Cirrhosis and HCC. Dr.Abonyi Margit PhD SE 1st.Medical Clinic

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Cirrhosis and HCC

Dr.Abonyi Margit PhD SE 1st .Medical Clinic

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Cirrhosis

 6.000-8.000 deaths in Hungary

 A 4. cause of death in Hungary

 Kb. 1.000.000 suffering of chronic hepatic problem

 M:F 2:1

 5-20 years developing HCC

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Etiology of cirrhosis

 Hepatitis C

– 50 - 70% in Europe and North America

– 70% in Japan

– 20% in Asia and Africa

 Hepatitis B

– 70% in Asia and Africa

– 10 - 20% in Europe and North America

– 10 - 20% in Japan

 Alkohol

– 10%- 20%

 Other cause

– 10% (PBC, PSC, PCT, hemochomatosis etc.)

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Hepatocellular carcinoma (HCC)

complex pathogenezis

 A HCC pathogenesis multifactorial

– Hepatitis vírus infection

– Immun diseases( PBC,PSC, AIH)

– Toxins(alkohol,aflatoxin, pesticides)

– Genetic diseases(HH, M: Wilson)

 HCC is developing in 85% in cirrhosis hepatis Chronic liver damage Hepatocita regeneration Cirrhosis Genetic changes HCC

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Cirrhosis -classification

 By morphology

– Micronodular(mainly alkoholic origin)

– Macronodularis (mainly post- hepatitis origin)

– Mixed form

 By clinical data

– Latent

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Diagnosis of cirrhosis

 Physical signs – Icterus – Spider naevus – Caput medusae – Palmar eryhtema – Splenomegaly – Ascites  Laboratory data

– ALT-AST-GGT-LDH –SeBilirubin elevation

– Low level of albumin, prothrombin, kolinesterase

 US- CT- MRI-MRCP

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NASH: non-alcoholic steatohepatitis

 Clinical picture

– Obesitas( BMI over 30), diabetes mellitus, hypertension

– US- focal deposition or bright liver  Laboratory

– Elevated liver enzymes-ALT/AST, high triglycerid and cholesterol

– High inzulin (inzulin resistency  Prevalencia

– Is elevating , because of obesity and DM type 1 and 2, and insulin resistency

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Gyomor

Leukaemia Non-Hodgkin lymphoma

Incidency and mortality of HCC in

Europe

Ferlay J, et al. Ann Oncol 2007;18:581–592.

A daganat incidenciája * Esetszám 0 100,000 200,000 300,000 400,000 Larynx Oesophagus Ovarium Máj Pancreas Bőr melanoma Leukaemia Vese Szájüregi/pharynx Non-Hodgkin lymphoma Gyomor Uterus Hólyag Tüdő Colon és rectum Prostata Emlő Daganatos mortalitás* Halálozások száma 0 100,000 200,000 300,000 Larynx Oesophagus Ovarium Máj Pancreas Bőr melanoma Vese Szájüreg/pharynx Uterus Hólyag Tüdő Colon ésrectum Prostata Emlő

*Becsült incidencia és mortalitás 2006-ban

48 000 new cases / year

46 000 deaths / year

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HCC

Infection

Hepatitis C krónikus infekció Hepatitis B krónikus infekció Hepatitis delta krónikus infekció Metabolic disease

Herediter haemochromatosis Alfa-1-antitripszin deficiencia Porphyria cutanea tarda Herediter thyrosinaemia Toxins Alcohol Aflatoxin B1 Smoking Hormons Anabolic steroids Oestrogen

Oral antibaby drugs

Megelőző májbetegség: Bármely okból kialakult cirrhosis Other

„ Non alcoholic fatty liver disease=NAFLD”, non-alcoholic steatohepatitis=NASH Obesity and diabetes mellitus

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HCC and HCV

 3-8 % of HCV developing carcinoma

 Hungarian HCC incidency : 600-900 new cases /year

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Tumor- surveillance

6 monthly must control the patients with

cirrhosis hepatis : US, AFP and CEA and liver

laboratory tests

Peck-Radosavljevic M, et al. Eur J Gastroenterol Hepatol 2009; epub ahead of print.

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Sangiovanni A, et al. Gastroenterol 2004;126:1005–1014.

HCC survival can be better by the

surveillance

HCC diagnózis óta eltelt idő( év )

10 T úl él és (%) 100 0 75 50 25 0 1 2 3 4 5 6 7 8 9 1987–1991 (n=52) 1992–1996 (n=37) 1997–2001 (n=23) p=0.009 vs. 1987–1991 p=0.018 vs. 1992–1996

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Clinical picture of HCC

 40% without any signs

 Non specific clinical data

– Abdominal pain – Loss of appetite – Losing weight – anorexia – Hepatomegaly – Ascites – Icterus

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HCC

 Anamnesis and physical status

 Liver laboratory parameters

 Tumormarkers ( AFP, CEA )

 Abdomainal US

 Abdominal CT / MRI

 In specific cases: angiography, ERCP, MRCP, PET

 Looking for metastases : X-ray of the chest, abdominal US, bone scan

 Biopsy from the tumor:

– FNAB

– Core biopssy by Menghini needle

– Laparoscopy

– Laparotomy

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HCC (AASLD)

Stabil

>18–24 month Getting larger

Surveillance

i 6–12 month Ismételt biopszia _{vagy ellenőrzés}

CT/ MRI/PET and biopsy Diagnostic for HCC <1 cm 1–2 cm >2 cm 1 dinamic scanning 2 results are +for vascular signs 1 is +for vascular signs Atípical Vascular signs HCC 2 different dinamic scanning

–

+

Bruix J, et al. Hepatology 2005;42:1208–1236.

US every 6th month Atípical Vascular signs 1 is +for vascular signs and AFP 200 ng/ml or higher Ismételt biopszia vagy ellenőrzés Repeated bopsy Biopsy Not diagnostic

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HCC komplex therapy

 Curative therapy ( early stage)-30% of HCC pts -5 year survival 40-70%

 Surgery

– Liver transplantation

– Resection

Intervencious radiology therapy -50% of HCC pts-survival 11-20 months

• Radiofrekvens ablation (RFA)

• Percutan ethanol infiltration (PEI)

 Palliatív treatment (in advanced stage)-20 % -survival 3-11 months

• Transarterial kemoembolization (TACE)

– Systematic treatment: Nexavar (Sorafenib) per os tablets

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Take home message

 Regular control of the cirrhotic patients and physical examination ,

 Every 6. month( or if it is possible, every 3. month) abdominal US, and AFP!!!

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Pre HCC stages

 Adenoma

 Focal nodular hyperplasia( FNH)

 TBC

 Sarcoidosis

 Fungal infection

 Hematological infiltration

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Thrombosis

-vena portae thrombosis: suddenly developed ascites,

abdominal pain, elevated D-dimer, US or CT or MRI or Angiography

Th: sc heparin 2x/ day and diuretics

-venae hepaticae thrombosis: Budd-Chiari syndrom- ( clinicsl signs are the same as above)