HEPATOCELLULAR

CARCINOMA
leonardo dairi
 PENDAHULUAN

 KHS urutan kelima yg paling sering

dijumpai dari kanker pada laki-laki dan
urutan kedelapan pada wanita
 Kejadian di Eropa dan US lebih sedikit
dibandingkan di Asia da Afrika
This is the external surface of a normal liver.
The color is brown and the surface is smooth.
A normal liver is about 1200 to 1600 grams.
Couinaud Segmentation

*
Surgical Treatment of HCC
 FISIOLOGI HEPAR
 Metabolisme garam empedu, pigment empedu
 Metabolisme Karbohidrat
 Pembentukan urea, penyimpanan protein (asam
amino)
 Metabolisme lemak, sintesis koleserol dan
penimbunan lemak
 Penimbunan vitamin dan mineral
 Metabolisme steroid
 Detoksifikasi
 Gudang darah dan filtrasi
Hepatocelluler adenoma
Tumor like lesion hepatocytes
Hemangioma
Benign hepatic tumor of cholangiocellular
origin
Benign hepatic tumor of mesenchymal origin
 HEPATOMA (HISTOLOGI)
 KHS (KARSINOMA HEPATOSELULAR)(85%)
HEPATOMA PRIMER DR SEL HEPATOSIT
 KARSINOMA KOLANGIOSARKOMA (10%)
HEPATOMA PRIMER YANG BERASAL DARI
EPITEL SALURAN EMPEDU INTRAHEPATIK
 KARSINOMA CAMPURAN HEPATOSELULAR
DAN KOLANGIOSARKOMA,KARSINOMA
JENIS LAIN (5%)
 HEPATOMA (MAKROSKOPIS)

 TIPE MASSIF,PD SATU LOBUS DAN HANYA

SATU NODUL SAJA
 TIPE NODULER, PALING SERING DIJUMPAI,
HATI MEMBESAR, NODUL YG BANYAK
(IRREGULER)
 TIPE DIFFUS,UMUMNYA SEL HATI MASIH
DALAM BATAS NORMAL TETAPI TERISI
OLEH SEL KARSINOMA YG DIFFUS
 EPIDEMOLOGI

Hepato cellular carcinoma (HCC) a primary

malignancy of the liver, hepatocellular origin
Tumor hati primer ( Karsinoma Hepato Selluler ) 
AS, jarang ditemukan, kejadian tertinggi dijumpai di
Asia Timur, Sahaqra Afrika dan Melanesia
HCC is a major cause of death from cancer in
Eastern Asia and sub-Saharan Africa
HCC causes 662,000 deaths per year, about half
of them in China.
Jarang ditemukan pada usia muda
Insidens meningkat pada usia tua
 OTHER RISK FACTORS
 Obesity
 Diabetes Mellitus
 Hemochromatosis
 Alpha-1 antitrypsin deficiency
 Autoimmune hepatitis
 15-50% of HCC in the US have no established risk
factors
 PATHOGENESIS

Thorgeirsson, S.S. and J.W. Grisham, Molecular pathogenesis of human hepatocellular carcinoma. Nat Genet, 2002. 31(4): p. 339-46.
 PATHOLOGY

“HCC with cholangiolar features, moderately differentiated”

Healthy Liver Hepatic Fibrosis

Cirrhosis Liver Cancer

Healthy Liver Hepatic Fibrosis

Cirrhosis Liver Cancer

KANKER HATI
 20% infeksi kronis 80%
Infeksi HCV: kronis
 berakhir dengan sirosis
 25% sirosis berakhir dengan
kanker hati atau gagal hati

Kelompok Risiko Tinggi HCV:

•Pengguna Narkoba Suntik
•Penerima Transfusi
•Pasien terpapar alat medis
yang tak steril
Here is another example of macronodular cirrhosis. Viral hepatitis (B or
C) is the most common cause for macronodular cirrhosis. Wilson's
disease and alpha-1-antitrypsin deficiency also can produce a
macronodular cirrhosis.
METASTASE TUMOR HATI
INTRAHEPETIK
EKSTRAHEPATIK
( V.Hepatika,V.Porta,V.Kava)
DIAFRAGMA,MEDIASTINUM,PERITONEUM
OESOPHAGUS
PARU - PARU
TULANG
ADRENAL
 GAMBARAN KLINIS
 RIWAYAT ALKOHOL ATAU SIROSIS
 RASA SAKIT ATAU TIDAK ENAK
 TERABA MASSA
 BERAT BADAN MENURUN
 ASITES
 JAUNDICE
 ANOREKSIA,PERUT GEMBUNG
 LETIH,BERAT BADAN MENURUN,
 PERDARAHAN
 DIAGNOSIS
1. Clinis
2. Imaging
3. Blood level of alphafetoprotein, PIVKA
4. Needle biopsy
 DIAGNOSIS
 Kriteria diagnosis KHS (PPHI)
1. Hati membesar berbenjol-benjol dengan/tanpa disertai
bising arteri
2. AFP meningkat lebih dari 500 mg/ml
3. USG,Nuclear medicine,CT scan,MRI,PET menunjukkan
adanya(HCC)
4. Peritoneoscopy dan biopsi menunjukkan (HCC)
5. Biopsi atau aspirasi biopsi jarum halus (HCC)
--- dijumpai 2 atau lebih dari kriteria diatas
DIAGNOSA
AFP MENINGGI  50 – 90 % .
 TUMOR KECIL  BISA NORMAL / SDKT  .
 AFP JUGA BISA ME  PADA SIROSIS HATI .
 TIDAK BERMAKNA.

AFP MONITOR KEBERHASILAN RESEKSI

KURATIF.
PARA NEOPLASTIC COMPLIKASI :
HIPOGLISEMIA
HIPERKALSEMIA
ERITROSITOSIS
HIPERTROFI PULMONARI
OSTEOARTROPATI
 IMAGING / RADIOLOGY
 CT Scan
 MRI Preferred
 USG
 Nuclear Medicine
 Angiography Less usefull
 Plain film
BIOPSI
 USG .
 STAGING .

STAGING SYSTEM HCC ( AJCC )’

KLASIFIKASI TNM
 STAGING SISTEM
TNM SISTEM,OKUDA,MORPHOLOGY,MET,VI
OKUDA SISTEM, BILLIRUBIN,ALB,ASC
CLIP (CANCER OF THE LIVER ITALIAN
PROGRAM),CHILD PUGH
JIS SCORE (JAPAN INTEGRATED STAGING)
BCLC(BARCELONA CLINIC LIVER CANCER)
,CHILD PUGH, PH, BILLIRUBIN
STAGE GROUP
- STAGE I T1 N0 M0
- STAGE II T2 N0 M0
- STAGE III T3 N0 M0
 T 1-3 N1 M0
- STAGE IVa T4 Any N M0
- STAGE IVb Any T Any N M1
 DIAGNOSA BANDING
HEMANGIOMA
ABSESS HEPAR
TUMOR METASTASE
KISTA HATI
PENATALAKSANAAN
 TERAPI DEFINITIF  OPERASI
 HANYA 10 – 30 %  MASIH OPERABLE
 HANYA 50 – 70 % YANG CURATIVE

KRITERIA NON OPERATIF :

 ADA PENYAKIT EKTRA HEPATIK
 GANGGUAN FUNGSI HATI BERAT
 MASA TUMOR YANG MASIF
 V. PORTA ATAU V. CAVA SUDAH TERLIBAT
 KONTRA INDIKASI RELATIF
 PENGOBATAN
TERAPI OPERASI
RESEKSI
TRANSPLANTASI HATI
TERAPI NON OPERATIP
RFA (RADIO FREKWENSI ABALATIO)
INJ.ETANOL MRNI (95%),INTRA TUMOR
PERKUTANTAS
 PENGOBATAN
KEMOEMBOLISASI ARTERI HEPATIK
PERKUTANERAPI OPERASI
KEMOTERAPI SISTEMIK
RADIOTERAPI
TAMOXIPEN
INJ.ASAM ASETAT PERKUTAN
SORAFENIF (95%)
 Available treatment options for
hepatic neoplasm
Treatment modality
1. Liver transplantation
2. Hepatic resection
3. Thermal ablation
(Radiofrequency,microwa
ve,laser)
4. Cryotherapy
Limitations
1.Donor avaibility, Three or
fewer lesions, none > 3 cm ,
Solitary lesion < 5 cm
2.Minimal or no cirrhosis, three
or fewer lesions
3.Three or fewer lesions, each <
5 cm
4.Small lesions, rarely done
percutaneously
Available treatment options for hepatic
neoplasm
5. Conformal radiation 5. Solitary lession
6. Proton beam therapy 6. Radiation-induced liver
disease
7. Intra-arterial
7. Radiation hepatitis,
radiotherapy renal/pancreatic damage
8. Intralesional ethanol 8. Few, small lesions, difficulty
viewing during injections,
9. Chemoembolization requires multiple sessions
9. Adequate hepatic function,
patent portal vein,
10.Systemic or intra considerable local toxicity
arterial chemothrapy 10.Toxicity, lack of efficacy
 Currative Treatments for Early HCC

