STEP 7

1 Mengapa pasien mudah lelah dan demam ?

Selain menyebabkan demam, IL-1 juga bertanggung jawab terhadap gejala lain
seperti timbulnya rasa kantuk/tidur, supresi nafsu makan, dan penurunan
sintesis albumin serta transferin. Penurunan nafsu makan merupakan akibat dari
kerjasama IL-1 dan TNF-. Keduanya akan meningkatkan ekspresi leptin oleh sel
adiposa. Peningkatan leptin dalam sirkulasi menyebabkan negatif feedback ke
hipothalamus ventromedial yang berakibat pada penurunan intake makanan
Pusat otak yang berpengaruh terhadap nafsu makan a.
1 Pusat kenyang (medial) : nucleus ventromedial i.
a Rangsangan : berhenti makan ii.
b Lesi : hiperfagia dan bila persediaan makanan banyak akan
mengakibatkan terjadinya sindrom obesitas
2 Pusat lapar (lateral) : area hipotalamik lateral (anyaman nucleus berkas
proensefalon medial pada pertemuan dengan serabut polidohipotalamik)
a Rangsangan : membangkitkan perilaku makan ii.
b Kerusakan : anoreksia (kehilangan nafsu makan) yang fatal pada
manusia sehat, kadangkala menyebabkan kematian karena kelaparan
(lethal starvation)
3 Badan mamilaria : menjilat-jilat bibir dan menelan
Sumber : Fisiologi Kedokteran Guyton & Hall

Nyeri perut kanan atas kerusakan sel-sel hepar kemungkinan karena

virus/obat-obatan (infeksi/inflamasi) hepar tdk bs menyimpan glukosa
glukosa dlm darah meningkat penderita tetap merasa kenyang tidak
nafsu makan.
Kalau misalkan heparnya membesar menekan gaster gaster terasa
penuh merangsang untuk mengirim sinyal kalau gaster penuh
Kerusakan hepar yg disebabkan virus mengeluarkan sinyal ke reseptor
timbul gejala salah satunya nafsu makan menurun
Tjd kerusakan hepar sel kupffer menghasilkan tnf alfa- dan il-6
peningkatan serotonin merangsang pusat akan di hipotalamus
kurang nafsu makan
Serotonin reseptor 5ht3 (mual-muntah) terangsang timbul gejala
mual-muntah
Demam (interaksi pirogen eksogen dan endogen) merangsang il-1 dan
il-2 keluar merangsang hipotalamus keluar serotonin peningkatan
serotonin merangsang pusat akan di hipotalamus kurang nafsu
makan

Efektor
Hipotalamus, suatu bagian otak merupakan pusat pengatur utama dari
napsu makan. Neuron-neuron yang mengatur napsu makan tampaknya
didominasi oleh neuron serotoninergik, walaupun neuropeptidea Y (NPY)
dan Agouti-related peptide (AGRP) juga memainkan peran penting.
Cabang-cabang Hypothalamocortical dan hypothalamolimbic projections
berkontribusi terhadap kesadaran adanya rasa lapar. Proses-proses
somatik yang dikendalikan oleh hipotalamus meliputi tonus vagus
(aktivitas sistem saraf parasimpatis), stimulasi tiroid (tiroksin mengatur
laju metabolisme), poros hipotalamus-hipofisis-adrenal serta sejumlah
mekanisme lain.
Sensor
Hipotalamus merasakan rangsang-rangsang eksternal melalui sejumlah
hormon, seperti leptin, ghrelin, PYY 3-36, orexin dan CCK
(cholecystokinin); semua ini memodifikasi respon hipotalamus. Beberapa
diproduksi di saluran cerna dan lainnya oleh jaringan adiposa (leptin).
Mediator sistemik, seperti tumor necrosis factor-alpha (TNF), interleukin
1 dan 6 serta corticotropin-releasing hormone (CRH) mempengaruhi
napsu makan secara negatif; mekanisme ini menjelaskan mengapa orang
sakit makan lebih sedikit. Sitokin-sitokin ini bekerja dengan menambah
jumlah serotonin (5-hidroksitriptofan atau 5-HT) di hipotalamus. Kadar
serotonin yang meninggi ini pada gilirannya akan merangsang sistem
melanocortin dan menyebabkan anoreksia.
dr Iyan Darmawan

