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Complain: right quadrant pain intermittently for 2 months.

A case:. Complain: right quadrant pain intermittently for 2 months. Concomitant : anorexia usually and diarrhea occasionally P.E: no special sign Blood-RT: normal Stool-RT: normal Past-H: HBV infection for 20 ys.

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Complain: right quadrant pain intermittently for 2 months.

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  1. A case: Complain: right quadrant pain intermittently for 2 months. Concomitant : anorexia usually and diarrhea occasionally P.E: no special sign Blood-RT: normal Stool-RT: normal Past-H: HBV infection for 20 ys. Family-H: mother died of HBV-cirrhosis Male, 41 y.o. Diagnosis ?

  2. Hepato-Cellular Carcinoma (HCC) !

  3. Hepato-Cellular Carcinoma (HCC) Chang-qing Yang, MD & PhD Tongji Hospital of Tongji University 同济大学附属同济医院　杨长青

  4. Special Terms • Hepatocellular Carcinoma (HCC) 肝细胞癌 • Aflatoxin β1 黄曲霉素B1 •  -Fetoprotein (AFP) 甲胎球蛋白 • -Glutamyl Transferase ( -GT)-谷氨酰转移酶 • -L-Fucosidase (ALF)-盐藻糖苷酶 • Des- -Carboxy Prothrombin (D -- CP)脱羧基凝血酶原 • Hepatomegaly肝肿大 • TACE (transarterial chemoembolization ) 介入化疗

  5. Background: HCC • most common solid organ tumor worldwide • incidence is rising: USA 2.4 /100,000 China 20.4 /100,000 South Africa 60 / 100,000 • in China, marginal waters > hinterland eastern > western one million died annually, Top 2 in tumors

  6. Sex distribution • Male ：Female = 3~5 ：1 in China • Almost equal in developed countries

  7. Age distribution • Middle aged man in predominance (43.7 y) • It is rare in children • It rises progressively with age, although it tends to level off in the oldest age group

  8. Etiology & Pathogenesis • Four major causal associations of HCC • The etiologic agents differs with different area

  9. Risk factors Major • Chronic HBV infection • Chronic HCV infection • Aflatoxin β 1 • Liver fibrosis & Cirrhosis

  10. Hepatitis B virus • Chronic infection with HBV may cause as much as 80% of human HCC • It is closest in ethnic Chinese and black Africans • Early infection carries a greater risk

  11. HBV & HCC

  12. Hepatitis B Virus • HBV DNA could be integrated into cellular DNA in about 95% of patients with HBV-related tumors • The site of integration is random • Integration perturbing the function of cellular oncogenes or tumor suppressor genes, which may contribute to hepatocellular carcinogenesis

  13. Hepatitis C Virus • HCV is carcinogenic in human • In Japan, Italy, Spain, chronic HCV infection is the major risk factor for hepatocellular carcinoma • A far smaller percentage of ethnic Chinese and black African have HCV-induced tumors • HCV does not integrate into host DNA, its mechanism differs from that of HBV

  14. HCV & HCC

  15. HCV & HCC HCV(+) in HCC Developed countries : 50% - 70% Developing countries : 13.3 – 38.5%

  16. Cirrhosis HCC frequently coexists with cirrhosis (80%) Cirrhosis HCC

  17. Cirrhosis • In ethnic Chinese and black Africans, it is usually of the macronodular variety and is the result of chronic HBV infection • In other populations, it is commonly of the micronodular variety and is usually caused by alcohol abuse, or both

  18. Aflatoxin β1 • It is a major risk factor for HCC in certain geographic regions • Epidemiologic studies have shown a positive correlation between intake of aflatoxin β1 and the incidence of HCC

  19. Main Risk Factors The main risk factors of HCC are _____ ?

  20. Alcohol Tobacco Obesity Diabetes Iron-overloading Copper-overloading 1–antitrypsin deficiency Glycogen storing disease Obstruction of the inferior vena cava ▲ ▲ Progress HCC Clin Liver Dis. 2005; 9(2):281-5 Gastroenterology. 2004; 127(5 Suppl 1):S79-86

  21. Minor risk factors • As many as 45% of persons who suffer from hereditary hemochromatosis develop into HCC • This complication was thought to occur only in the presence of cirrhosis • Patients with Wilson disease occasionally develop into HCC, although only in the presence of cirrhosis • Other inherited metabolic disturbances predispose to that HCC may also induced by cirrhosis (α1–antitrypsin deficiency)

  22. Minor Risk Factors • In patients with the use of contraceptive steroids, the risk is related directly to the duration of use • Controversy exists over whether cigarette smoking

  23. Pathology • Gross appearance • Microscopic appearance Well-Differentiated appearance Moderate-Differentiated appearance Undifferentiated appearance Fibrolaminar hepatocellular carcinoma

  24. Gross appearance • Nodular <5cm, usually coexists with cirrhosis (either single or two) • Massive > or =5cm, most common form most prone to rupture • Diffuse It is rare, may be difficult to distinguish from regenerating nodules of cirrhosis