• Liver transplant / Resection (< 5% of cases)

– 5 yr survival , 41-93%
• Radiofrequency ablation (RFA)
– 5 yr survival , 33-40%
– Solitary tumors, max 3-5 cm
• Percutaneous ethanol injection.
– 5 yr survival , 29-71%
– Solitary tumors, max 3-5cm
 Palliative Treatment for Advanced HCC

• Transarterial chemoembolization (TACE)

– 2 yr survival 24-63%
– No vascular invasion, preserved liver function, no
extrahepatic spread

• Radiation therapy

• Systemic chemotherapy
 Poor prognosis with advanced HCC
Five-year survival rates, based upon the newer staging
system are as follows,
 Stage I – 55 percent
 Stage II – 37 percent
 Stage III – 16 percent
 Stage IV - 0 percent

 75% of HCCs present when stage III/IV

 Most patients with advanced HCC die within 1 year of
diagnosis, with <10% of patients surviving after
5 years
 Main challenge in treating advanced HCC is the
underlying liver dysfunction
 PENCEGAHAN
Usaha difokuskan kepada pencegahan.
Dpt dilakukan beberapa tindakan prevention seperti,
Vaksinasi anak-anak pada usia dini terhadap hepatitis
B,
Mengurangi risiko untuk tertular hepatitis C
Menggurangi atau menghindarkan konsumsi minuman
beralkohol yang berlebihan. ‘
Makan makanan bergizi seperti buah dan sayuran.
Modifikasi gaya hidup.
 KESIMPULAN
o KHS adalah suatu tumor ganas primer pada hati yang
paling sering ditemukan
o Faktor resiko KHS adalah infeksi
HBV,HCV,alkohol,aflatoksin B1, dan sirosis
o Gejala klinis adalah sakit perut,bengkak pada perut
kanan, nafsu makan berkurang,dan rasa lemas
o Diagnosa dapat menggunakan kriteria PPHI
o Pemeriksaan KHS tdd, laboratorium,radiologi, biopsi
o Pengobatan KHS tdd bedah,transplantasi,tindakan
non bedah
 DIAGNOSIS
D/ SUBKLINIS HEPATOMA, STAD.DINI,TANPA
GEJALA DAN TANDA FISIK YG JELAS
 D/NON INVASIF
 D/PATOLOGIS
 MAJOR RISK FACTOR
 HBV
o 70-90% of chronic cases in cirrhosis
o Treatment decrease risk
 HCV
o 1-3% of HCV develop HCC
o Treatment decrease risk
 Co-infection
 Aflatoxins (Aspergillus fumigatus)
o 4 fold increased risk HCC
 Alcohol
o > 50-70g/day
o Synergist with HCV and HBV
 Nonalcoholic Steatohepatitis?
El-Serag, H.B. and K.L. Rudolph, Hepatocellular carcinoma: epidemiology and molecular carcinogenesis. Gastroenterology, 2007. 132(7): p. 2557-76.
Brunetto M.R., O.F., Koehler M., et al., Effect of interferon-alpha on progression of cirrhosis to hepatocellular carcinoma: a retrospective cohort study.
International Interferon-alpha Hepatocellular Carcinoma Study Group. Lancet, 1998. 351(9115): p. 1535-9.