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Triple-phasic CT during hepatic angiography of pelioid hepatocellular carcinoma
European Journal of Radiology Extra 79 (2011) e5–e9
Contents lists available at ScienceDirect
European Journal of Radiology Extra journal homepage: intl.elsevierhealth.com/journals/ejrex
Triple-phasic CT during hepatic angiography of pelioid hepatocellular carcinoma Yasushi Itou a,∗ , Shigenori Nagata b , Yasuhiko Tomita b , Katsuyuki Nakanishi a a b
Department of Diagnostic Radiology, Osaka Medical Center for Cancer and Cardiovascular, 1-3-3, Nakamichi, Higashinari-ku, Osaka 537-8511, Japan Department of Pathology, Osaka Medical Center for Cancer and Cardiovascular, Osaka, Japan
a r t i c l e
i n f o
Article history: Received 4 January 2011 Accepted 4 April 2011
Keywords: Pelioid hepatocellular carcinoma Dilated sinusoid-like blood space CT during hepatic angiography
a b s t r a c t We present a case of pelioid hepatocellular carcinoma detected by computed tomography during hepatic angiography and confirmed by pathology. On computed tomography angiography, the lesion showed slight enhancement in the early phase, and enhancement subsequently increased. Lesion enhancement then attenuated in the delayed phase. On T2-weighted image, the lesion was hyperintense, and the inner part of the lesion was hyperintense when compared with the outer part of the lesion. Pathologically, dilated sinusoid-like blood spaces were present within the lesion, and the proportion of these in the inner part of the tumor was greater than that in the outer part. © 2011 Elsevier Ireland Ltd. All rights reserved.
1. Introduction Peliosis hepatis is rare and is histologically characterized by randomly distributed multiple blood-filled cavities representing dilated sinusoids in liver [1,2]. Findings of pelioid hepatocellular carcinoma (HCC) mimicking peliosis hepatis in the triple-phasic CT during angiography are herein presented. 2. Case report A liver mass was incidentally discovered in a 68-year-old male on abdominal sonography at a health screening. The patient was subsequently referred to our hospital for evaluation and treatment of the mass. He had been a habitual drinker for 40 years. Laboratory test results were as follows: serum aspartate aminotransferase (AST), 49 U/l; serum alanine aminotransferase (ALT), 54 U/l; ␥glutamyltransferase, 270 U/l; and ICG 15-min retention ratio, 14.3%. Serum ␣-fetoprotein (AFP) levels and protein induced by Vitamin K absence or antagonist (PIVKA-II) were in the normal range. These data indicated chronic liver damage due to alcohol intake. Triple-phasic helical CT was performed using a 16-detector row CT scanner (Aquilion 16; Toshiba, Tokyo, Japan) at 120 kVp and a revolution time of 0.5 s. After pre-contrast CT scan, 100 ml of iopamidol (Iopamiron; Bayer Schering Pharma, Osaka, Japan) with an iodine concentration of 370 mg/dl was injected at a rate
∗ Corresponding author. Tel.: +81 6 6972 1181; fax: +81 6 6981 3329. E-mail address: [email protected] (Y. Itou). 1571-4675/$ – see front matter © 2011 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ejrex.2011.04.001
of 3 ml/s by a power injector via the antecubital vein. Arterialdominant phase and portal-dominant phase scans were obtained using 35- and 80-s delay times, respectively, from the initiation of contrast material injection. Scans were obtained at a 1 mm collimation and pitch of 0.8. Pre-contrast CT image showed fatty liver, and a focal hypoattenuating lesion measuring 3 cm in segment 7 (Fig. 1a). In the arterial-dominant phase of contrast enhancement, the lesion showed peripheral ring enhancement (Fig. 1b). In the portal-dominant phase, the lesion was isodense to intrahepatic portal veins (Fig. 1c). A centripetal progression (from the periphery to the center of the lesion) of enhancement was observed. MR images were obtained with a 3 Tesla system (Magnetom Trio; Siemens Medical