LIVER NEOPLASMS


See also Biliary Tract Neoplasms

Hepatomas have same degree of vascularity as normal liver tissue; metastases to liver have decreased vascularity; hemangiomas have elevated vasc. See also under "Gastroenterology"

Hepatocellular carcinoma (HCC)

I. Risk factors and epidemiology

  1. Major risk factors
    1. Chronic hepatitis B infectrion (commonly occurs in absence of hepatic cirrhosis; presence of HBeAg is an indicator of risk)
    2. Chronic hepatitis C virus infection (rarely seen in absence of hepatic cirrhosis annual incidence is 1-4% in patients with chronic HCV infection + cirrhosis)
    3. Alcohol abuse
    4. Hemochromatosis (much more common in hepatic cirrhosis is present)
    5. Alpha-1-antitrypsin deficiency (5-10% lifetime risk for developing HCC)
    6. Primary biliary cirrhosis
    7. Non-alcoholic fatty liver disease
    8. Aflatoxin exposure
  2. Male:Female 4:1
  3. Median age at onset is 62yo
II. Clinical presentation
  1. About 2/3 of patients are symtpomatic at presentation
  2. Abdominal pain, weight loss, early satiety are common
  3. Symptoms of decompensating cirrhosis (ascites, jaundice, splenomegaly, edema, variceal bleeding, encephalopahy)
  4. Metastases
    1. 60% of patients are in advanced stages at the time of diagnosis
    2. Most frequent to lung, intra-abdominal lymph nodes, bone, adrenal
III. Treatment
  1. Excision or transplant is generally considered if Child-Pugh class A or B, single lesion < 5cm, and no metastases, major vascular invasion, or portal hypertension (i.e. hepatic pressure gradient < 10mm Hg)
  2. Direct tumor destruction e.g. by percutaneous injection of ethanol, RF ablation, cryoablation, transarterial embolization, microwave, etc.-Often used as bridging to transplant
  3. Systemic chemotherapy is not highly effective but Sorafenib (Nexavar), an orally-active tyrosine kinase inhibitor, which inhibits vascular endothelial growth factor, can be effecive in palliation for unresectable HCC

IV. Prevention-See under specific diseases

V. Screening in patients with chronic liver disease

  1. Surveillance generally includes Q6mo (hepatic ultrasound + serum alpha-fetoprotein with cutoff of 20 ng/mL)
  2. In a study in 855 pts with histologically advanced chronic hepatitis C who underwent serum AFP measurement Q3mos x 4y (plus yearly ultrasound), AFP > 20ng/mL had sensitivity of 60% for development of hepatocellular Ca in the subsequent 24mos, but positive predictive value was only 10%.  At cutoff of 200 ng/mL, PPV was 31% but sensitivity was only 20%. (Am. J. Gastroent. 107:64, 2012-JW)
  3. If AFP is progressively rising often proceed to  three-phase CT or MRI; "classic" appearance on imaging may preclude need for biopsy
  4. However, 40% of patients with HCC have a normal AFP
  5. Associated with 35-40% reduction in mortality in patients with chronic HCV infection + cirrhosis
  6. In a study in 360 pts with chronic liver disease (254 with cirrhosis, 106 with "chronic hepatitis") followed for 56 mos who underwent screening with ultrasound and serum AFP Q6 mos, 6.6% of pts were dx'd with hepatocellular Ca over study period; only 50% of these had elevated serum AFP; all but one case occurred in pts with cirrhosis (Am. J. Gastroenterol. 91:1189, 1996; cited in Journal Watch)

(Sources include Core Content Review of Family Medicine, 2012)