatik
Inflamasi (+) aktif
SGPT ↑ persisten / intermitent
HBeAg (+)
HBV DNA Tinggi
Serokonversi HBeAg → anti HBe
FASE INACTIVE CARRIER
HBeAg (-) Anti HBe (+)
SGPT N persisten
HBV DNA low / undetected

FASE REACTIVATION
HBeAg (-) anti HBe (+)
(kadang reversi HBeAg)
HBV DNA ↑
SGPT ↑ fluktuasi
 Hepatitis B Kronis Hepatitis B kronis
HBeAg (+) HBeAg (-)

HBeAg (+) HBeAg (-) Anti HBe (+)

 HUBUNGAN USIA DENGAN
KRONISITAS DAN GEJALA
100 100

80 80

60 60
Chronic Symptomatic
Infection Infection
(%) 40 40 (%)

20 20

0 0
Birth 1 to 6 7 to 12 1 to 4 Older
months months years Children
& Adults

Age at Infection
 HBsAg, Anti HBs

Anti HBc IgM

IgG
 SGPT/SGOT

 HBeAg, Anti HBe

 HBV DNA Kuantitatif

ANTIGEN DAN ANTIBODI HEPATITIS B

Antigen HBsAg, HBeAg, HBcAg

Antibodi Anti-HBs, Anti-HBe, Anti-HBc

INFEKSI AKUT VHB DENGAN KESEMBUHAN

GEJALA
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
Minggu setelah infeksi
 PROGRESI KE INFEKSI KRONIK
Akut Kronik
(6 months) (years)
HBeAg Anti-HBe
HBsAg

Total anti-HBc
Titer

IgM anti-HBc

0 4 8 12 16 20 24 28 32 36 52 Tahun

Minggu setelah infeksi

MAKNA TES SEROLOGI

HBsAg Anti-HBs Anti HBc IgM anti HBeAg HBV DNA

HBc

Hepatitis B + - + + +
+
Akut

Hepatitis B + +/- - +/- +

Kronik
+

Pengidap + +/- + - - -

Vaksinasi - + - - - -

Sembuh - + + - - -
 KORELASI
HBeAg
ALT
HBV DNA
terhadap progresifitas Penyakit

25
HBeAg
(Hep. B e Antigen)

26
 HBeAg yang persistence, berhubungan dengan
Insidensis Sirosis lebih tinggi
50
Cumulative incidence of cirrhosis

Non-seroconverters
40

30

20

10 Seroconverters

(Months)
0
0 24 48 72 96 120 144 168 192 216
74 60 49 39 32 22 14 6 4
134 106 81 64 52 39 17 5 2
Lin SM et al. J Hepatol. 2007;46:45−52
 HBeAg Positif menyebabkan pogresifitas
penyakit lebih cepat
Disease progression
100
cirrhosis development (%)
Cumulative incidence of

80

60 HBeAg reversion (4%)

40
HBeAg-negative hepatitis (24%)
20
Sustained remission (67%)
0
0 2 4 6 8 10 12 14 16 18
Years after HBeAg seroconversion

No. at risk
9 8 8 8 8 7 7 7 4 3 2

62 61 61 59 54 52 49 43 36 33 30 25 23 17 15 11 9 5 2

184 184 181 163 141 130 121 112 98 87 76 63 49 32 23 15 8 2

Hsu YS et al. Hepatology. 2002;35:1522−1527

Status HBeAg dan tingkat HBV DNA

 HBeAg+ CHB: 90% > 105 copies/mL1

 HBeAg– CHB: 50% < 105 copies/mL1

 Usulan cutoff level dari HBK aktif:

– HBeAg+ CHB: > 105 copies/mL

– HBeAg– CHB: > 104 copies/mL

29
1. Chu CJ et al. Hepatology 2002; 36: 1408–15.
HBeAg dan Risiko terhadap Kanker Hati

 11,893 Taiwanese men; 92,359 person-years (PYs) follow-up

 111 cases of HCC diagnosed during follow-up
 Overall incidence rate, 120.2 cases/100,000 PYs
 Incidence highest among individual HBeAg- and HBsAg-positive