2 Mengapa pasien nyeri tekan perut kanan atas dan sub ikterik
sklera?
RIGHT UPPER QUADRANT ABDOMINAL PAIN
ORGAN DI REGIO KANAN ATAS
-

Hepar
Vesica Fellea
Flexura Coli dextra

NYERI KANAN ATAS

Hal ini disebabkan oleh karena adanya proses perlawanan terhadap
antigen yang masuk kedalam hepar, di hepar ada makrofag ( sel kuppfer )
yang untuk melawan antigen tersebut serta ada aktivasi dari mediator
madiator inflamasi dan terjadilah proses peradangan, proses peradangan
tersebut membuat sel hati menjadi rusak dan terjadi penyumbatan pada
hepatosit.
SUB SKLERAL JAUNDICE

(ROBIN KUMAR, PATHOLOGY)

3 Mengapa nafsu makan menurun ?

Penurunan nafsu makan

Nukleus arcuatus adalam kumpulan neuron terletak dekat dengan dasar

ventrikel 3 dan berperan dalam rasa lapar dan kenyang. Nukleus lateral
(pusat lapar), nukleus ventromedial (pusat kenyang)
Memproduksi dua subset yaitu NPY (perangsang nafsu makan) dan
melanokortin (menekan nafsu makan) terutama alfa melanosit stimulating
hormone
Leptin -> salah satu adipokin yaitu hormon yang dikeluarkan oleh lemak.
Bila tubuh kelebihan lemak maka leptin akan meningkat -> leptin
menginaktivasi NPY dan aktivasi melanokortin sehingga nafsu makan
menurun, begitupun sebaliknya
Insulin -> bila sekresi insulin menurun -> mengaktivasi NPY dan in-aktivasi
melanokortin sehingga nafsu makan meningkat
Adipokin lain yang bisa menghambat NPY dan aktivasi melanokortin : TNFalfa dan IL-6
(SHERWOOD)

4 Apa hubungan riwayat tranfusi dengan keluhan pasien ?

TRANSMISSION

Modes of transmission of HCV can be divided into percutaneous

(blood transfusion and needlestick inoculation) and
nonpercutaneous (sexual contact and perinatal exposure).
Patients are often unwilling to disclose percutaneous risk factors,
and therefore nonpercutaneous transmission may represent
occult percutaneous exposure.
Percutaneous Transmission
Blood transfusion, before the introduction of screening, and
injection drug use are the most clearly documented risk factors
for HCV infection. Following the introduction of anti-HCV
screening of blood donors between 1990 and 1992, the number of
transfusion-related cases of HCV infection declined sharply, and
currently less than 1 case occurs per 2,000,000 units
transfused.76,77
Injection drug use has always been the major route of HCV
acquisition in the United States and accounts for an increasingly
large portion of cases, at least 68% of new cases of HCV infection,
since the virus was essentially eliminatedfrom the blood supply.74
The prevalence of HCV infection in injection drug users ranges
from 57% to 90%.1,78 Although risk factors for hepatitis B virus
(HBV) and human immunodeficiency virus (HIV) infection overlap
with those for HCV infection, the prevalence of HCV infection in
this population is the highest among the three viruses. The
majority of injection drug users become anti-HCV positive within
six months of initiating injection drug use with shared
paraphernalia.
Chronic hemodialysis is also associated with increased rates of
HCV infection. The frequency of anti-HCV in patients on
hemodialysis ranges from 11.6% in the United States to 55% to
85% in Jordan, Saudi Arabia, and Iran.79 Serologic assays for antiHCV may underestimate the frequency of HCV infection in this
relatively immunocompromised population, and virologic assays
may be necessary for accurate diagnosis.80
Transmission may occur from infected patients to health care
workers. A serologic survey of emergency department patients
found that 18% were infected with HCV.81 The proportion with
HCV infection was even higher in patients with a history of
intravenous drug use (83%), past blood transfusion (21%), or a
male homosexual lifestyle (21%). Although all potential routes of
transmission of HCV infection to hospital workers are not obvious,
needlestick injuries probably account for a large proportion of
cases. Anti-HCV seroconversion rates are approximately 0.3% to
4% in longitudinal studies of health care workers after
percutaneous inoculation from antiHCV-positive sources,
although the risk is dependent on the type of needle (hollow
versus solid, infusion versus withdrawal), volume of inoculum,
depth of injury, time the body fluid has spent ex vivo, level of

