Gastrointestinal ImagingHepatocellular carcinoma
(HCC), most common primary
malignant tumour of the liver occurring predominantly in patients with underlying parenchymal liver disease. The prevalence of HCC is different according to the geographical area concerned. In Western Europe and the USA an autopsy incidence between 0.2 and 0.7% is reported, whereas, in Asia and sub-Saharan Africa a prevalence of 5.5% is indicated. In general, men are affected more frequently than women and male dominance may reach a ratio of 8 to 1 in high-incidence areas.
The main aetiological factors of HCC are cirrhosis, hepatitis B and C infection and carcinogens. Other risk factors are primary haemochromatosis, glycogen storage disease and thoriumdioxide deposition in the liver. Alcohol related cirrhosis is considered the most frequent cause of HCC in the Western world.
The development of HCC in cirrhosis is probably related to a disturbance of the regenerative processes such as adenomatous hyperplastic nodules occurring in the liver. Hepatitis virus B infection is considered to be responsible for the majority of HCC cases worldwide. A strong correlation exists between dietary aflatoxin contamination and HCC in south-east Asia and Africa.
HCC can be expansive (solitary, multifocal or more rarely diffusely infiltrating). Multifocal tumours may present as dominant massive masses with satellite nodules or as multiple nodular structures of similar size. The expansive type of tumour displays a slower and less aggressive growth pattern than the infiltrative one, and may be surrounded by a capsule.
Microscopically the cells of HCC resemble normal hepatocytes but have cytological features of malignancy such as hyperchromatic nuclei and mitotic figures, and it is often difficult to distinguish them from normal cells or cells of hepatocellular adenoma. The most frequent of the different HCC histological patterns is the trabecular pattern in which the tumour cells tend to recapitulate the cords seen in the normal liver. Areas of necrosis, haemorrhage or fatty metamorphosis are commonly seen in HCC. Calcification is present in 510% of tumours. A central fibrous scar can occasionally be present.
The blood supply of HCC comes mainly from the hepatic artery. Arterioportal blood shunting due to portal invasion is not uncommon. Portal vein invasion is frequently present whereas hepatic vein invasion occurs more rarely.
Ultrasound
Tumours smaller than 3 cm in diameter are mostly hypoechoic. If small tumours are hyperechoic; fatty metamorphosis is present. Multifocal tumours are mostly hyperechoic. The hyperechogenic pattern (Fig.1) visible in some larger tumours has been attributed to fatty metamorphosis or marked sinusoidal dilatation within the tumour. Sonography is able to display portal or hepatic vein invasion, as well as, extension into the bile duct system and enlarged metastatic lymph nodes in the liver hilum. Colour Doppler sonography visualizes routinely the high vascularization of HCC but no specific vascular pattern, allowing differentiation between hypervascular primary or secondary liver tumours can be displayed.
Computed tomography
On precontrast CT (Fig.2), HCC may appear hypo- or isoattenuating relative to the surrounding parenchyma. A tumour capsule may be visible in isoattenuating lesions as a thin peripheral hypoattenuating rim. Contour deformity may be detectable in lesions originating in subcapsular areas or in larger tumours. Most HCC appear homogeneous but inhomogeneous attenuation may be due to areas of calcification, necrosis or fatty metamorphosis. Intrahepatic biliary duct dilatation can also be seen on precontrast CT. On dynamic contrast enhanced CT (Fig. 2), HCC display an early moderate to high degree of homogeneous enhancement similar to that of focal nodular hyperplasia (FNH) and hepatocellular adenoma (HA) although in most instances less marked than with benign tumours. The contrast enhancement is transien demonstrated by CT because of the lack of specific features before or after contrast enhancement.
Magnetic Resonance Imaging
On T1-weighted images HCC has been reported as iso- or hyperintense in 47% to 62% of patients in Japan. The capsule, as well as the central scar, are usually markedly hypointense on T1-weighted images. Hyperintensity on T1-weighted images has been related to fatty metamorphosis, recent haemorrhage, excessive glycogen or copper deposition. On T2-weighted images the majority of HCC are hyperintense. Frequently the signal intensity is inhomogeneous due to localized hyperintense foci which correspond to dilated sinusoids and necrosis within the tumour. The central scar is high in signal intensity on T2-weighted images.
Dynamic contrast enhanced MRI with Gadolinium DTPA, which is able to detect more lesions than unenhanced MRI, shows an enhancement pattern similar to that observed on contrast enhanced dynamic CT. While undifferentiated HCC does not take up specific liver contrast agents directed to the reticuloendothelial system (SPIOs, USPIOSs) (Fig.5), well-differentiated HCC may show a distinct uptake. Quantitative evaluation of the percentage signal intensity loss after contrast administration may be the most useful approach to distinguish well-differentiated HCCs from benign liver neoplasms. It has also been shown that malignant liver tumours frequently show ring enhancement after administration of USPIOs.
MRI may be specifically helpful in differentiating regenerative nodules, siderotic nodules and dysplastic nodules that are frequently present in cirrhosis from HCC. Regenerative nodules tend to be hypo-, iso-, or hyperintense on T1-weighted images and hypo- or isointense on T2-weighted images. Most dysplastic nodules are hyperintense on T1-weighted and hypointense on T2-weighted images. Nodules in a cirrhotic liver presenting hypointensity on T2-weighted images are likely not to correspond to HCC.
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