INFORMASI DASAR

DAN TATA LAKSANA

HEPATITIS B DAN HEPATITIS C
J. MANURUNG

SMF ILMU PENYAKIT

DALAM
RSU DR. SLAMET
GARUT
 DEFINISI HEPATITIS VIRUS

GEJALA DAN TANDA

BERVARIASI :
INFLAMASI ATAU • DEMAM
PERADANGAN • SKLERA MATA
HATI AKIBAT KUNING
INFEKSI VIRUS • MUAL MUNTAH
HEPATITIS A, B, C, • KURANG SELERA
D ATAU E MAKAN
• MUDAH LELAH
• PEGAL LINU
 HEPATITIS VIRUS
A B C D E
PENULARAN MAKANAN DARAH DARAH DARAH MAKANAN
PENCEGAHAN VAKSIN VAKSIN -- VAKSIN [ B ] --
SANITASI ++ ? ? ? ++++
POTENSI --/<< +++ ++++ +++++ --/<<
FATAL
TERAPI SUPORTIF KAUSAL KAUSAL ???? SUPORTIF
 KELAINAN HISTOPATOLOGI

• NEKROINLAMASI

•TRIAS • FIBRONEKROSIS

• NODUL REGENERASI
TATALAKSANA
 MASALAH KESEHATAN DUNIA

• TERAPI HEPATITIS B KRONIK YG TIDAK

TEPAT :

• 5 TAHUN, 8 – 20 % JADI SIROSIS HATI

• 5 TAHUN, 20 % JADI SH
DEKOMPENSATA
• 5 TAHUN, 20 % JADI KARSINOMA SEL
HATI
 NEW NOMENCLATURE FOR CHRONIC PHASES
• THE NATURAL HISTORY OF CHRONIC HBV INFECTION HAS BEEN SCHEMATICALLY DIVIDED INTO fiVE PHASES

HBeAg positive HBeAg negative

Chronic
Phase 1 Phase 2 Phase 3 Phase 4 Phase 5
hepatitis B
Chronic HBV Chronic Chronic HBV Chronic Resolved HBV
Chronic HBV infection hepatitis B infection hepatitis B infection
infection
High/
HBsAg High Low Intermediate Negative
intermediate

HBeAg Positive Positive Negative Negative Negative

HBV DNA >107 IU/mL 104–107 IU/mL <2,000 IU/mL* >2,000 IU/mL <10 IU/mL‡
ALT Normal Elevated Normal Elevated† Normal

Moderate/ Moderate/
Liver disease None/minimal None None§
severe severe

Immune HBsAg negative

Old HBeAg negative
Immune tolerant reactive Inactive carrier /anti-HBc
terminology chronic hepatitis
HBeAg positive positive

*HBV DNA LEVELS CAN BE BETWEEN 2,000 AND 20,000 IU/ML IN SOME PATIENTS WITHOUT SIGNS OF CHRONIC
HEPATITIS;
†PERSISITENTLY OR INTERMITTENTLY, BASED ON TRADITIONAL ULN (~40 IU/L). ‡CCCDNA CAN FREQUENTLY BE

DETECTED IN THE LIVER;

§RESIDUAL HCC RISK ONLY IF CIRRHOSIS HAS DEVELOPED BEFORE HBSAG LOSS.

EASL CPG HBV. J HEPATOL 2017;67:370–98

 PERJALANAN PENYAKIT
HEPATITIS B
• PAJANAN VIRUS HEPATITIS B ( HBV DNA ), BERAKIBAT :
• 1. HEPATITIS B AKUT, LALU SEMBUH SPONTAN DAN TIMBUL KEKEBALAN.
• 2. HEPATITIS B KRONIK, 4 FASE :
• IMMUNE TOLERANT ( HBV DNA >>>, SGPT N )
• IMMUNE CLEARANCE ( HBV DNA >>, SGPT >>> }
• INACTIVE ( HBV DNA <<, SGPT N )
• REACTIVE ( HBV DNA >>, SGPT >>> )