Systems, Erlangen, Germany) using a phased-array coil. The following sequences were performed. T2-weighted half-Fourier acquisition single-shot turbo spin-echo imaging (T2WI): TR/TE = 1200/67 ms; flip angle (FA) = 120◦ ; echo train length (ETL) = 256; number of excitations (NEX) = 1; matrix = 320 × 238; slice thickness = 8 mm; and no gap. In-phase (TR/TE = 120/2.46) and opposed-phase (TR/TE = 120/1.23) T1-weighted two-dimensional gradient-echo imaging (T1WI): FA = 60◦ ; ETL = 1; matrix = 256 × 164; slice thickness = 8 mm; and no gap. Diffusion-weighted imaging (DWI) using a single-shot spin echo-planner imaging (EPI) sequence with water selective excitation and free-breathing Prospective Acquisition and Correction (PACE): TR/TE = 6000/82 ms; FA = 90◦ ; matrix = 128 × 86; slice thickness = 5 mm; no gap; and b-values = 0, 1000 s/mm2 . After these images were obtained, a volumetric three-dimensional fat-suppressed spoiled gradient echo acquisition (volumetric interpolated breath-hold examination, VIBE; Siemens) with mSENSE was performed using following param-
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Y. Itou et al. / European Journal of Radiology Extra 79 (2011) e5–e9
Fig. 1. (a) Pre-contrast CT image showing fatty liver, and a focal hypoattenuating lesion (black arrow) in segment 7. (b) In the arterial-dominant phase of contrast enhancement, the lesion shows peripheral ring enhancement. (c) In the portal-dominant phase, the lesion is isodense with intrahepatic portal veins. Centripetal progression (from the periphery to the center of the lesion) of enhancement is observed.
eters: TR/TE = 3.64/1.32 ms; FA = 10◦ ; matrix = 256 × 141; slice thickness = 5 mm; no gap. After the unenhanced image was acquired, 0.2 ml/kg gadolinium-ethoxybenzyl-diethylenetriamine penta-acetic acid (Gd-EOB-DTPA; Bayer Schering Pharma, Osaka, Japan) was injected at a rate of 2 ml/s by a power injector via the antecubital vein, followed by a 40-ml saline flush. The delay
times for the arterial dominant, portal dominant, and equilibrium phases were 32, 80 and 120 s, respectively. A hepatocyte-specific phase was acquired at 20 min after administration of contrast media. The lesion in segment 7 was hypointense on axial inphase and opposed-phase gradient-echo MR images (Fig. 2a and b). On T2WI, the lesion was hyperintense and the inner part
Fig. 2. Chemical shift imaging on axial in-phase (a) and opposed-phase (b) gradient-echo MR images revealed a hypointense lesion in segment 7. (c) Axial T2-weighted fast spin-echo image showing a hyperintense lesion in segment 7. The inner part of the lesion is more hyperintense than outer part of the lesion. (d) ADC values for the inner part of the lesion and the outer part of the lesion are 2 × 103 mm2 /s and 1.6 × 103 mm2 /s, respectively.
Y. Itou et al. / European Journal of Radiology Extra 79 (2011) e5–e9
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Fig. 3. Dynamic Gd-EOB-DTPA-enhanced T1-weighted images are showed. (a) Pre-contrast image. (b) Arterial-dominant phase image. (c) Portal-dominant phase image. (d) Equilibrium-phase image. (e) Hepatocyte-specific phase image (20-min post-injection). On dynamic Gd-EOB-DTPA-enhanced T1WI, the lesion shows peripheral enhancement in the arterial-dominant phase (Fig. 3b), followed by progressive centripetal enhancement during the portal-dominant phase and equilibrium phase (Fig. 3c and d). In the hepatocyte-specific phase, the lesion is hypointense when compared with liver parenchyma (Fig. 3e).
of the lesion was hyperintense when compared with the outer part of the lesion (Fig. 2c). On dynamic Gd-EOB-DTPA-enhanced T1WI, the lesion showed peripheral enhancement in the arterialdominant phase (Fig. 3b), followed by progressive centripetal
enhancement during the portal-dominant phase and equilibrium phase (Fig. 3c and d). In the hepatocyte-specific phase, the lesion was hypointense when compared with liver parenchyma (Fig. 3e).
