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I./3.4.: Hepatocellular carcinoma – HCC
I./3.4.1.: General remarks
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Most often hepatocellular carcinoma originates from cirrhotic liver. Non-cirrhotic hepatitis, metabolic disorder (haemochromatosis, Wilson’s disease) or chronic liver toxicity (for ex. aflatoxin) can be also in the background. In the imaging point of view three forms are known: (i) focal, (ii) multifocal, (iii) diffuse. Fibrolamellar type of HCC is a separate entity, occurs in young patients, includes calcification which can be detected by CT frequently. MR appearance: slightly hypointense in T1-weighed, slightly hyperintense in T2-weighted images.
I./3.4.2.: Ultrasound – US
US is usually the first examination. In early phase, hypoechogenic, inhomogenous echogenic space occupying pattern is visible, which demarcates later, and necrotic signs may be observed in the center. Reclining upon the echo pattern does not provide a sure diagnosis (e.g. small hyperechoic lesion may look like similarly to a hemangioma). In experienced hands with US machines of good capacity, smaller lesions can be also detected. The enlargement of lymph nodes in liver hilum are well visible too. Vascular invasion of HCC is also visible on US. Color Doppler US can demonstrate the hepatofugal circulation.
I./3.4.3.: Computed tomography, CT
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HCC demonstrated as a hypodense (sometimes isodense) lesion on CT, usually in a cirrhotic liver. There is a hypodense demarcating zone around it towards the normal liver parenchyma. Very important to know that well vascularised HCC enhances the contrast agent in early arterial phase, but it becomes isodense later in portal venous phase. „Wash-out” is typical in venous phase images, when the tumour becomes hypodense. If the HCC is less vascularised, contrast enhancement is longlasting.
Multiple dynamic series are necessary: in arterial, portal and venous phases as well as in late phase, when the capsule becomes annularly hyperdense. Contrast enhancement dynamics of regenerative and dysplastic nodules may be similar to HCC. Necrosis suggesting hypodensity and lack of contrast enhancement might be present in its center. Due to the previously mentioned reasons, to detect multifocality CT angiography is recommended to be performed which demonstrated the arterioportal shunts well. Important to know that very small nodules of multifocal HCC might remain accidentally undetected even on triphasic CT.
I./3.4.4.: Magnetic resonance (imaging), MR(I)
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Advantage of MRI is the high tissue contrast, thus also the small lesions can be nicely visible. Due to the good tissue resolution of MRI, fibrosis, haemorrhagia, necrosis and degenerative lesions (steatosis) can be demonstrated well. HCC is mostly hypointense in T1, but it might appear iso- or hyperintense, respectively. Its signal is inhomogenous in T2 weighted images, its signal intensity is usually higher than the signal intensity of liver. „Capsule” may be present in focal forms. The (older) internal hemorrhages can be well differentiated. High signal intensity nodules in T2 images are usually HCCs. If the nodule has a poor signal in T1- and T2-weighted images, iron content can be supposed: siderotic regenerative nodule (might be dysplastic as well).
Nodules with high signal intensity on T1-weighted images and iso- or hypointensity on T2-weighted images are most likely dysplastic nodules or low-grade HCCs. MRI demonstrates the vascular invasion well. T1 type contrast agents produce the same result as CECTs (Contrast Enhanced Computed Tomography – contrast weighted CT-examination): fast, arterial phase enhancement is seen most likely in case of small lesions – in this case, differentiation from a rapidly enhancing small hemangioma includes that the contrast wash-out of HCC is fast, in contrast to the hemangioma which „keeps” the contrast within it. Difference between contrast enhancement dynamics of regenerative dysplastic nodules and HCCs have a differential diagnostic value with CT and MRI, but an overlap is possible between these two kinds of lesions. Injecting T2-type contrast agent (SPIO), the signal of lesions depends on the differential grade of HCCs in T2-weighted images. There are no or a few Kupffer cells in HCC.
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