• HBV DNA >> : > 2000 IU/ML

• SGPT >> : 2 X BATAS ATAS N
 INDICATIONS FOR TREATMENT
• PRIMARILY BASED ON THE COMBINATION OF 3 CRITERIA
• HBV DNA, SERUM ALT AND SEVERITY OF LIVER DISEASE

Recommendations Grade of evidence Grade of recommendation

Should be treated

• Patients with HBeAg-positive or -negative chronic hepatitis B* I 1

• Patients with cirrhosis, any detectable HBV DNA, regardless of
I 1
ALT level
• Patients with HBV DNA >20,000 IU/mL and ALT >2x ULN,
II-2 1
regardless of severity of histological lesions
May be treated
• Patients with HBeAg-positive chronic HBV infection† III 2
>30 years old, regardless of severity of liver histological lesions
Can be treated
• Patients with HBeAg-positive or -negative chronic HBV infection
III 2
and family history of HCC or cirrhosis and extrahepatic
manifestations‡
*DEFINED BY HBV DNA >2,000 IU/ML, ALT >ULN AND/OR AT LEAST MODERATE LIVER NECROINFLAMMATION OR FIBROSIS;
†DEFINED BY PERSISTENTLY NORMAL ALT AND HIGH HBV DNA LEVELS;

‡ EVEN IF TYPICAL TREATMENT INDICATIONS ARE NOT FULFILLED

EASL CPG HBV. J HEPATOL 2017;67:370–98

SEROMARKER
SEROMARKER
 KRITERIA DIAGNOSTIK
HEPATITIS B KRONIK

HBSAG + > 6 BLN HBV DNA SGPT HBEAG

AKTIF +++ > 20000 IU >>> +
INAKTIF ++ 2000 - 20000 N ----/ ANTI HBE +
SEMBUH ---- <<</---- N ----
 TARGET TERAPI HEPATITIS B KRONIK

IDEAL HBSAG (-)

MEMUASKAN RELAPS KLINIK (-) SETELAH TERAPI SELESAI , ANTI HBE (+), HBEAG (-)

DIINGINKAN HBV < 2000 IU, HBEAG (+)/HBEAG (-)

 INDIKASI TERAPI

• JUMLAH HBV DNA

SERUM
• STATUS HBEAG
KOMBINASI • NILAI SGPT
4 HAL : • HISTOLOGI/DERAJAD
FIBROSIS
• ( DITANGGUNG BPJS-
KAH..??? )
 PILIHAN TERAPI
INTERFERON ANALOG NUKLEOSIDA
HARGA >>>>> BPJS ( AAMIIN...!!!!! )
DURASI MAX 48 MINGGU JANGKA PANJANG
CARA PEMBERIAN S.K ORAL
PADA SIROSIS TIDAK YA
DAYA SUPRESI SETAHUN RENDAH > TINGGI
SEROKONVERSI HBEAG JADI (-) RENDAH > TINGGI
SEROKONVERSI HBSAG JADI (-) TINGGI RENDAH
RESISTENSI (-) ADA
RESPON JGK PANJANG  BAIK SERING KAMBUH
 TERAPI DENGAN ANALOG NUKLEOSIDA
PPHI 2017
• LINI PERTAMA • PEMANTAUAN :
• TENOFOVIR 300 MG/HARI, ATAU
• ENTECAVIR 0,5 MG/HARI • TIAP 3-6 BLN CEK : HBV DNA, HBEAG, ANTI
HBE, SGPT
• LINI KEDUA
• PADA SIROSIS CEK JUGA
• LAMIVUDIN 100 MG/HARI
UREUM/KREATININ
• ADEFOVIR 10 MG/HARI
• PADA AKHIR TERAPI CEK HBSAG
• TELBIVUDIN 600 MG/HARI
 TERAPI HEPATITIS B
PADA IBU HAMIL