viremia (viral load), and HIV status of the inoculating body

fluid.82,83 In one study, 99% of surgeons in training experienced
at least one needlestick by their final year of residency. Fiftythree percent of these injuries involved a high-risk patient, and
only 49% were reported to the employee health service.84 As a
result, as many as 16,000 new cases of HCV are estimated to have
been transmitted to health care workers worldwide in 2000.85
Although less common, transmission of HCV also may occur from
health care workers to patients. Because acute HCV infection
often is subclinical, nosocomial transmission may occur with
greater frequency than has been recognized previously. Strict
adherence to universal precautions to protect health care workers
and patients is critically important. At this time, no treatment is
effective for post-exposure prophylaxis, and no data support
such treatment even if it were available.
Nonpercutaneous Transmission
Nonpercutaneous modes of HCV transmission include sexual
practices and childbirth. Available evidence indicates that
transmission by nonpercutaneous routes occurs but is inefficient.
From 10% to 20% of patients with HCV infection report that their
only risk factor is sexual exposure to a partner with HCV infection.
Most seroepidemiologic studies, however, have demonstrated
anti-HCV in only a small proportion of sexual contacts of infected
persons. In a large prospective study of monogamous
seronegative partners of HCV-infected patients who denied anal
intercourse and intercourse during menstruation, no instances of
HCV transmission of the same sequenced virus occurred over a
10-year period of time.86 Therefore, many of the cases
presumed to be the result of sexual transmission are likely the
result of other, perhaps unreported or unrecognized, exposures.
If the index sexual partner is infected with HIV or the partners
engage in high-risk sexual practices, such as anal intercourse,
however, the transmissibility of HCV is likely increased.87
Furthermore, epidemiologic studies have shown that persons with
multiple sex partners have a higher prevalence of HCV infection.1
Whether sexually transmitted diseases promote transmission of
HCV through breakdown of mucosal or immune barriers is unclear.
HCV-infected persons commonly are counseled to notify sexual
partners of their HCV status. The risk of sexual transmission is
negligible in monogamous couples that do not engage in high-risk
sexual practices.86 Barrier methods should be recommended,
however, to persons in non-monogamous relationships or those
engaging in high-risk sexual practices.
Compared with the high efficiency of perinatal transmission of
HBV infection (see Chapter 78), the risk of perinatal transmission
of HCV infection is low, averaging 5.1% to 6.7% for HCVmonoinfected patients and two to three times higher for HIV-HCVcoinfected patients.88,89 Mothers with a high viral load are more

likely to transmit HCV to their infants, a finding that may explain

why infants born to mothers with HIV-HCV coinfection are at
higher risk of HCV infection. Interestingly, the use of highly active
antiretroviral therapy (HAART) in HIV-HCV-coinfected mothers
may decrease the risk of perinatal transmission of both HIV and
HCV.89 Data regarding the risk associated with vaginal delivery
as opposed to cesarean delivery are uncontrolled, but evidence
for a higher risk of HCV transmission with vaginal delivery is
unconvincing. This issue remains controversial, and some
authorities recommend elective cesarean section before
membrane rupture.88
Although little data exist, the risk of HCV transmission from
breastfeeding is negligible to small. The Centers for Disease
Control and Prevention have concluded that breastfeeding by
HCV-infected mothers is generally safe. Some authorities have
suggested, however, that mothers with a high viral load (greater
than 108 copies/mL, see later) may pose a risk.90 Because antiHCV can be acquired passively by the infant, molecular testing
for HCV RNA is required if the diagnosis of HCV infection is
suspected. Infants of infected mothers should not undergo
serologic testing for anti-HCV before the age of 18 months
because maternal antibodies may persist in the infants serum
and lead to diagnostic confusion.
Sporadic HCV Infection
The source of transmission is unknown in 9% to 27% of cases of
HCV infection.78 Such sporadic HCV infection probably results
from an undisclosed or unrecognized percutaneous route of
infection. This presumption is supported by the observation that
intranasal cocaine use is not considered a risk factor for HCV
transmission (although it was considered a risk factor in the
past).91 HCV infection can be acquired from non-commercial
tattooing and body piercing when equipment is reused, shared, or
improperly sterilized. Commercial tattooing is now well controlled
and probably conveys little risk of HCV infection. Iatrogenic
transmission of HCV is well documented in a variety of
circumstances, most notably via contaminated multi-use vials and
inadequately sterilized multi-use instruments and syringes, as
seen with schistosomal treatment campaigns in Egypt.92
(Zakim and Boyers hepatology : A textbook of liver disease,
Elsevier)
5 Apa interpretasi dari hasil lab ?
1 ASPARTAT AMINOTRANSFERASE (AST)
SERUM GLUTAMIC OXALOACETIC TRANSAMINASE (SGOT)
a Peningkatan tegas (5x/>): hepatitis akut, hepatitis krn obat,
sirosis krn alkohol, pankreatitis akut, mononukleosis
infeksiosa, AMI, trauma otot
b Peningkatan sedang (3-5x): Obstr tr.biliaris, hepatitis kronik,
tumor hati

