The annual incidence of HCC in HBV carriers is 0.5% to 1% per year in noncirrhotic patients and 2.5% per year in cirrhotic patients. The relative risk of HCC is 100 (i.e., HBV carriers are 100 times more likely to develop HCC than uninfected persons).[12,13]
In a single, prospective, population-based study that included 12,008 patients, the presence of anti-HCV positivity conferred a twentyfold increased risk of HCC compared with anti-HCV negative persons. HCC may occur in HCV-infected patients with bridging fibrosis even in the absence of overt cirrhosis. However, the risk is highest among those patients with HCV-related established cirrhosis, which has an incidence rate of HCC of 2% to 8% per year.
Several reports suggest that alcoholic cirrhosis is a risk factor for HCC. However, the true incidence of HCC in alcoholic cirrhosis is unknown because most epidemiology reports on this subject were published before the identification of hepatitis C virus.
Recently, the risk factors associated with the metabolic syndrome, including insulin resistance, hypertension, dyslipidemia, and obesity have been recognized as potential causes of nonalcoholic hepatosteatosis, cirrhosis, and HCC. However, no study to date has followed a sufficiently large group of these patients for long enough to describe an incidence rate for HCC.
Hemochromatosis is also a significant risk factor for HCC and has an increased relative risk twenty times that of the normal population.
The incidence of HCC in stage IV primary biliary cirrhosis is approximately the same as in cirrhosis resulting from hepatitis C.
Aflatoxin B1 is produced by fungi of the Aspergillus species and is a common contaminant of grain, nuts, and vegetables in some parts of Asia and Africa. Aflatoxin B1 has also been implicated as a cofactor in the etiology of primary liver cancer in HBV carriers because it enhances the neoplastic risk threefold.
(Refer to the PDQ summary on Liver (Hepatocellular) Cancer Screening for more information.)
For lesions that are smaller than 1 cm and are detected during screening in patients at high risk for HCC, no detailed investigation is required because most of these lesions will be cirrhotic nodules rather than HCC.[Level of evidence: 3iii] Close follow-up at 3-month intervals is recommended using the same technique that first documented the presence of the nodules.