P < .001
Cases/100,000 PYs
Incidence of HCC,

1400
1200 1169.4
1000
800
600 P < .001
400 324.3
200 39.1
0
HBsAg(-) HBsAg(+) HBsAg(+)
HBeAg(-) HBeAg(-) HBeAg(+)

Yang et al. N Engl J Med. 2002;347:168-174. 30

Fakta 1

Orang yang mengidap Hepatiti B Kronik dengan

HBeAg Positive memiliki risiko komplikasi sirosis dan
kanker hati lebih tinggi jika dibandingkan dengan
orang yang :
1. HBsAg -
2. HBsAg +, HBeAg -

31
ALT NORMALIZATION

32
 ALT and Komplikasi Hati
 Korea Medical Insurance Corporation
- 94,533 men; 47,522 women
- 35-59 yrs old
- Relative risk for liver mortality compared with AST
and ALT <20 IU/l

Men Women
AST (IU/l)
20-29 2.5 3.3
30-39 8.0 18.2
ALT (IU/L)
20-29 2.9 3.8
30-39 9.5 6.6
Conclusion: People with AST and ALT levels in the upper ranges of
“normal” are at risk of liver disease/mortality
33
Kim HC, et al. BMJ 2004;
 ALT and Hepatic Complications
 3,233 Chinese CHB patients
Stratified: ALT < 0.5 x ULN
30 ALT > 0.5-1 x ULN, ALT > 1-2 x ULN
ALT > 2-6 x ULN, ALT > 6 x ULN
Risk of
Complications
ALT >6 X ULN
(%) 20

ALT >2 - 6 X ULN

10
ALT >1 - 2 X ULN

ALT 0.5 - 1 X ULN

ALT <0.5 X ULN

0 30 60 90 120 150 180

Months of Follow-up

34
Yuen MF et al. Gut 2005; 54:1610
 Fakta 2

Perbandingan ke 3 kelompok ALT

Risiko komplikasi Hati :

- Terendah ketika ALT < 0.5 x ULN;

- Lebih tinggi jika ALT 0.5-1 x ULN;

- Tetinggi jika ALT >1-2 x ULN

Yuen MF et al. Gut 2005; 54:1610

35
HBV DNA Viral Load

36
 R.E.V.E.A.L: high HBV viral load is associated with
increased incidence of HCC

Cumulative Incidence of HCC: All Subjects (n=3,653)

Relative Risk
(95% CI)
16
14.89% 10.7
Cumulative incidence of HCC, %

14 Baseline HBV DNA Level, copies/mL (5.7-20.1)

≥106
12 12.17% 8.9
105–<106 (4.6-17.5)
104–<105
10
300–<104
8 <300

4 3.57% 2.7
(1.3-5.6)
2 1.37%
1.0
1.30% (0.5-2.2)
0 1.0
(reference)
0 1 2 3 4 5 6 7 8 9 10 11 12 13

Year of follow-up
Chen CJ, et al. JAMA. 2006; 295:65–73.
 R.E.V.E.A.L: high HBV viral load is associated with increased incidence
of HCC – independent of ALT level

Cumulative Incidence of HCC:

HBeAg(-), normal ALT, no liver cirrhosis at entry (n=2,925)

14
Cumulative incidence of HCC, %

Baseline HBV DNA Level 13.50%

12 ≥106
105–<106
10 104–<105
300–<104
8 <300 7.96%

4
3.15%
2
0.89%
0 0.74%

0 1 2 3 4 5 6 7 8 9 10 11 12 13
Year of follow-up
Chen CJ, et al. JAMA. 2006; 295:65–73.
VARIABLE MULTIVARIATE ADJUSTED
RELATIVE-RISK

Gender
Female 1.0
Male 2.1 (1.4-3.2)‡

Age (yr) 1.10 (1.08-1.12)‡

Cigarette smoking
No 1.0
Yes 1.2 (0.8-1.6)

Alcohol drinking
No 1.0
Yes 1.6 (1.1-2.3)*

Anti-HCV
Negative 1.0
Positive 1.4 (0.8-2.5)