  25. Gross appearance Nodular Type

  26. Gross appearance Massive Type

  27. Gross appearance Diffuse Type

  28. Small HCC • <3cm • Well differentiated, low grade malignancy • Usually encapsulated • cancer embolism rate is low with relative good liver function

  29. Microscopic appearance • Hepatocyte (90%) • Bile duck cell (less) • Mixed (least)

  30. Metastasis of HCC • Intrahepatic metastasis: through portal vein • Extrahepetic metastasis : through hepatic vein or lymph route 5 most common sites of HCC metastasis are: (1)regional lymph nodes (2) lung (3) adrenal glands (4) bone (5) peritoneal surface

  31. Metastasis of HCC Intrahepatic metastasis:

  32. Metastasis of HCC Extrahepetic metastasis: Tumor embolus in inferior cava vein HCC

  33. Clinical manifestation Symptoms Prevalence(%) Abdominal pain 59-95 Weight loss 34-71 Weakness 22-53 Abdominal swelling 28-43 Nonspecific 25-28 Gastrointestinal symptoms common

  34. Clinical manifestation Physical signs Prevalence(%) Hepatomegaly 54-98 Hepatic bruit 6-25 Ascites 35-61 Splenomegaly 27-42 Jaundice 4-35 Wasting 25-41 Fever 11-54

  35. Paraneoplastic Syndromes associated with HCC Hypoglycemia Polycythemia (erythrocytosis) Hypercalcemia Osteoporosis Polymyositis Neuropathy Sexual changes: gynecomastia feminization

  36. Clinical stages Stage I (subclinical stage): • High risk factors, hepatitis history or HBsAg + over 5 years • No specific symptoms • Elevated AFP • Single or multiple nodules, size <= 5cm • No vascular invasion

  37. Clinical stages Stage IIa • Present some symptoms or signs of HCC • Abnormal laboratory findings • Single or double nodules >5~10cm • No portal vein cancerous embolism • No lymph nodes enlargement • No distant metastasis

  38. Clinical stages Stage IIb • Single or double nodules ≥10cm or triple ≤ 10cm in one hepatic lobule • Single or double nodules 5~10 cm in two hepatic lobule • Portal vein cancerous embolism

  39. Clinical stages Stage III • More advanced than stage IIb • or with vascular invasion or with intrahepatic invasion or with peritoneal lymph nodes enlargement or distant metastasis

  40. Complications • Hepatic encephalopsy end stage deadly complication, 1/3 death cause • Gastrointestinal bleeding esophageal varices, erosive GI mucosa • Rupture of hepatic cancer mass accounts for 9~14% • Secondary infection

  41. Laboratory tests and others • Tumor markers of HCC • Radiologic investigations • Needle biopsy

  42. Tumor markers •  -Fetoprotein (AFP) •  –Glutamyl Transferase ( -GT) •  –L-Fucosidase (ALF) • Des- -Carboxy Prothrombin (D -- CP)

  43. -Fetoprotein (AFP) • high concentration in fetal serum, in normal adult usually<20g/L • In patients with pregnancy, neonatal, testis tumor or ovarian tumor, the serum AFP may also elevated (<200g/L) • Reappearance of high serum levels of alpha-fetoprotein in serum (>500g/L) is a strong pointer to the diagnosis of HCC • Below this level may be found in patients with variety of acute and chronic benign hepatic disease or GI tumor with liver metastasis

  44. –Glutamyl Transferase ( -GT) • Normal serum contains as many as 10 isoenzymes of  -GT • Three isoenzymes may be present in serum from patients with HCC:  -GT- I 27%  -GT -II 60%  -GT-III 30%

  45. Des- γ-Carboxy Prothrombin • It is raised in the majority of patients with HCC • ≥ 250μg /L is considered positive

  46. –L-Fucosidase (ALF) • It was first reported to have a sensitivity of 75% and specificity 90% in HCC • In a subsequent study, it failed to distinguish between cirrhosis and HCC • In black Africans, this marker is less sensitive, less specific and has lower predictive value than alpha-fetoprotein

  47. Tumor markers Sensitivity(%) Specificity (%) Advantages Disadvantages AFP80~90(high) 90 Relatively quick Relative easy to measure expansive D-γ –CP58-91 84 Easy and quick Far more tomeasure expansive ALF 75 70-90 Easy and quick to measure, relative inexpansive γ-GT-II60 96 Relatively easy and Expansive quick to measure

  48. Hepatic imaging • Ultrasonography (U-S) • Computed Tomography (CT) • Magnetic Resonance Imaging (MRI) • Hepatic Arteriography (DSA) • Position emission computed tomography (PECT)

  49. Ultrasonography • Detects tumor which size >2cm • Shows the size, sharp, site and its relationship with vessel • Identifies the hepatic vein, portal vein cancerous embolism • Doppler sonography are useful

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