c
2

Peningkatan ringan (2-3x): sirosis, perlemakan hati

ALANINE AMINO TRANSFERASE (ALT)

SERUM GLUTAMIC PYRUVIC TRANSAMINASE (SGPT)
a Peningkatan 20-50X: hepatitis virus/obat
b Peningkatan 10-<20x: hepatitis kronik, kolestasis/kolesistitis,
penyembuhan hepatitis
c Peningkatan 3-10X: obat-obatan hepatotoksik (allopurinol,
aspirin, ampisilin, heparin, barbiturat), AMI, pankreatitis akut
d Peningkatan 1-2x: kongesti hepatik
Patofisiologi vol 1, Sylvia & Wilson, EGC

The AST/ALT ratio in serum is also regarded as a useful indicator, with a

ratio greater than 2 being highly suggestive of alcohol-induced hepatic
injury. In contrast, in patients with acute or chronic viral hepatitis or
extrahepatic biliary obstruction, an AST/ALT ratio of less than 1 is typically
observed, although a correlation between an AST/ALT ratio greater than 1
and the presence of underlying cirrhosis has been described in patients
with chronic hepatitis B infection. An AST/ALT ratio of greater than 1 in the
setting of nonalcoholic chronic liver disease
should raise suspicion regarding underlying cirrhosis, but in the presence
of cirrhosis the AST/ALT ratio may be less useful in differentiating alcoholic
from nonalcoholic forms of liver disease.
The presence of anti-HCV supports a diagnosis of acute hepatitis
C.Occasionally, testing for HCV RNA or repeat anti-HCV testing later during
the illness is necessary to establish the diagnosis.Absence of all serologic
markers is consistent with a diagnosis of non-A, non-B, non-C hepatitis, if
the epidemiologic setting is appropriate. In patients with chronic hepatitis,
initial testing should consist of HBsAg and anti-HCV.Anti-HCV supports and
HCV RNA testing establishes the diagnosis of chronic hepatitis C.

Harrison infectious disease

6 Apa hubungan anti-hcv + dengan keluhan pasien ?

7 Pemeriksaan penunjang untuk menegakkan diagnosis ?

8 Apa DD dan diagnosis dari skenario ?
DD :
1 Hepatitis kronis et causa hepatitis c anti hcv + , tranfusi darah 10
tahun yang lalu, sub ikterik sklera
2 Sirosis et causa hepatitis C
3 HCC
4 Kolestasis
5 Fatty Liver
9 Bagaimana etiologi dan patogenesis dari DD ?
Hepatitis C Kronis :
Patogenesis
Bila enam bulan atau lebih parenteral setelah serangan hepatitis virus akut,
masih tetap ada tanda-tanda biokimia atau gejala dari penyakit hati, maka
kita pikirkan penyakit ini menjadi kronik. Dari beberapa variasi hepatitis
kronik, hanya ada dua bentuk yang menunjukkan perubahan yang khas,
menurut kritria histopatologi : ( 1 ) hepatitis kronik persisten dan ( 2 )
hepatitis kronik aktif, yang kadang-kadang disebut hepatitis kronik agresif.