HBeAg
Negative 1.0
Positive 2.3 (1.6-3.3)‡

ALT
<1x ULN 1.0
≥1x ULN 1.7 (1.2-2.6)†

HBV DNA level

<104 1.0
104-<105 2.5 (1.5-4.3)‡
≥105 6.4 (4.1-10.1)‡
 R.E.V.E.A.L: HIGH VIRAL LOAD IS ASSOCIATED WITH INCREASED
INCIDENCE OF CIRRHOSIS

Cumulative Incidence of Liver Cirrhosis Relative Risk

All Subjects (n=3,582) (95% CI)
40
Baseline HBV DNA level, copies/ml 36.2% 9.8
≥106 (n=602) (6.7-14.4)
Cumulative incidence of liver

105–<106 (n=333)
30
cirrhosis (% subjects)

104–<105 ( n=628)
300–<104 ( n=1,150)
23.5% 5.9
<300 (n=869)
20 (3.9-9.0)

Log rank test of trend 2.5

p<0.001 (1.6-3.8)
10 9.8%
5.9%
1.4
4.5% (0.9-2.2)
1.0
0 (reference)

0 1 2 3 4 5 6 7 8 9 10 11 12 13
Years of follow-up
 R.E.V.E.A.L: high HBV viral load is an independent risk factor for
cirrhosis

All participants (n=3,582) HBeAg(-), normal ALT (n=2,923)

18 #p <0.001 18 #p <0.001
16 16
Adjusted relative risk* of

14 14
cirrhosis (95% CI)

#
12 12
#
10 10 #
#
8 8
6.5 6.6
6 5.6 6 5.6
#
#
4 4
2.5 2.5
2 1.4 2 1.4

0 0
300–<104 104–105 105–106 >106 300–<104 104–105 105–106 >106
HBV DNA copies/mL HBV DNA copies/mL
*Cox proportional hazards regression analysis. Risk relative to HBV DNA <300 copies/mL. Relative risk adjusted for
age, gender, cigarette smoking, alcohol consumption.
 Fakta 3

Faktor yang paling penting yang berkaitan

dengan perkembangan komplikasi ( sirosis hati
dan kanker hati) adalah Viral Load

43
Chen CJ.et al JAMA, 2006
 MANFAAT PEMERIKSAAN
HBV-DNA

 Menunjukkan adanya partikel Dane

(partikel VHB utuh) dalam tubuh pasien

 Kadar HBV-DNA dapat dipergunakan

sebagai prediktor progresi penyakit

 Untuk menentukan kandidat

pengobatan, efektifitas dan juga
kegagalan terapi
PERAN BIOPSI HATI

 Biopsi hati merupakan baku

emas dalam penilaian
beratnya nekroinflamasi dan
fibrosis pada pasien hepatitis
B kronik
 Karena keterbatasan sarana
di Indonesia, konsensus PPHI
tidak mengharuskan biopsi
hati
 Tujuan Akhir Pengobatan Hep.B Kronis

 Mencegah terjadinya Sirosis Hati

 Mencegah terjadinya Kanker Hati

 Mencegah risiko kematian yang

behubungan dengan penyakit Hepatitis B.

G Dusheiko and N Antonakopoulus, Current treatment of Hepatitis B, GUT, 108

 Tujuan pengobatan Jangka Pendek Hep.B Kronis

HBeAg Positive
 Menghilangkan HBV-DNA serum.
 Menghilangkan HBeAg serta mencapai serokonversi
menjadi Anti HBeAg.
 Normalisasi ALT.
 Perbaikan histologi hati.
HBeAg Negative
 Menghilangkan HBV-DNA serum.
 Normalisasi ALT.
 Perbaikan histologi hati.

G Dusheiko and N Antonakopoulus, Current treatment of Hepatitis B, GUT, 111

Algoritma Pengobatan
Hepatitis B Kronik
 Treatment Algorithm
Patients with Compensated Disease

HBeAg Positive

HBV DNA HBV DNA

<20,000 IU/mL ≥20,000 IU/mL

ALT ALT
Normal Elevated

• No treatment • Monitor ALT every 3- • Treat

12 months (immune • Adefovir, entecavir,
• Monitor every 6–12 months tolerant) peginterferon, and
• Consider biopsy, if telbivudine* are first-
age >35–40, and line options
treat if significant
disease *If HBV DNA (-) at week 24