• HBV DNA > 2 x

1000000 iu/ ml Pilihan :
• HBeAG +
KRITERIA: • Mulai TM 3 sd 3 bln pp
• Mulai lebih awal jika
fibrosis/risiko
dekompensata Tenofovir Telbivudin
 SPECIAL PATIENT GROUPS: PREGNANT WOMEN

• MANAGEMENT MAY DEPEND ON SEVERITY OF LIVER DISEASE AND TIMING OF A FUTURE

PREGNANCY
Recommendations
Grade of evidence Grade of recommendation
Screening for HBsAg in the first trimester is strongly recommended I 1
In women of childbearing age without advanced fibrosis planning a pregnancy in the near
future, it may be prudent to delay therapy until the child is born II-2 2

In pregnant women with chronic hepatitis B and advanced fibrosis or cirrhosis, therapy with
TDF is recommended II-2 1

In pregnant women already on NA therapy, TDF should be continued while ETV or other
NA should be switched to TDF II-2 1

In all pregnant women with HBV DNA >200,000 IU/ml or HBsAg

>4 log10 IU/ml, antiviral prophylaxis with TDF should start at Week 24–28 of gestation and I 1
continue for up to 12 weeks after delivery

Breast feeding is not contraindicated in HBsAg-positive untreated women or those on TDF-

based treatment or prophylaxis III 2

EASL CPG HBV. J HEPATOL 2017;67:370–98

PENCEGAHAN TRANSMISI HEPATITIS B PERINATAL

Pemberian HB
IG 12 jam pp

Vaksinasi
 SPECIAL PATIENT GROUPS: HEALTHCARE WORKERS
Recommendations Grade of evidence Grade of recommendation

HBV infection alone should not disqualify infected persons

from the practice or study of surgery, dentistry, medicine, or III 1
allied health fields
Healthcare workers performing exposure-prone procedures
with serum HBV DNA >200 IU/ml may be treated with NAs II-2 2
to reduce transmission risk

EASL CPG HBV. J HEPATOL 2017;67:370–98

 SPECIAL PATIENT GROUPS: ACUTE HEPATITIS B
• PREVENTING THE RISK OF ACUTE OR SUBACUTE LIVER FAILURE IS THE MAIN TREATMENT GOAL
• TREATING TO IMPROVE QUALITY OF LIFE AND REDUCING RISK OF CHRONICITY ARE
ALSO RELEVANT TREATMENT GOALS

Recommendations Grade of evidence Grade of recommendation

More than 95% of adults with acute HBV hepatitis do not

II-2 1
require specific treatment
Only patients with severe acute hepatitis B, characterized by
coagulopathy or protracted course, should be treated with II-2 1
NAs and considered for liver transplantation

EASL CPG HBV. J HEPATOL 2017;67:370–98

TATALAKSANA HEPATITIS C
 EPIDEMIOLOGY OF HCV
• ESTIMATED GLOBAL PREVALENCE OF HCV IN 2015: 1.0% (95% UNCERTAINTY INTERVAL 0.8–
1.1)1

• CORRESPONDS TO 71.1 MILLION (62.5–79.4) VIRAEMIC INFECTIONS1,2

• ~399,000 DEATHS EACH YEAR, MOSTLY FROM CIRRHOSIS AND HCC2

• GT 1 AND 3 ARE THE MOST COMMON CAUSES OF INFECTION (44% AND 25%,
RESPECTIVELY)1
Incidence of HCV infection and new HCV infections in the general population, by WHO region, 20152
HCV incidence rate per New HCV infections
100,000: (x 1,000):
Map Best estimate Best estimate
WHO region key (uncertainty level) (uncertainty level)
African 31.0 (22.5–54.4) 309 (222–544)
Americas 6.4 (5.9–7.0) 63 (59–69)
Eastern
62.5 (55.6–65.2) 409 (363–426)
Mediterranean
European 61.8 (50.3–66.0) 565 (460–603)
South-East Asia 14.8 (12.5–26.9) 287 (243–524)
Western Pacific 6.0 (5.6–6.6) 111 (104–124)
1,751
Global 23.7 (21.3–28.7)
(1,572–2,120)

