HCC in cirrhotic patients is diagnosed by (1) alpha fetoprotein (AFP) level, (2) imaging studies, and (3) histologic diagnosis. The AFP level is normally less than 15 to 20 ng/mL in adults. The higher the AFP level, the more specific it is for HCC. An AFP greater than 400 ng/mL in a cirrhotic with a vascular hepatic mass on imaging is diagnostic. Unfortunately, many HCC cases have only modestly elevated AFP values. Sensitivities are as low as 45% even for a low cutoff of 20 ng/mL [4]. Moreover, hepatocyte regeneration during and after flares in chronic hepatitis may increase AFP levels in the absence of HCC. Other serologic markers, such as des g-carboxyprothrombin and glypican-3, have shown promise but are not widely used clinically in the United States [5,6].

Imaging studies, including abdominal ultrasound (US), contrast-enhanced CT, and MRI, are useful. The latter two modalities rely on characteristic vascular qualities to identify lesions. Virtually all HCCs are perfused by the hepatic artery rather than the portal venous system. Large HCCs are usually easy to identify, but small lesions (<2-3 cm) may have subtle vascular markings. CT and MRI scans must include images taken before, during, and after contrast administration (multiphased). An experienced body-imaging radiologist is invaluable in interpreting these tests. Indeed, the choice of CT or MRI for HCC diagnosis often depends on center expertise and preference. US is also quite useful, but a lesion detected on US generally requires an MRI or CT for better characterization. Nevertheless, positive predictive values for CT and MRI can be as low as 37% to 69%, particularly for lesions less than 1 to 2 cm [7,8]. Sonographic contrast materials can be injected into a peripheral vein and cross pulmonary microvasculature to produce air bubbles in the hepatic artery. This diagnostic technique is currently experimental [9,10]. Finally, invasive imaging studies, such as hepatic artery angiogram, and CT and MRI angiography, may increase accuracy [11,12] but are not widely used.

Some experts recommend needle biopsy under imaging guidance partly because lymphoma and nonmalignant lesions can masquerade as HCC [13]. Tissue diagnosis, however, is neither always necessary nor feasible. Biopsies entail some risk. Patients with HCC often have end-stage cirrhosis with coagulopathy, thrombocytopenia, or ascites, all of which increase the risk of bleeding. Small tumors may be difficult to reach by percutaneous biopsy. Cancer cells can rarely seed along the biopsy needle track. Earlier large studies reported a risk of about 0.003% to 0.009% of seeding [14], but more recent studies report a 1% to 2% risk [15,16]. In some studies, the false-negative rate of biopsies is as high as 10% to 40%, particularly for small tumors, because of inadequate samples or sampling error [15,16]. The histo-pathologic criterion separating dysplastic regenerative nodules from malignancy can be ambiguous. Repeat biopsy does not significantly decrease the false-negative rate [13,16].

Generally accepted guidelines provide criteria for HCC, as published by the European Association for the Study of Liver Disease in 2001 (Box 1) [17]. Note that criteria 2 and 3 apply only in the setting of cirrhosis. The United Network for Organ Sharing (UNOS) in the United States has similar guidelines as described later in the liver transplantation section.


Screening for HCC remains controversial. HCC meets several criteria for cost-effective screening, including an identifiable risk group (cirrhotic

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