Fig. 4. (a) CTAP image showing a portal perfusion defect in segment 7. (b)–(d) Triple-phasic CTHA was performed. Early-phase (b), late-phase (c), and delayed-phase scans (d) were obtained using 8-, 35-, and 180-s delay times, respectively, from the initiation of contrast material injection. On CTA, the lesion in segment 7 shows slight enhancement in the early phase, followed by gradual enhancement during early phase and late phase. Although the enhancement of the lesion was attenuated in the delayed phase, it remained slightly hyperdense when compared with liver parenchyma.
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Y. Itou et al. / European Journal of Radiology Extra 79 (2011) e5–e9
Fig. 5. Cut surface of surgical specimen. Encapsulated tumor, 3.0 cm in diameter, showing a dark red color at the center of the lesion.
40 s. Triple-phasic CTA was performed by placing the catheter tip in the proper hepatic artery, and 30 ml of iopamidol with an iodine concentration of 150 mg/dl was injected at a rate of 2 ml/s. Early-phase, late-phase, and delayed-phase scans were obtained using 8-, 35- and 180-s delay times, respectively, from the initiation of contrast material injection. CTAP showed a well-defined, round perfusion defect in segment 7 (Fig. 4a). On CTA, the lesion showed slight enhancement in the early phase (Fig. 4b), followed by gradual enhancement during the early and late phases (Fig. 4c). Although lesion enhancement was attenuated in the delayed phase, it remained slightly hyperdense when compared with liver parenchyma (Fig. 4d). The tumor in segment 7 was surgically resected. The cut surface of the surgical specimen revealed a well-encapsulated tumor, measuring 3.0 cm in diameter and dark red in color at the center of the lesion (Fig. 5). Microscopic examination showed welldifferentiated HCC with a thin fibrous capsule (Fig. 6a and b). Dilated sinusoid-like blood spaces were present within the tumor, and relative proportion of those in the inner part of the tumor was higher than that in the outer part (Fig. 6c). On CD31 antibody staining, the endothelial lining was almost absent in the dilated sinuisoid-lke blood spaces (Fig. 6d).
3. Discussion CT during arterial portography (CTAP) and triple-phasic CT during hepatic angiography (CTA) were performed using a 4-detector row CT scanner (Aquilion 4; Toshiba, Tokyo, Japan) at 120 kVp and a revolution time of 0.5 s. After pre-contrast CT was performed, 90 ml of iopamidol (Iopamiron; Bayer Schering Pharma, Osaka, Japan) with an iodine concentration of 150 mg/dl was injected at a rate of 3 ml/s by placing the catheter tip in the superior mesenteric artery, with CT scanning started at 25 and
Peliosis hepatis has been reported in association with chronic wasting diseases (e.g., tuberculosis, acquired immunodeficiency syndrome) [3,4] and drugs (e.g., anabolic steroids, oral contraceptives, and azathioprine) [5,6]. Two histological patterns of peliosis hepatis were described by Yanoff and Rawson [1]. In the phlebectatic type, blood-filled spaces are lined by endothelium and are associated with aneurysmal dilatation of the central vein. In the
Fig. 6. (a) Histopathological examination revealed a tumor with a thin fibrous capsule (arrow) (H&E stain, 20×). (b) Photomicrograph of pathological section showing welldifferentiated hepatocellular carcinoma in the outer part of the tumor. Tumor cells are arranged in a thin trabecular pattern (H&E stain, 200×). (c) Histopathologically, dilated sinusoid-like blood spaces are present within the tumor, and the distribution of dilated sinusoid-like blood spaces is predominantly in the inner part of the tumor when compared with the outer part of the tumor (Fig. 6b) (H&E stain, 400×). (d) Endothelial cells are positive for CD 31 immunostaining in the cancer cell nest (black arrow). On the other hand, endothelial lining was largely absent in the dilated sinuisoid-lke blood spaces (CD 31 stain, 400×) (DS, dilated sinusoid-like blood space).