1. POLARIS OBSERVATORY HCV COLLABORATORS. LANCET GASTROENTEROL HEPATOL 2017;2:161–76; 2. WORLD HEALTH
ORGANIZATION. GLOBAL HEPATITIS REPORT 2017. AVAILABLE AT:
HTTP://APPS.WHO.INT/IRIS/BITSTREAM/HANDLE/10665/255016/9789241565455-ENG.PDF?SEQUENCE=1;
EASL CPG HCV. J HEPATOL 2018;69:461–511.
 PERJALANAN PENYAKIT HEPATITIS C
20%
HANYA 20% YG Clear the
BERGEJALA Virus

Healthy Acute Chronic

Liver Infection Infection

80% Virus
Continues
to Damage
Liver
Adapted from Lauer and Walker, NEJM 2001
 NATURAL HISTORY/DISEASE BURDEN
• LONG-TERM NATURAL HISTORY OF HCV INFECTION IS HIGHLY VARIABLE
• CHRONIC HCV INFECTION IS ACCOMPANIED BY
• EXTRAHEPATIC MANIFESTATIONS REPORTED IN UP TO 75% OF PATIENTS, INCLUDING:1
• MIXED CRYOGLOBULINAEMIA VASCULITIS, RENAL DISEASE (ELEVATED CREATININE), TYPE 2 DIABETES, CARDIOVASCULAR DISEASE
(VASCULITIS, ARTERIAL HYPERTENSION), PORPHYRIA CUTANEA TARDA, LICHEN PLANUS AND LYMPHOPROLIFERATIVE DISORDERS
• NON-SPECIFIC SYMPTOMS: FATIGUE, NAUSEA, ABDOMINAL PAIN, WEIGHT LOSS
• RAPID DEVELOPMENT OF HEPATIC FIBROSIS AND ACCELERATED TIME TO CIRRHOSIS2

F4 F4 F4
F0 F1 F2 F3 HCC
CTP A CTP B CTP C

• INCREASED RISK FOR LIVER FAILURE, HCC AND LIVER-RELATED MORTALITY

• OVERALL ESTIMATED ANNUAL RISK FOR LIVER FAILURE OF 2.9%, HCC 3.2% AND
LIVER-RELATED DEATH 2.7% IN PATIENTS WITH ADVANCED FIBROSIS1,3

FIGURE ADAPTED FROM ASSELAH T, ET AL. J HEPATOL 2014;61:193–5

1. VAN DER MEER AJ, ET AL. J HEPATOL 2016;65:S95–S108; 2. BUTT AA, ET AL. JAMA INTERN MED 2015;175:178–85;
3. SINGH AG, ET AL. CLIN GASTROENTEROL HEPATOL 2010;8:280–8;
EASL CPG HCV. J HEPATOL 2018;69:461–511.
 FAKTOR RISIKO

IDU/snorting
NARKOBA
TIDAK TAHU (51%)

Incarceration (3%)

Transfusion/dialysis
blood contact (4%) HCV-infected household
member/sexual partner
Hospitalization Tattooing (7%)
dental work piercing
Source: Health Canada Enhanced Surveillance, Oct 98-Oct 99, Calgary, Edmonton, Winnipeg, Ottawa
(6%) (6%)
SCREENING FOR CHRONIC HCV INFECTION
Recommendations
Screening strategies
• Screening according to local epidemiology and within framework
Grade of
of evidence A 1
Grade of recommendation
national plans
• May include at-risk populations, birth cohort testing and general population testing in B 2
areas of intermediate to high seroprevalence (≥2–5%)
• Based on detection of serum/plasma anti-HCV Abs using EIA A 1
Anti-HCV Ab testing
• Should be offered with linkage to prevention, care and treatment A 1
• Dried blood spots can be used as alternative to serum or plasma* A 2
• Use RDTs† (as an alternative to classical EIA) at patient’s care site to facilitate screening A 2
and improve access to care
HCV RNA testing
• If anti-HCV Ab detected, test for serum/plasma HCV RNA (or HCV core antigen)‡ to A 1
identify patients with ongoing infection
• Dried blood spots can be used as alternative to serum or plasma* A 2
• Reflex testing for HCV RNA in patients who are anti-HCV Ab+ should be applied to B 1
increase linkage to care
• Anti-HCV Ab screening can be replaced by a point-of-care HCV RNA assay (LLOD: C 2
≤1000 IU/mL) or HCV core antigen testing§

