Address for correspondence: Giuseppe Montalto, M.D., Istituto di Medicina Interna e Geriatria, via del Vespro 141, 90127 Palermo, Italy. Voice: 39 091 6552991; fax: 39 091 6552936.
gmontal{at}unipa.it
Ann. N.Y. Acad. Sci. 963: 13-20 (2002).
The incidence of hepatocellular carcinoma is increasing in many
countries. The estimated number of new cases annually is over
500,000, and the yearly incidence comprises between 2.5 and
7% of patients with liver cirrhosis. The incidence varies between
different geographic areas, being higher in developing areas;
males are predominantly affected, with a 2:3 male/female ratio.
The heterogeneous geographic distribution reflects the epidemiologic
impact of the main etiologic factors and environmental risk,
which are the hepatitis B (HBV) and hepatitis C (HCV) viruses.
The percentage of cases of hepatocellular carcinoma attributable
to HBV worldwide is 52.3% and is higher in Asia where the seroprevalence
of HBsAg in the population is high. However, the vaccination
campaign against this virus in some eastern countries has tended
to lower the incidence of new cases of hepatocellular carcinoma.
The percentage of cases of hepatocellular carcinoma attributable
to HCV is 25%, and it is more prevalent in Japan, Spain, and
Italy where the association between hepatocellular carcinoma
and antibodies to HCV ranges between 50 and 70%. In most cases
hepatocellular carcinoma develops in cirrhotic livers, where
the persistent proliferation of liver cells represents the key
factor of progression to hepatocellular carcinoma independent
of the etiology. Another minor risk factor is aflatoxin B1 consumption,
which is responsible for most cases of hepatocellular carcinoma
in Africa, where the consumption of contaminated foods is common.
Other known risk factors are some hereditary diseases, such
as hemochromatosis, porphyria cutanea tarda, hereditary tyrosinemia,
and
1 anti-trypsin deficiency. The natural history of hepatocellular
carcinoma is heterogeneous and is influenced by nodule dimension,
the mono- or plurifocality of lesions at diagnosis, the growth
rate of the tumor, and the stage of the underlying cirrhosis.
Available data to date suggest that tumor growth in a cirrhotic
liver is variable and that the time in which a lesion in undetectable
until it becomes 2 cm is between 4 and 12 months. Therefore,
the suggested interval for surveillance screening with ultrasound
in patients with liver cirrhosis has been set at 6 months. Patients
who should benefit from screening programs are those who would
be treated with curative therapy if diagnosed with hepatocellular
carcinoma. Thus, the ideal target population should be limited
to Child-Pugh's class A cirrhotic patients without significant
comorbidity.
