Hepatocellular Carcinoma (Hepatoma)

50% of cases, the tumor appears in the absence of cirrhosis

M>F (3:1) in low incidence area and (8:1) in high incidence area

5th leading cause of death in males

Causes: Aflatoxin (Carcinogen), Hep B and C

CHILDS criteria,

Pathogenesis:

 Chronic liver diseases – most common cause of the HCC. It is usually identified in a background
of cirrhosis, (But cirrhosis it self is not a pre malignant lesion)
 Most important underlying factors in Hepatocarcinogenesis are HBV and HCV and toxic injuries
such as chronic alcoholism and aflatoxin exposures (produced by a Aspergillus species fungal
toxin or mycotoxin) usually contaminate crop products
 Metabolic diseases such as hereditary hemochromatosis and α1AT deficiency increase risk HCC
 Obesity DM and NAFLD increase risk of HCC
 Activation of oncogene (B-catenin) and inactivation of p53 are the early mutational events
(injury-regenerate-injury-inc risk)
 High-grade dysplastic nodules are probably the most important primary pathway for emergence
of HCC
 HCC may appear grossly as (1) a unifocal (usually large) mass, (2) multifocal, widely distributed
nodules of variable size, or (3) a diffusely infiltrative cancer
 Can metastasize either vascular invasion or direct extension, (hematogenous metastases that
can cause lung cancer, and long, snakelike masses that can cause portal vein HTN or IVC
 - Unifocal neoplasm + table 18-12

Diagnostics:

Clinical feature: ill-defined upper abdominal pain, malaise, fatigue, weight loss, and sometimes
awareness of hepatomegaly or an abdominal mass or abdominal fullness. Jaundice, fever, and
gastrointestinal or esophageal variceal bleeding are inconstant findings.

Serum alpha feto protein 50% in person with advanced HCC (insensitive screening for premalignant or
early lesions)

Most valuable for detection UTZ for distinctive nodule, CT and MRI with contrast studies (HCCs are
typically hypervascular with blood supplied predominantly from the hepatic artery. Thus, the lesion often
appears hypervascular during the arterial phase, hypodense during the delayed phases due to early washout of
the contrast medium by the arterial blood)

Death usually occurs from (1) cachexia, (2) gastrointestinal or esophageal variceal bleeding, (3) liver
failure with hepatic coma, or, rarely, (4) rupture of the tumor with fatal hemorrhage. The 5-year survival
of large tumors is dismal, the majority of patients dying within the first 2 years.

Management:

HCC, resection is TOC (Child’s class A cirrhosis with preserved liver function and
no portal hypertension), if poor liver finction transplant is TOC