*AFTER SHIPMENT TO A CENTRAL LABORATORY WHERE THE EIA WILL BE PERFORMED; †USING SERUM, PLASMA, FINGERSTICK WHOLE
BLOOD OR SALIVA AS MATRICES; ‡IF HCV RNA ASSAYS ARE NOT AVAILABLE AND/OR NOT AFFORDABLE; §IF AVAILABLE AND SCREENING
STRATEGY IS COST EFFECTIVE
EASL CPG HCV. J HEPATOL 2018;69:461–511.
SEROMARKER
 KRITERIA DIAGNOSIS
HEPATITIS C
ANTI HCV HCV RNA INTERPRETASI
POSITIF POSITIF AKUT ATAU KRONIK, TGT GJL KLINIK
POSITIF NEGATIF MUNGKIN VIREMIA INTERMITEN
NEGATIF POSITIF AKUT AWAL/KRONIK IMUNOCOMPROMISED/POSITIF PALSU
NEGATIF NEGATIF TAK TERINFEKSI
 DIAGNOSIS OF ACUTE AND CHRONIC HCV
INFECTION
Recommendations Grade of evidence Grade of recommendation

All patients with suspected HCV infection should be tested for anti-HCV Ab in serum or
A 1
plasma as first-line diagnostic test
In cases of suspected acute hepatitis C, in immunocompromised patients and patients on
haemodialysis, serum or plasma HCV RNA testing should be part of A 1
the initial evaluation
If anti-HCV Ab detected, HCV RNA should be determined by a sensitive molecular method
A 1
(LLOD: ≤15 IU/mL)
Anti-HCV Ab+, HCV RNA individuals should be retested for HCV RNA 12 and
A 1
24 weeks later to confirm definitive clearance
In low- and middle-income countries, and specific high-income country settings, a qualitative
HCV RNA assay (LLOD: ≤1000 IU/mL) can be used to provide broad affordable access to B 2
HCV diagnosis and care
Serum or plasma HCV core antigen (a marker of HCV replication) can be used instead of
HCV RNA to diagnose acute or chronic HCV infection when HCV RNA assays are not A 1
available and/or not affordable

EASL CPG HCV. J HEPATOL 2018;69:461–511.

 PENILAIAN FIBROSIS

FIB-4 {( USIA X SGOT ) : (PLT X SGPT)} X 100

APRI {(SGOT : BTS ATAS NILAI NORMAL SGOT) : PLT } X 100
 DERAJAD KEPARAHAN
HEPATITIS

USG APRI c.off rdh APRI c.off tgi FIB-4 c.off rdh FIB-4 c.off tgi FIBROSCAN
FIBROSIS 0,5 1,5 1,45 3,25 7- 8,5 kpa
SIROSIS 1,0 2,0 -- -- 11-14 kpa
 TUJUAN TERAPI

• ERADIKASI VIRUS HEPATITIS C

• MENCEGAH KOMPLIKASI
• TERCAPAINYA SUSTAINED VIROLOGICAL
RESPONSE ( SVR )
 PRIMARY GOAL AND IMPACT OF HCV THERAPY
Primary goal of therapy – cure HCV infection (SVR12 or SVR24)