Updated from Keeffe EB, et al. Clin Gastroenterol Hepatol. 2006;4:936-962. 49

 Treatment Algorithm
Patients with Compensated Disease

HBeAg Negative

HBV DNA HBV DNA

<2,000 IU/mL ≥2,000 IU/mL

ALT ALT
Normal Elevated

• No treatment • Monitor ALT and • Treat

HBV DNA, or • Adefovir, entecavir,
• Monitor every 6–12 months
• Consider biopsy, peginterferon, and
since ALT often telbivudine* are first-
fluctuates, and treat line options
if significant disease • Long-term treatment
required (oral agents)
*If HBV DNA (-) at week 24
Updated from Keeffe EB, et al. Clin Gastroenterol Hepatol. 2006;4:936-962. 50
 Treatment Algorithm Update
Compensated Cirrhosis

HBV DNA HBV DNA HBV DNA

≥2000 IU (PCR) <2000 IU

1 IU = 5.6 copies/mL

Treat May choose to treat or observe

Long-term treatment recommended

Nucleoside Analogue
Consider combination therapy

Keeffe EB, et al. Clin Gastroenterol Hepatol. 2006;4:936.

51
 Treatment Algorithm Update
Decompensated Cirrhosis

HBV DNA <200 or ≥200 IU

 Consider treatment
(long-term required)
 Wait list for transplant

Combination therapy with NA

PEG IFN alfa-2a contraindicated

1 IU = 5.6 copies/mL
Keeffe EB, et al. Clin Gastroenterol Hepatol. 2006;4:936.
52
 Fresh APASL 2008 - Seoul
guidelines for HBV management
HBeAg Positive

HBV DNA
> 20,000 IU/mL
( 105 copies/ml )

ALT Normal ALT > 2x ULN

Biopsi
Treat:
• Conventional IFN
If :Advanced Fibrosis / Cirrhosis • Peg IFN
• Lamivudine
Treat • Adefovir
• Entecavir
• Telbivudine
Yun FL.al.Liver Int 2005;25:472
Yun FL. Guidelines for HBV management, APASL 2008 53
 Fresh APASL 2008 - Seoul
guidelines for HBV management
HBeAg Negative

HBV DNA
> 2,000 IU/mL
( 104 copies/ml )

ALT Normal ALT > 2x ULN

Biopsi
Treat:
• Conventional IFN
if: Advanced Fibrosis / Cirrhosis • Peg IFN
• Lamivudine
Treat • Adefovir
• Entecavir
• Telbivudine
Yun FL.al.Liver Int 2005;25:472
Yun FL. Guidelines for HBV management, APASL 2008 54
 Fresh APASL 2008 - Seoul
guidelines for HBV management

Decompensated
Patient

Start as early as possible

Treat:
• Lamivudine
• Entecavir
• Telbivudine

Yun FL.al.Liver Int 2005;25:472

Yun FL. Guidelines for HBV management, APASL 2008 55
 Fresh APASL 2008 - Seoul
guidelines for HBV management

Pasien HBeAg Positif

Terapi dapat diberhentikan bila serokonversi HBeAg dengan 2 x pemeriksaan
HBV DNA negatif berselang 6 bulan

6 month
Serokonversi HBeAg Stop Check ALT & HBV DNA
Check HBV DNA (-) / 3 month
Check HBV DNA (-) Therapy

Serokonversi HBeAg Serokonversi HBeAg

Check HBV DNA (-)
Check HBV DNA (+) Check HBV DNA (-)
Stop
6 month 6 month
Therapy
-Continue
-Add on or switch Check ALT & HBV DNA / 3
month
 Fresh APASL 2008 - Seoul
guidelines for HBV management

Pasien HBeAg negatif

Terapi dipertimbangkan berhenti bila bila 3 x
pemeriksaan HBV DNA negatif berselang 6 bulan

1 Check HBV DNA (-)

6 month
2 Check HBV DNA (-)
6 month
3 Check HBV DNA (-)

Stop Therapy

Check ALT & HBV DNA /3 month

 Fresh APASL 2008 - Seoul
guidelines for HBV management

Wanita yang mendapatkan Terapi antiviral, dalam perjalanan terjadi

kehamilan dapat diteruskan dengan Antiviral kategori B

A Adequate, well-controlled studies in pregnant women have not shown an

increased risk of fetal abnormalities.