Y. Itou et al. / European Journal of Radiology Extra 79 (2011) e5–e9
parenchymal type, the spaces have no endothelial lining and are usually associated with hemorrhagic parenchymal necrosis. Pathologically, peliosis hepatis-like blood-filled spaces are frequently observed in HCC [7]. Kadoya et al. reported that peliotic changes were observed in 22 (31%) of 72 resected HCC [8]. Kojiro reported that the incidence of peliotic change parallels the increase in tumor diameter, and all tumors are completely or incompletely encapsulated [7]. It was therefore speculated that the development of peliotic change in HCC could be explained by endothelial damage due to sinusoidal dilatation following increased intratumoral pressure. On the other hand, few cases regarding the radiologic findings on pelioid HCC have been reported [8–10]. Peripheral enhancement in the arterial phase and centripetal progression of contrast enhancement have been observed during portal venous phase on dynamic CT and MR imaging [9,10]. Kim et al. speculated that dilated sinusoid-like blood spaces might have been responsible for the gradual fill-in enhancement patterns, as in cavernous hemangioma [9]. Kadoya et al. reported that the peliotic change in HCC was significantly correlated with localized hyperintense foci on T2weighted MR image [8]. In the present case, the lesion showed a gradual fill-in enhancement pattern during the early and late phases, and this enhancement diminished during the delayed phase on CTA. On T2WI, the lesion was hyperintense and the inner part of the lesion was more hyperintense than the outer part of the lesion. On microscopic examination, a mix of well-differentiated HCC cells and dilated sinusoid-like blood spaces was found in the lesion, and the relative proportion of dilated sinusoid-like blood space in the inner part of the lesion was greater than that in the outer part. The enhancement pattern and MR appearance in our case may depend on the proportion of dilated sinusoid-like blood space to HCC cells. Although the diagnosis of HCC can usually be made based on characteristic enhancement patterns; hypervascularity during the arterial-dominant phase and washout during the portal-dominant phase on dynamic CT and MR imaging [11], we occasionally encounter HCC with atypical radiologic findings, such as the present case. If we encounter a hypervascular liver mass without washout during the portal-dominat phase, delayed-phase imaging may be helpful in correctly diagnosing HCC.
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To our knowledge, this is the first case report to show the enhancement pattern of pelioid HCC on triple-phasic CTA, and delayed-phase imaging was helpful in making a diagnosis of HCC, as dilated sinusoid-like blood spaces may affect the enhancement pattern and MR appearance of HCC. 4. Conclusion We herein presented the radiologic findings of pelioid HCC with triple-phasic CTA and MRI. Based on the enhancement pattern of pelioid HCC on triple-phasic CTA, delayed-phase imaging was helpful in diagnosing HCC, as dilated sinusoid-like blood spaces may affect the enhancement pattern and MR appearance of HCC. Conflict of interest Authors have no conflict of interest. References [1] Yanoff M, Rawson AJ. Peliosis hepatis – an anatomic study with demonstration of two varieties. Arch Pathol 1964;77:159–65. [2] Zafrani ES, Alain C, Baudelot AM, et al. Ultrastructual lesions of the liver in human peliosis – a report of 12 cases. Am J Pathol 1984; 114:349–59. [3] Zak FG. Pelisis hepatis. Am J Path 1950;26:1–16. [4] Czapar CA, Weldon-Linne CM, Moore DM. Pelisis hepatis in the acquired immunodeficiency syndrome. Arch Pathol Lab Med 1986;110:611–3. [5] Muzzo JL, Manz HJ, Maxted WC. Peliosis hepatis after long-term androgen therapy. Urology 1985;25:518–9. [6] Burger RA, Marcuse PM. Pelisis hepatis-report of case. Am J Clin Path 1952;22:569–73. [7] Kojiro M. Pathology of hepatocellular carcinoma. Blackwell; 2006. p. 70–1. [8] Kadoya M, Matsui O, Takashima T, et al. Hepatocellular carcinoma: correlation of MR imaging and histological findings. Radiology 1992; 183:819–25. [9] Kim YK, Jang KY, Cho BH, et al. Three-phase dynamic CT of pelioid hepatocellular carcinoma. AJR 2007;189:160–2. [10] Hoshimoto S, Morise Z, Suzuki K, et al. Hepatocellular carcinoma with extensive peliotic change. J Hepatobilially Pancreat Surg 2009;16:566–70. [11] Silva AC, Evans JM, McCullough AE, et al. MR Imaging of hypervascular liver masses: a review of current techniques. RadioGraphics 2009;29:385–402.
