PMC6104347_01
Ultrasound examination of the abdomen revealing well-defined, hypoechogenic incidental lession in the liver (a). Color dopler analysis demonstrates a hypervascularity of the lession (b).
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Colour Doppler analysis demonstrated hyperemia in the lesion in comparison with normal hepatic tissue (Fig. 1).
Contrast enhanced ultrasound examination showing a homogeneous enhancing vascular lesion in arterial phase - 9 s (a) and 11 s (b) after the injection of contrast media.
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The lesion showed homogenous hyperechogenic enhancement in the arterial phase (20-40 s post injection) (Fig. 2) and stayed iso- to hyperechogenic in comparison to surrounding liver parenchyma in portal venous (60-120 s post injection) and late phase (2-4 min post injection).
MRI shows a well-defined lesion in liver segment IV. Lesion is moderately hyperintense on T2 HASTE sequence (a) and shows restriction of diffusion (b). In-phase GRE (c) and out-of-phase GRE (d) sequences were performed and no drop of signal was noted in the lesion.
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MRI with the hepatobiliary-specific contrast agent demonstrated a 25 mm liver lesion that was hypointense on T1 and hyperintense on T2 weighted sequences and showed no notable signal drop on GRE opposed-phase sequences (Fig. 3).
MRI of the liver with hepatobiliary-specific contrast agent. (a) Lesion is hypointense on T1 VIBE pre-contrast mage. (b) Lesion shows intense homogeneous enhancement in the arterial phase. (c) Lesion is hypointense in comparison with liver parenchyma in venous and in hepatospecific phase (d).
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The lesion was completely hypointense in hepatospecific phase (Fig. 4), a feature not specific for FNH and ultrasound guided histologic puncture was subsequently indicated.
Well-demarcated and unencapsulated proliferation of neoplastic epithelioid cells in the liver. Hematoxylin and eosin, magnification 100x.
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The nuclei of tumor cells were bland with occasional regular mitoses (Fig. 5).