Abdominal imagingCase Type
Charlotte Harth1, Pieter De Mulder1, Lieven Van Hoe2.Patient
68 years, female
A 68-year-old Caucasian woman, with a history of breast cancer, was referred to the radiology department for a follow-up abdominal ultrasonography.
A hypoechoic focal liver lesion with a diameter of 2cm was visualized in segment 4. MRI with gadoxetic acid (Primovist) showed a T2 slightly hyperintense and T1 almost isointense nodule of 2 cm in segment 4 (figure 1a, b). The lesion was hyperenhancing in the arterial and portal venous phases and had a central scar (figure 1c, d). The hepatobiliary phase showed a central scar and two additional slightly hypointense focal “defects” in the otherwise homogenously hyperintense lesion (figure 1e). FNH was suggested. An MRI study 4 years later showed significant interval growth to 7 cm. On hepatobiliary phase images, the lesion still showed a rather homogeneous hyperintense aspect, with however presence of several hypointense intralesional foci (Figure 2).
Hepatocellular carcinoma (HCC) is the fifth most common cancer and the second largest cause of cancer mortality in the world. Although most HCC’s occur in cirrhotic livers, up to 20% appear in non-cirrhotic livers .
HCC is diagnosed on the basis of imaging features alone, without histologic confirmation .
Hepatocyte-specific contrast agents are actively taken up by functioning hepatocytes. Gadoxetic acid (Primovist) is the most widely used hepatocyte-specific contrast agent worldwide. 50% of the injected dose is rapidly taken up by hepatocytes. Images visualizing uptake by normal liver parenchyma can be obtained 10-20 minutes after administration [2,3]. Hyperintense lesions in her hepatobiliary phase include FNH or FNH-like nodules, hepatocellular adenoma, dysplastic nodules and HCC. FNH is the most common cause of hepatobiliary phase hyperintense lesions in patients without chronic liver disease. Malignant lesions represent 1% of the incidentalomas.
FNHs are characterized by (1) lesion homogeneity (except for the central scar); (2) slightly different signal from the adjacent liver signal on precontrast imaging; (3) strong and homogeneous enhancement on arterial phase images, which becomes similar to the adjacent liver on portal and delayed phase; (4) a central scar that is hypointense on precontrast T1-weighted images and typically hyperintense on T2-weighted images; (5) hyperintensity in the HBP (with the exception of the central scar), or presence of a hyperintense rim .
In this case, one additional feature proved to be the hallmark of HCC rather than FNH: although the lesion was mostly hyperintense on the images obtained in the HBP, a smaller and a larger uptake defect were seen. The presence of focal uptake defects in lesions otherwise mimicking the features of FNH at HBP can be considered the hepatobiliary phase variant of the nodule-in-nodule pattern that is typically seen on arterial phase images in HCC lesions [5-7]. Other features that should herald the diagnosis of HCC are the presence of a thick perilesional hypointense rim, and hypointense septa completely dividing the lesion into more than two compartments [5-7].
Once the diagnosis of HCC has been made, clinical staging should be performed to assess prognosis and to guide therapeutic intervention. In our case, the diagnosis of HCC was confirmed after biopsy of the lesion.
Potentially curative partial hepatectomy is the optimal treatment for solitary HCC confined to the liver that shows no radiographic evidence of hepatic vascular invasion, no evidence of portal hypertension, and well-preserved hepatic function . In our case, the patient was treated with partial hepatectomy with complete resection of the tumour. Follow-up during a five-year period revealed no local recurrence or metastatic disease.
Take-Home Message / Teaching Points
Atypically hyperintense HCC is characterized by the presence of a thick fibrous pseudocapsule, mosaic/nodule-in-nodule pattern and a focal defect in contrast uptake.
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