Contents lists available at ScienceDirect
European Journal of Radiology Extra journal homepage: intl.elsevierhealth.com/journals/ejrex
Triple-phasic CT during hepatic angiography of pelioid hepatocellular carcinoma Yasushi Itou a,∗ , Shigenori Nagata b , Yasuhiko Tomita b , Katsuyuki Nakanishi a a b
Department of Diagnostic Radiology, Osaka Medical Center for Cancer and Cardiovascular, 1-3-3, Nakamichi, Higashinari-ku, Osaka 537-8511, Japan Department of Pathology, Osaka Medical Center for Cancer and Cardiovascular, Osaka, Japan
a r t i c l e
i n f o
Article history: Received 4 January 2011 Accepted 4 April 2011
Keywords: Pelioid hepatocellular carcinoma Dilated sinusoid-like blood space CT during hepatic angiography
a b s t r a c t We present a case of pelioid hepatocellular carcinoma detected by computed tomography during hepatic angiography and confirmed by pathology. On computed tomography angiography, the lesion showed slight enhancement in the early phase, and enhancement subsequently increased. Lesion enhancement then attenuated in the delayed phase. On T2-weighted image, the lesion was hyperintense, and the inner part of the lesion was hyperintense when compared with the outer part of the lesion. Pathologically, dilated sinusoid-like blood spaces were present within the lesion, and the proportion of these in the inner part of the tumor was greater than that in the outer part. © 2011 Elsevier Ireland Ltd. All rights reserved.
1. Introduction Peliosis hepatis is rare and is histologically characterized by randomly distributed multiple blood-filled cavities representing dilated sinusoids in liver [1,2]. Findings of pelioid hepatocellular carcinoma (HCC) mimicking peliosis hepatis in the triple-phasic CT during angiography are herein presented. 2. Case report A liver mass was incidentally discovered in a 68-year-old male on abdominal sonography at a health screening. The patient was subsequently referred to our hospital for evaluation and treatment of the mass. He had been a habitual drinker for 40 years. Laboratory test results were as follows: serum aspartate aminotransferase (AST), 49 U/l; serum alanine aminotransferase (ALT), 54 U/l; ␥glutamyltransferase, 270 U/l; and ICG 15-min retention ratio, 14.3%. Serum ␣-fetoprotein (AFP) levels and protein induced by Vitamin K absence or antagonist (PIVKA-II) were in the normal range. These data indicated chronic liver damage due to alcohol intake. Triple-phasic helical CT was performed using a 16-detector row CT scanner (Aquilion 16; Toshiba, Tokyo, Japan) at 120 kVp and a revolution time of 0.5 s. After pre-contrast CT scan, 100 ml of iopamidol (Iopamiron; Bayer Schering Pharma, Osaka, Japan) with an iodine concentration of 370 mg/dl was injected at a rate
∗ Corresponding author. Tel.: +81 6 6972 1181; fax: +81 6 6981 3329. E-mail address: [email protected] (Y. Itou). 1571-4675/$ – see front matter © 2011 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ejrex.2011.04.001
of 3 ml/s by a power injector via the antecubital vein. Arterialdominant phase and portal-dominant phase scans were obtained using 35- and 80-s delay times, respectively, from the initiation of contrast material injection. Scans were obtained at a 1 mm collimation and pitch of 0.8. Pre-contrast CT image showed fatty liver, and a focal hypoattenuating lesion measuring 3 cm in segment 7 (Fig. 1a). In the arterial-dominant phase of contrast enhancement, the lesion showed peripheral ring enhancement (Fig. 1b). In the portal-dominant phase, the lesion was isodense to intrahepatic portal veins (Fig. 1c). A centripetal progression (from the periphery to the center of the lesion) of enhancement was observed. MR images were obtained with a 3 Tesla system (Magnetom Trio; Siemens Medical Systems, Erlangen, Germany) using a phased-array coil. The following sequences were performed. T2-weighted