• SVR CORRESPONDS TO A DEFINITIVE CURE OF HCV INFECTION IN NEARLY ALL CASES AND IS
FREQUENTLY ASSOCIATED WITH
• IMPROVEMENT IN EXTRAHEPATIC MANIFESTATIONS1
• IMPROVEMENT/DISAPPEARANCE OF LIVER NECROINFLAMMATION AND FIBROSIS1
• REGRESSION OF ADVANCED HEPATIC FIBROSIS (F3) OR CIRRHOSIS (F4)2
• REDUCED RISK OF HCC, HEPATIC DECOMPENSATION, NON-LIVER- AND LIVER-RELATED MORTALITY, AND LIVER
TRANSPLANTATION3–7
• HCV THERAPY IS ONE OF THE INTERVENTIONS NECESSARY TO REDUCE GLOBAL BURDEN OF DISEASE8
1. VAN DER MEER AJ, ET AL. J HEPATOL 2016;65:S95–S108; 2. D’AMBROSIO R, ET AL. HEPATOLOGY 2012;56:532–43; 3. NAHON P, ET
AL. GASTROENTEROLOGY 2017;152:142–56; 4. VAN DER MEER AJ, ET AL. JAMA 2012;308:2584–93; 5. BRUNO S, ET AL. J HEPATOL
2016;64:1217–23; 6. LEE M-H, ET AL. J INFECT DIS 2012;206:469–77; 7. SINGH AG, ET AL. CLIN GASTROENTEROL HEPATOL 2010;8:280–
8;
8. HEFFERMAN A, ET AL. LANCET 2019; DOI: 10.1016/S0140-6736(18)32277-3;
EASL CPG HCV. J HEPATOL 2018;69:461–511.
 INDIKASI TERAPI

TERAPI KELOMPOK PASIEN

INDIKASI HEPATITIS C KASUS BARU/GAGAL TERAPI, KOMPENSATA/DEKOMPENSATA
PRIORITAS FIBROSIS BERAT, KOINFEKSI HIV/HBV, KANDIDAT CANGKOK, RISIKO MENULAR TINGGI
PERTIMBANGAN FIBROSIS SEDANG
DITUNDA FIBROSIS RINGAN/TIDAK FIBROSIS
DILARANG KOMORBIDITAS BERAT
INDICATIONS FOR TREATMENT: WHO SHOULD BE
TREATED?
Recommendations Grade of evidence
All patients with HCV infection must be considered for therapy, including
Grade of recommendation

A 1
treatment-naïve and treatment-experienced* patients
Patients who should be treated without delay
• Significant fibrosis or cirrhosis (METAVIR score ≥F2): including compensated
(Child–Pugh A) and decompensated (Child–Pugh B or C) cirrhosis
• Clinically significant extra-hepatic manifestations†
• HCV recurrence after liver transplantation
• Patients at risk of rapid evolution of liver disease due to concurrent comorbidities‡
A 1
• Individuals at risk of transmitting HCV
– PWID
– MSM with high-risk sexual practices
– Women of child-bearing age who wish to get pregnant
– Haemodialysis patients
– Incarcerated individuals
• In patients with decompensated cirrhosis and an indication for liver transplantation (MELD score B 1
≥18–20), transplant first and treat after transplantation
• For waiting time >6 months, treat before transplant (clinical benefit not well established) B 2
• Treatment is generally not recommended in patients with limited life expectancy due to non-liver-
B 2
related comorbidities

*INDIVIDUALS WHO FAILED TO ACHIEVE SVR AFTER PRIOR TREATMENT; †SYMPTOMATIC VASCULITIS ASSOCIATED WITH HCV-RELATED
MIXED CRYOGLOBULINAEMIA, HCV IMMUNE COMPLEX-RELATED NEPHROPATHY AND NON-HODGKIN B-CELL LYMPHOMA; ‡NON-LIVER
SOLID ORGAN OR STEM CELL TRANSPLANT RECIPIENTS, HBV COINFECTION, DIABETES
EASL CPG HCV. J HEPATOL 2018;69:461–511.
 ENDPOINTS OF THERAPY
Recommendations Grade of evidence Grade of recommendation