Diferensiasi dari kedua bentuk ini mempunyai arti klinik yang penting.
Hepatitis kronik aktif, berarti meneruskan proses kerusakan hati, yang
menyebabkan terjadinya sirosis dan kegagalan hati. Sebaliknya hepatitis
kronik persisten, merupakan kelainan jinak yang akhirnya sembuh dengan
sendirinya. Sayangnya, tidak ada kriteria yang dapat dipercaya selama
stadium hepatitis virus akut, untuk mengidentifikasi penderita yang
mempunyai risiko tinggi menjadi hepatitis kronik.
Terutama, beratnya serangan akut mempunyai kolerasi dengan menetapnya
infeksi virus. Penemuan serologi yang memberi kesan kemungkinan
terjadinya proses kronik pada hepatitis B adalah HbsAg, HbeAg yang menetap
dalam serum, titer anti-HBc yang tinggi, HBV-DNA dan DNA polimerase dalam
serum. Pada beberapa penderita, setelah suatu periode yang berubah-ubah
dari 1 sampai 20 tahun, munculnya antibodi anti-Hbe secara spontan
menunjukkan pengendalian terhadap viremia dan penghentian kerusakan
hati.
( Buku Ajar Patologi 2, Robins dan Kumar edisi IV )

HCV ( melalui parenteral ) Partikel Dane ( peredaran darah ) hati

( mengalami replikasi virus ) partikel Dane utuh HCV mengakifkan respon
imun non spesifik ( dibantu oleh sel NK dan NKT respon imun spesifik aktif (
oleh sel limfosit B dan T ) aktivasi sel CD8 + terjadi setelah kontak reseptor
sel T dg kompleks peptide VHC MHC kelas I yg ada pada permukaan dinding
sel hati dan pada permukaan APC dan dibantu oleh rangsangan sl CD4+ yg
sebelumnya mengalami kontak dengan komplek peptida VHC MHC kelas II pd
dinding APC sel T CD8+ mengeliminasi virus pada sel hati yg terinfeksi
nekrosis hati meningkatnya ALT ( mekanisme sitolitik ) sel T CD4+ akan
mengaktivasi sel limfosit B memproduksi antibody
Buku Ajar Ilmu Penyakit Dalam.Edisi III
Common to all forms of chronic hepatitis are histopathologic distinctions
based on localization and extent of liver injury.These vary from the milder
forms, previously labeled chronic persistent hepatitis and chronic lobular
hepatitis, to the more severe form, formerly called
chronic active hepatitis.When first defined, these designations were felt to
have prognostic implications, which have been challenged by more recent
observations. Categorization of chronic hepatitis based primarily on
histopathologic features has been replaced by a more
informative classification based on a combination of clinical, serologic, and
histologic variables. Classification of chronic hepatitis is based on (1) its
cause; (2) its histologic activity, or grade; and (3) its degree of
progression, or stage. Thus, neither clinical features alone nor histo-logic
featuresrequiring liver biopsyalone are sufficient to characterize and
distinguish among the several categories of chronic hepatitis.

CLASSIFICATION BY CAUSE
Clinical and serologic features allow the establishment of a diagnosis of
chronic viral hepatitis, caused by hepatitis B, hepatitis B plus D, or
hepatitis C; autoimmune hepatitis, including several subcategories, I and II
(perhaps III), based on serologic distinctions; drug-associated chronic
hepatitis; and a category of unknown cause, or cryptogenic chronic
hepatitis (Table 93-1). These are addressed in more detail below.

CLASSIFICATION BY GRADE
Grade, a histologic assessment of necroinflammatory activity, is based on
examination of the liver biopsy. An assessment of important histologic
features includes the degree of periportal necrosis and the disruption of
the limiting plate of periportal hepatocytes by inflammatory cells
(so-called piecemeal necrosis or interface hepatitis); the degree of
confluent necrosis that links or forms bridges between vascular structures
between portal tract and portal tract or even more important bridges
between portal tract and central veinreferred to as bridging necrosis; the
degree of hepatocyte degeneration and focal necrosis within the lobule;
and the degree of portal inflammation. Several scoring systems that take
these histologic features into account
have been devised, and the most popular are the histologic activity index
(HAI) and the METAVIR score . Based on the presence and degree of these
features of histologic activity, chronic hepatitis can be graded as
mild,moderate, or severe.

CLASSIFICATION BY STAGE
The stage of chronic hepatitis, which reflects the level of progression of
the disease, is based on the degree of hepatic fibrosis.When fibrosis is so
extensive that fibrous septa surround parenchymal nodules and alter the
normal architecture of the liver lobule, the histologic lesion
is defined as cirrhosis. Staging is based on the degree of fibrosis as
categorized on a numerical scale from 06 (HAI) or 04 (METAVIR).