half-Fourier acquisition single-shot turbo spin-echo imaging (T2WI): TR/TE = 1200/67 ms; flip angle (FA) = 120◦ ; echo train length (ETL) = 256; number of excitations (NEX) = 1; matrix = 320 × 238; slice thickness = 8 mm; and no gap. In-phase (TR/TE = 120/2.46) and opposed-phase (TR/TE = 120/1.23) T1-weighted two-dimensional gradient-echo imaging (T1WI): FA = 60◦ ; ETL = 1; matrix = 256 × 164; slice thickness = 8 mm; and no gap. Diffusion-weighted imaging (DWI) using a single-shot spin echo-planner imaging (EPI) sequence with water selective excitation and free-breathing Prospective Acquisition and Correction (PACE): TR/TE = 6000/82 ms; FA = 90◦ ; matrix = 128 × 86; slice thickness = 5 mm; no gap; and b-values = 0, 1000 s/mm2 . After these images were obtained, a volumetric three-dimensional fat-suppressed spoiled gradient echo acquisition (volumetric interpolated breath-hold examination, VIBE; Siemens) with mSENSE was performed using following param-
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Y. Itou et al. / European Journal of Radiology Extra 79 (2011) e5–e9
Fig. 1. (a) Pre-contrast CT image showing fatty liver, and a focal hypoattenuating lesion (black arrow) in segment 7. (b) In the arterial-dominant phase of contrast enhancement, the lesion shows peripheral ring enhancement. (c) In the portal-dominant phase, the lesion is isodense with intrahepatic portal veins. Centripetal progression (from the periphery to the center of the lesion) of enhancement is observed.
eters: TR/TE = 3.64/1.32 ms; FA = 10◦ ; matrix = 256 × 141; slice thickness = 5 mm; no gap. After the unenhanced image was acquired, 0.2 ml/kg gadolinium-ethoxybenzyl-diethylenetriamine penta-acetic acid (Gd-EOB-DTPA; Bayer Schering Pharma, Osaka, Japan) was injected at a rate of 2 ml/s by a power injector via the antecubital vein, followed by a 40-ml saline flush. The delay
times for the arterial dominant, portal dominant, and equilibrium phases were 32, 80 and 120 s, respectively. A hepatocyte-specific phase was acquired at 20 min after administration of contrast media. The lesion in segment 7 was hypointense on axial inphase and opposed-phase gradient-echo MR images (Fig. 2a and b). On T2WI, the lesion was hyperintense and the inner part
Fig. 2. Chemical shift imaging on axial in-phase (a) and opposed-phase (b) gradient-echo MR images revealed a hypointense lesion in segment 7. (c) Axial T2-weighted fast spin-echo image showing a hyperintense lesion in segment 7. The inner part of the lesion is more hyperintense than outer part of the lesion. (d) ADC values for the inner part of the lesion and the outer part of the lesion are 2 × 103 mm2 /s and 1.6 × 103 mm2 /s, respectively.
Y. Itou et al. / European Journal of Radiology Extra 79 (2011) e5–e9
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Fig. 3. Dynamic Gd-EOB-DTPA-enhanced T1-weighted images are showed. (a) Pre-contrast image. (b) Arterial-dominant phase image. (c) Portal-dominant phase image. (d) Equilibrium-phase image. (e) Hepatocyte-specific phase image (20-min post-injection). On dynamic Gd-EOB-DTPA-enhanced T1WI, the lesion shows peripheral enhancement in the arterial-dominant phase (Fig. 3b), followed by progressive centripetal enhancement during the portal-dominant phase and equilibrium phase (Fig. 3c and d). In the hepatocyte-specific phase, the lesion is hypointense when compared with liver parenchyma (Fig. 3e).
of the lesion was hyperintense when compared with the outer part of the lesion (Fig. 2c). On dynamic Gd-EOB-DTPA-enhanced T1WI, the lesion showed peripheral enhancement in the arterialdominant phase (Fig. 3b), followed by progressive centripetal
enhancement during the portal-dominant phase and equilibrium phase (Fig. 3c and d). In the hepatocyte-specific phase, the lesion was hypointense when compared with liver parenchyma (Fig. 3e).