Main endpoint
• Undetectable serum or plasma HCV RNA by sensitive assay
A 1
(LLOD ≤15 IU/mL) 12 weeks (SVR12) or 24 weeks (SVR24)
after EOT
Alternative endpoint
• Undetectable HCV core antigen in serum or plasma by EIA 24 weeks
(SVR24) after EOT A 1
– In patients with detectable HCV core antigen prior to therapy, if HCV RNA assays
are not available and/or not affordable
Additional endpoint
• Undetectable serum or plasma HCV RNA (SVR24) after EOT by qualitative B 1
HCV RNA assay with LLOD ≤1000 IU/mL
– In areas where sensitive assays are not available and/or not affordable
• In patients with advanced fibrosis and cirrhosis, HCC surveillance must be
continued: an SVR will reduce, but not abolish, the risk A 1
of HCC

EASL CPG HCV. J HEPATOL 2018;69:461–511.

 PILIHAN TERAPI PPHI 2017
SOFOSBUVIR
DAA: DIRECT ACTING FDA APPROV 2013
ANTIVIRAL

NUCLEOTIDE ANALOG
INHIBITOR OF NS5B DI INDONESIA 2016
POLYMERASE

PANGENOTYPIC REKOMENDASI PPHI 2017

ACTIVITY

SOFOSBUVIR/RIBAVIRIN: WHO
DOSIS SEKALI SEHARI 2018

INTERAKSI OBAT 2019,

SOFOSBUVIR/VELPATASVIR :
MINIMAL STR
 HCV DAAS APPROVED IN EUROPE IN 2018 AND
RECOMMENDED IN THIS DOCUMENT
Product Presentation Posology
Pangenotypic drugs or drug combinations

Sofosbuvir Tablets containing: 400 mg SOF 1 tablet QD

Sofosbuvir/velpatasvir Tablets containing: 400 mg SOF, 100 mg VEL 1 tablet QD

Sofosbuvir/velpatasvir/ Tablets containing: 400 mg SOF, 100 mg VEL, 100 1 tablet QD

voxilaprevir mg VOX

Glecaprevir/pibrentasvir Tablets containing: 100 mg GLE, 40 mg PIB 3 tablets QD

Genotype-specific drugs or drug combinations

Sofosbuvir/ledipasvir Tablets containing: 400 mg SOF, 90 mg LDV 1 tablet QD

Ombitasvir/ Tablets containing: 75 mg PTV, 12.5 mg OBV, 50 mg 2 tablets QD

paritaprevir/ritonavir RTV

Dasabuvir Tablets containing: 250 mg DSV 1 tablet BID (am & pm)

Grazoprevir/elbasvir Tablets containing 100 mg GZR, 50 mg EBR 1 tablet QD

EASL CPG HCV. J HEPATOL 2018;69:461–511.

 CONTRAINDICATIONS TO THERAPY
• THERE ARE FEW CONTRAINDICATIONS TO TREATMENT WITH DAAS

Recommendations Grade of evidence Grade of recommendation

Certain CYP/P-gp-inducing agents (e.g. carbamazepine, phenytoin) are contraindicated
A 1
with all regimens; risk of significantly reduced DAA concentrations
PIs must not be used in patients with Child–Pugh B or C decompensated cirrhosis or in
A 1
patients with previous episodes of decompensation
In patients with eGFR <30 mL/min/1.73 m2, SOF should only be used if no alternative
treatment approved for use in patients with severe renal impairment B 1
is available

EASL CPG HCV. J HEPATOL 2018;69:461–511.

 TERAPI HEPATITIS C
PADA IBU HAMIL

Stop terapi jika terjadi

kehamilan saat Pilihan : ( tapi
pengobatan. data blm cukup )
Tidak ada vaksinasi
• Ledipasvir
• sofosbuvir
 TERIMA
KASIH
DISAMPAIKAN PADA PERTEMUAN PROGRAM HEPATITIS DAN ISP
DETEKSI DINI HEPATITIS B & C
TGL 15 & 16 APRIL 2019