10 Apa faktor risiko, pencegahan dan penatalaksanaan dari DD

Fakror Risiko

VHC ditularkan melalui kontak dengan darah yang terinfeksi,misalnya

pada:
1 Penggunaan instrumen medis yang terkontaminasi.
2 Penggunaan jarum suntik yang tidak steril atau digunakan secara
bergantian.
3 Tindik (telinga, hidung, dan bagian tubuh lain), tato, dan cukur dengan
alat yang tidak steril.
4 Penerima transfusi atau produk darah sebelum tahun 1992 atau
dengan sumber yang belum di-skrining.
5 Aktivitas seksual yang tidak terproteksi atau penularan pada bayi dari
ibu yang terinfeksi, walaupun kasusnya sangat jarang
Sumber : http://hepatitis.roche.co.id/content/dam/indonesiahepatitis/doc/Hepatitis%20C%20Booklet.pdf
Protab

Chronic Hepatitis C Treatments

Treatment of chronic hepatitis C depends on the person. Even
though you have chronic hepatitis C, you may not need or get help from
treatment. Some people may not be able to handle treatment because of
side effects.
The FDA has approved the following treatments for hepatitis C:

Incivek (telaprevir)

Olysio (simeprevir)

Pegylated interferon alfa-2a

Pegylated interferon alfa-2b

Ribavirin

Sovaldi (sofosbuvir)

Harvoni (sofosbuvir, ledipasvir)

Standard interferon alfa

Victrelis (boceprevir)

Viekira Pak (ombitasvir, paritaprevir, dasabuvir, ritonavir)

Hepatitis C treatments are changing quickly. Until recently, the most

common treatment was a blend of shots and pills that usually came with
some unpleasant side effects. It typically combined a shot of interferon or
pegylated interferon with the pills ribavirin and another drug. But recently,
two new drugs have been approved as hepatitis C treatments.

The newer drugs Olysio (simeprevir) and Sovaldi (sofosbuvir) cure more
people in less time with fewer side effects. The drugs are taken together with
interferon and ribavirin. Doctors hope that soon more people will be able to
stop taking interferon, the treatment that causes so many side effects.

Kriteria yang harus dipenuhi sebelum pemberian terapi Interferon:

(Sulaiman HA,Julitasari, 2004, hal 21)
1.Anti HCV [+] dengan informasi stadium dan aktivitas penyakit, HCV
RNA [+], genotip virus, biopsi.
2.Ada / tidaknya manifestasi ekstra hepatic.
3.Kadar SGOT/ SGPT berfluktuasi diatas normal.
4.Tidak ada dekompensasi hati.
5.Pemeriksaan laboratorium:
a. Granulosit > 3000/ cmm
b. Hb > 12 g/dl
c. Trombosit > 50000/ cmm.
d. Bilirubin total < 2 mg/ dl
e. Protrombin time < 3 menit.
Berdasarkan rekomendasi konsensus FKUI PPHI (2003, hal 21) :
1 Terapi antivirus diberikan bila ALT >2 N
2 Untuk pengobatan hepatitis C diberikan kombinasi Interferon dengan
Ribavirin
3 Ribavirin diberikan tiap hari, tergantung berat badan selama
pemberian interferon dengan dosis :
a. < 55 kg diberikan 800 mg/hari
b. 5675 kg diberikan 1000 mg/hari
c. > 75 kg diberikan 1200 mg/hari
4 Dosis Interferon konvensional 3,41/2,5 MU seminggu 3 kali, tergantung
kondisi pasien
5 Pegylated Intenfenon Alfa 2a diberikan 180 ug seminggu sekali selama
1 bulan pada genotipe 1&4, dan 6 bulan pada genotipe 2 dan 3. pada
Pegylated Interferon Alfa 2b diberikan dengan dosis 1,5ug/kgBB/kali
selama 12 bulan atau 6 bulan tergantung genotip
6 Dosis Ribavirin sedapat mungkin dipertahankan. Bila terjadi efek
samping anemia, dapat diberikan enitropoitin.
Sumber :
http://elib.fk.uwks.ac.id/asset/archieve/jurnal/Vol1.no2.Juli2008/DETEKSI
%20HEPATITIS%20C.pdf