Fig. 4. (a) CTAP image showing a portal perfusion defect in segment 7. (b)–(d) Triple-phasic CTHA was performed. Early-phase (b), late-phase (c), and delayed-phase scans (d) were obtained using 8-, 35-, and 180-s delay times, respectively, from the initiation of contrast material injection. On CTA, the lesion in segment 7 shows slight enhancement in the early phase, followed by gradual enhancement during early phase and late phase. Although the enhancement of the lesion was attenuated in the delayed phase, it remained slightly hyperdense when compared with liver parenchyma.
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Fig. 5. Cut surface of surgical specimen. Encapsulated tumor, 3.0 cm in diameter, showing a dark red color at the center of the lesion.
40 s. Triple-phasic CTA was performed by placing the catheter tip in the proper hepatic artery, and 30 ml of iopamidol with an iodine concentration of 150 mg/dl was injected at a rate of 2 ml/s. Early-phase, late-phase, and delayed-phase scans were obtained using 8-, 35- and 180-s delay times, respectively, from the initiation of contrast material injection. CTAP showed a well-defined, round perfusion defect in segment 7 (Fig. 4a). On CTA, the lesion showed slight enhancement in the early phase (Fig. 4b), followed by gradual enhancement during the early and late phases (Fig. 4c). Although lesion enhancement was attenuated in the delayed phase, it remained slightly hyperdense when compared with liver parenchyma (Fig. 4d). The tumor in segment 7 was surgically resected. The cut surface of the surgical specimen revealed a well-encapsulated tumor, measuring 3.0 cm in diameter and dark red in color at the center of the lesion (Fig. 5). Microscopic examination showed welldifferentiated HCC with a thin fibrous capsule (Fig. 6a and b). Dilated sinusoid-like blood spaces were present within the tumor, and relative proportion of those in the inner part of the tumor was higher than that in the outer part (Fig. 6c). On CD31 antibody staining, the endothelial lining was almost absent in the dilated sinuisoid-lke blood spaces (Fig. 6d).
3. Discussion CT during arterial portography (CTAP) and triple-phasic CT during hepatic angiography (CTA) were performed using a 4-detector row CT scanner (Aquilion 4; Toshiba, Tokyo, Japan) at 120 kVp and a revolution time of 0.5 s. After pre-contrast CT was performed, 90 ml of iopamidol (Iopamiron; Bayer Schering Pharma, Osaka, Japan) with an iodine concentration of 150 mg/dl was injected at a rate of 3 ml/s by placing the catheter tip in the superior mesenteric artery, with CT scanning started at 25 and
Peliosis hepatis has been reported in association with chronic wasting diseases (e.g., tuberculosis, acquired immunodeficiency syndrome) [3,4] and drugs (e.g., anabolic steroids, oral contraceptives, and azathioprine) [5,6]. Two histological patterns of peliosis hepatis were described by Yanoff and Rawson [1]. In the phlebectatic type, blood-filled spaces are lined by endothelium and are associated with aneurysmal dilatation of the central vein. In the
Fig. 6. (a) Histopathological examination revealed a tumor with a thin fibrous capsule (arrow) (H&E stain, 20×). (b) Photomicrograph of pathological section showing welldifferentiated hepatocellular carcinoma in the outer part of the tumor. Tumor cells are arranged in a thin trabecular pattern (H&E stain, 200×). (c) Histopathologically, dilated sinusoid-like blood spaces are present within the tumor, and the distribution of dilated sinusoid-like blood spaces is predominantly in the inner part of the tumor when compared with the outer part of the tumor (Fig. 6b) (H&E stain, 400×). (d) Endothelial cells are positive for CD 31 immunostaining in the cancer cell nest (black arrow). On the other hand, endothelial lining was largely absent in the dilated sinuisoid-lke blood spaces (CD 31 stain, 400×) (DS, dilated sinusoid-like blood space).
