PMC5173492_01
Ultrasonography findings (arrows). B-mode conventional ultrasonography showed a 15 mm hypoechoic mass in liver segment 4 (S4) (a), the liver parenchyma had a coarsened appearance consistent with cirrhosis, and ascites and splenomegaly were observed (b, c).CEUS using Sonazoid showed a homogeneously enhanced mass in the arterial dominant phase (d), a hypoechoic mass relative to the adjacent liver parenchyma during the portal dominant phase (e), and a contrast defect with a clear border in the postvascular phase (f).
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B-mode conventional US showed a 15 mm hypoechoic mass in liver segment 4 (S4) (Fig. 1a), and an 18 mm hyperechoic mass in liver segment 2 (S2) (Fig. 2a). Furthermore, the liver parenchyma had a coarsened appearance consistent with cirrhosis, and ascites and splenomegaly were observed (Fig. 1b and c). The mass lesion in S4 was homogeneously enhanced in the arterial dominant phase (from 10 to 30 seconds) (Fig. 1d). The lesion became progressively hypoechoic relative to the adjacent liver parenchyma during the portal dominant phase (from 30 to 120 seconds) (Fig. 1e), and provided a contrast defect with a clear border in the postvascular phase (10 minutes later) (Fig. 1f).
B-mode conventional ultrasonography showed an 18 mm hyperechoic mass in liver segment 2 (S2) (a); and CEUS showed a homogeneously enhanced mass in the arterial dominant phase (b), isoechoic mass relative to the adjacent liver parenchyma during the portal dominant phase (c), and no defects in the postvascular phase (d).
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The mass lesion in S2 was homogeneously enhanced in the arterial dominant phase (Fig. 2b). The lesion became isoechoic mass relative to the adjacent liver parenchyma during the portal dominant phase (Fig. 2c) and provided no defects in the postvascular phase (10 minutes later) (Fig. 2d).
There was radiographic evidence of liver cirrhosis with portal hypertension, including a nodular surface, a coarse texture, ascites, and splenomegaly on MRI (a, b). Gd-EOB-DTPA MRI showed a 15 mm S4 mass with a moderately low intensity in T1-WI (c), moderately high intensity in T2-WI (d), moderately high intensity in diffusion (e), homogeneous arterial enhancement (b, f), and complete washout in the hepatobiliary phase (g).
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T2-weighted imaging (WI) before and after contrast media administration, including diffusion imaging. The contrast media used was hepatocyte-specific Primovist [gadolinium ethoxybenzyl diethylenetriamine pentaacetic acid (Gd-EOB-DTPA); Bayer Schering Pharma, Berlin, Germany]. There was radiographic evidence of liver cirrhosis with portal hypertension, including a nodular surface, a coarse texture, ascites, and splenomegaly on MRI (Fig. 3a and b). This imaging revealed a mass lesion in S4 with a moderately low intensity in T1-WI (Fig. 3c) and moderately high intensity in T2-WI (Fig. 3d). In diffusion imaging, the lesion showed a moderately high intensity (Fig. 3e). In the postcontrast phases, the lesion revealed homogeneous enhancement in the arterial phase at 20 seconds (Fig. 3b and f), and washout in the portal phase at 70 seconds and interstitial phase at 180 seconds. At 20 minutes (hepatobiliary phase) after the contrast uptake the lesion showed washout (Fig. 3g).
Gd-EOB-DTPA MRI showed an 18 mm S2 mass with a moderately high intensity in T1-WI (b), moderately low intensity in T2-WI (c), moderately low intensity in diffusion (d), homogeneous arterial enhancement (a, e), and high intensity in the hepatobiliary phase (f).
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In addition, MRI imaging revealed a mass lesion in S2 with a moderately high intensity in T1-WI (Fig. 4b) and moderately low intensity in T2-WI (Fig. 4c). In diffusion imaging, the lesion showed a moderately low intensity (Fig. 4d). In the postcontrast phases, the lesion revealed a homogeneous enhancement in the arterial phase (Fig. 4a and e), an isoenhancement relative to the adjacent liver parenchyma in the portal and interstitial phases, and a high intensity in the hepatobiliary phase (Fig. 4f).
A histological specimen was obtained by an ultrasound-guided needle biopsy of the S2 lesion. Microscopic histological findings revealed bridging fibrosis in the liver section. The parenchymal cells did not display cellular or structural atypia [Hematoxylin and Eosin staining (a), and silver impregnation (b) with a low-power field]. The liver mass in S2 was pathologically diagnosed as a regenerative nodule.
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Histological findings revealed that bridging fibrosis in the liver section, and the parenchymal cells did not display cellular or structural atypia (Fig. 5).
A macroscopic appearance of the resected S4 specimen revealed a yellowish-white encapsulated solid tumor measuring 15 mm in size (a). Microscopically, the growth pattern of the S4 liver tumor showed expansive growth with extracapsular invasions [b, Hematoxylin and Eosin (H&E) staining with a low-power field]. Tumor cells had an increased nuclear/cytoplasmic ratio, polymorphic, and chromatin-rich nuclei, and the pathological diagnosis was poorly differentiated HCC (c, H&E staining with a high-power field).
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Macroscopically, sections of the specimen revealed a yellowish-white encapsulated solid tumor measuring 15 mm in size (Fig. 6a). The growth pattern of the liver tumor showed expansive growth with extracapsular invasions (Fig. 6b). The tumor cells had an increased nuclear/cytoplasmic ratio, polymorphic, and chromatin-rich nuclei, and the pathological diagnosis was poorly differentiated HCC (Fig. 6c).
The noncancerous area of the resected specimen revealed bridging fibrosis without fat deposition, and the patient was diagnosed with liver cirrhosis [silver impregnation (a)]. Fibrosis was observed in both the portal and pericellular areas, the sinusoidal structure was maintained, and significant inflammation was not seen [silver impregnation (b, c) with a high-power field].
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The non-cancerous area of the resected specimen revealed that bridging fibrosis was observed without fat deposition, and the patient was diagnosed with liver cirrhosis (Fig. 7a). Fibrosis was observed in both the portal and pericellular areas, the sinusoidal structure was maintained, but no significant inflammation was observed (Fig. 7b and c).