B Animal studies have revealed no evidence of harm to the fetus. However, there
are no adequate and well-controlled studies in pregnant women.
Pregnancy Or

Drug Category
Animal studies have shown an adverse effect, but adequate and well-
controlled studies in pregnant women have failed to demonstrate a risk to
the fetus.

Adefovir C C Animal studies have shown an adverse effect and there are no adequate and
well-controlled studies in pregnant women.
Or
Entecavir C No animal studies have been conducted and there are no adequate and
well-controlled studies in pregnant women.

Lamivudine C D Studies, adequate well-controlled or observational, in pregnant women have

demonstrated a risk to the fetus. However, the benefits of therapy may
outweigh the potential risk.

Telbivudine
B X Studies, adequate well-controlled or observational, in animals or pregnant
women have demonstrated positive evidence of fetal abnormalities. The
use of the product is contraindicated in women
who are or may become pregnant
 Pencegahan :
Sangat Penting!
Melindungi pasien…
Melindungi petugas kesehatan…
Promosi pelayanan kesehatan
yang berkualitas!
Virus Hepatitis C
(VHC)

60
• Virus golongan RNA
• Famili Flaviridae
• Terdiri dari 6 genotype
• Replikasi di hepatosit

61
 Penegakan diagnosis :
Serokonversi anti-HCV pada pasien yang
sebelumnya diketahui anti-HCV negatif

Pasien dengan gejala :

 ALT > 10x nilai batas atas normal,
ikterik
 Tidak ada riwayat penyakit hati kronik
atau penyebab lain hepatitis akut,
dan/atau
 Sumber penularan dapat diidentifikasi
62
Bila pasien diduga termasuk
GOLONGAN RISIKO TINGGI
ATAU PERNAH
TERPAPAR DARAH YANG
TERKONTAMINASI

• Skrining awal :
Pemeriksaan anti-HCV
• Tahap lanjutan :
HCV RNA kuantitatif, genotipe virus
63
 Tahapan Pemeriksaan

• Skrining dilakukan dengan pemeriksaan anti-

HCV menggunakan teknik enzyme linkage
immunosorbent assay (ELISA) atau
chemiluminescent immunoassay (CLIA)

• Bila anti-HCV (+), dilanjutkan pemeriksaan

HCV RNA dengan real time PCR
• nilai deteksi terendah < 50 IU/mL (dual therapy)

• nilai deteksi terendah < 15 IU/mL (triple therapy)

 SEROLOGI HEPATITIS C

• HCV RNA dapat terdeteksi dalam 7-10 hari setelah paparan

65
• Anti HCV dapat terdeteksi dalam 7-8 minggu setelah paparan
Sekelompok Orang
Terpajan Hepatitis C

Infeksi Hepatitis C

Hepatits C Akut

Sembuh Hepatitis C kronik

66
 Penegakan Diagnosis :
 Anti-HCV dan HCV RNA tetap
terdeteksi > 6 bulan sejak terinfeksi
(kriteria ideal)
 Dapat disertai maupun tanpa
gejala-gejala penyakit hati kronik
 Umumnya pasien tanpa sumber
penularan yang jelas dalam 6 bulan
terakhir dianggap sebagai kasus
hepatitis C kronik
67
HEPATITIS C KRONIK
(80% kasus asimtomatik)

68
Liver Fibrosis Staging

69
 Pengkajian Pra-terapi
Mencari etiologi lain penyakit hati kronik
 Koinfeksi HIV dan VHB
 Kemungkinan penyakit komorbid (NAFLD,
penyakit hati autoimun, penyakit hati alkohol)
 Pemeriksaan fungsi hati: AST/ALT, GGT,
alkalin fosfatase, bilirubin, PT, albumin,
globulin, darah perifer lengkap

Menilai derajat kerusakan hati

 Pemeriksaan awal : USG abdomen
 Gold standar : biopsi hati (menentukan
nekroinflamasi dan fibrosis)
 Pemeriksaan non-invasif: fibroscan, APRI70
Alur Tatalaksana
Hepatitis C

71