Y. Itou et al. / European Journal of Radiology Extra 79 (2011) e5–e9
parenchymal type, the spaces have no endothelial lining and are usually associated with hemorrhagic parenchymal necrosis. Pathologically, peliosis hepatis-like blood-filled spaces are frequently observed in HCC [7]. Kadoya et al. reported that peliotic changes were observed in 22 (31%) of 72 resected HCC [8]. Kojiro reported that the incidence of peliotic change parallels the increase in tumor diameter, and all tumors are completely or incompletely encapsulated [7]. It was therefore speculated that the development of peliotic change in HCC could be explained by endothelial damage due to sinusoidal dilatation following increased intratumoral pressure. On the other hand, few cases regarding the radiologic findings on pelioid HCC have been reported [8–10]. Peripheral enhancement in the arterial phase and centripetal progression of contrast enhancement have been observed during portal venous phase on dynamic CT and MR imaging [9,10]. Kim et al. speculated that dilated sinusoid-like blood spaces might have been responsible for the gradual fill-in enhancement patterns, as in cavernous hemangioma [9]. Kadoya et al. reported that the peliotic change in HCC was significantly correlated with localized hyperintense foci on T2weighted MR image [8]. In the present case, the lesion showed a gradual fill-in enhancement pattern during the early and late phases, and this enhancement diminished during the delayed phase on CTA. On T2WI, the lesion was hyperintense and the inner part of the lesion was more hyperintense than the outer part of the lesion. On microscopic examination, a mix of well-differentiated HCC cells and dilated sinusoid-like blood spaces was found in the lesion, and the relative proportion of dilated sinusoid-like blood space in the inner part of the lesion was greater than that in the outer part. The enhancement pattern and MR appearance in our case may depend on the proportion of dilated sinusoid-like blood space to HCC cells. Although the diagnosis of HCC can usually be made based on characteristic enhancement patterns; hypervascularity during the arterial-dominant phase and washout during the portal-dominant phase on dynamic CT and MR imaging [11], we occasionally encounter HCC with atypical radiologic findings, such as the present case. If we encounter a hypervascular liver mass without washout during the portal-dominat phase, delayed-phase imaging may be helpful in correctly diagnosing HCC.
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To our knowledge, this is the first case report to show the enhancement pattern of pelioid HCC on triple-phasic CTA, and delayed-phase imaging was helpful in making a diagnosis of HCC, as dilated sinusoid-like blood spaces may affect the enhancement pattern and MR appearance of HCC. 4. Conclusion We herein presented the radiologic findings of pelioid HCC with triple-phasic CTA and MRI. Based on the enhancement pattern of pelioid HCC on triple-phasic CTA, delayed-phase imaging was helpful in diagnosing HCC, as dilated sinusoid-like blood spaces may affect the enhancement pattern and MR appearance of HCC. Conflict of interest Authors have no conflict of interest. References [1] Yanoff M, Rawson AJ. Peliosis hepatis – an anatomic study with demonstration of two varieties. Arch Pathol 1964;77:159–65. [2] Zafrani ES, Alain C, Baudelot AM, et al. Ultrastructual lesions of the liver in human peliosis – a report of 12 cases. Am J Pathol 1984; 114:349–59. [3] Zak FG. Pelisis hepatis. Am J Path 1950;26:1–16. [4] Czapar CA, Weldon-Linne CM, Moore DM. Pelisis hepatis in the acquired immunodeficiency syndrome. Arch Pathol Lab Med 1986;110:611–3. [5] Muzzo JL, Manz HJ, Maxted WC. Peliosis hepatis after long-term androgen therapy. Urology 1985;25:518–9. [6] Burger RA, Marcuse PM. Pelisis hepatis-report of case. Am J Clin Path 1952;22:569–73. [7] Kojiro M. Pathology of hepatocellular carcinoma. Blackwell; 2006. p. 70–1. [8] Kadoya M, Matsui O, Takashima T, et al. Hepatocellular carcinoma: correlation of MR imaging and histological findings. Radiology 1992; 183:819–25. [9] Kim YK, Jang KY, Cho BH, et al. Three-phase dynamic CT of pelioid hepatocellular carcinoma. AJR 2007;189:160–2. [10] Hoshimoto S, Morise Z, Suzuki K, et al. Hepatocellular carcinoma with extensive peliotic change. J Hepatobilially Pancreat Surg 2009;16:566–70. [11] Silva AC, Evans JM, McCullough AE, et al. MR Imaging of hypervascular liver masses: a review of current techniques. RadioGraphics 2009;29:385–402.