Journal of Clinical Imaging 26 (2002) 35 – 38
Hepatic adenomatosis MRI demonstration with the use of superparamagnetic iron oxide N. Cem Balcia,*, Mustafa S¸irvancıa, Cihan Durana, Ahmet Akıncıb a
Department of Radiology, Florence Nightingale Hospital, Istanbul, Turkey Department of Gastroenterology, Florence Nightingale Hospital, Istanbul, Turkey
b
Received 18 June 2001
Abstract This case report describes a case of a 38-year-old woman with hepatic adenomatosis. MRI revealed five hyperintense nodular liver lesions on T1-weighted images which were hypo-isointense with the liver parenchyma on T2-weighted images. Serial gadolinium-enhanced images did not reveal distinctive imaging findings. With the use of superparamagnetic iron oxide (SPIO) particles, hyperintense adenomas revealed signal loss on T1-weighted images after SPIO. Two subcapsular adenomas were resected based on MRI findings and histopathology confirmed MRI diagnosis. D 2002 Elsevier Science Inc. All rights reserved. Keywords: Liver; Adenoma; Magnetic resonance; Contrast agent
1. Introduction Hepatic adenomatosis is defined as presence of arbitrarily more than four adenomas in the liver [1]. Its cross-sectional imaging findings have been reported [1– 3]. According to these reports, adenomas in hepatic adenomatosis have same MRI findings as solitary adenomas. T1- and T2-weighted images reveal no distinctive findings for hepatic adenomas. On serial postgadolinium images, early arterial enhancement with washout has been considered as a more characteristic imaging feature than noncontrast MRI findings [3 –5]. RESspecific contrast agent superparamagnetic iron oxide (SPIO) particles have been used to distinguish benign hepatocellular tumors from malignant liver lesions in indefinite cases [5,6]. We report a case of hepatic adenomatosis, in which the adenomas were characterized with the use SPIO.
2. Case report A 38-year-old woman was referred to our hospital with a right quadrant pain, which has been consistent for 3 months. * Corresponding author. Birlik sok. Bimak Apartment 13/8, 80600 Levent, Istanbul, Turkey. E-mail address:
[email protected] (N.C. Balci).
Laboratory examination revealed slight increase of ALT and AST. Total bilirubin was within normal limits. Serology for hepatitis B and C was negative. Blood alpha-fetoprotein level was within normal limits. There was no clinical sign of cholecystitis. She had no history of drug abuse or prolonged use of oral contraceptives. Patient underwent ultrasound examination, which revealed nodular lesions in the liver with mixed echogenity. MRI was ordered to further characterize nodular lesions in the liver. MRI was performed on a 1-T MR scanner (Magnetom Impact, Siemens Medical Systems, Erlangen, Germany) in all patients. The following imaging sequences were used: breath-hold T1-weighted spoiled gradient-echo (TR = 170 ms, TE = 6 ms, FA = 70), with and without fat suppression, breathing averaged STIR (TR = 5600 ms, TE = 80 ms, TI = 150 ms). Postgadolinium images were obtained using T1-weighted spoiled gradientecho sequence. Gadolinium chelate (Magnevist, Schering, Berlin, Germany) was administered at a dosage of 0.1 mmol/ kg as a 5-s hand-injected bolus followed by a rapid flush 10 ml of normal saline. Spoiled gradient-echo images were repeated immediately after contrast administration (arterial phase) and at 45 and 90 s (intermediate phase) and 5– 7 min (delayed phase) after completion of the normal saline flush. All sequences were acquired using 14– 16 sections and a thickness of 8– 10 mm. The matrix was 128– 145 256 (phase encoding frequency encoding).
0899-7071/02/$ – see front matter D 2002 Elsevier Science Inc. All rights reserved. PII: S 0 8 9 9 - 7 0 7 1 ( 0 1 ) 0 0 3 5 2 - 7
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Five lesions were identified on T1-weighted images in the following localizations: lateral segment of left liver lobe (n = 1), anterior segment of the right liver lobe (n = 2), and posterior segment of the right liver lobe (n = 2). All lesions had high signal on T1- and T1-weighted fat-saturated images. On T2-weighted fat-saturated images, lesions were isointense with the liver parenchyma. One lesion in the posterior segment of the right liver lobe revealed low signal in the central portion on T1-weighted images, which has high signal on T2-weighted images (Figs. 1 and 2). Contrast enhancement of the lesions over time was difficult to assess on serial postgadolinium images, because of their high signal on noncontrast T1-weighted images. The patient was referred to MRI to be further examined with SPIO. SPIO particles (AMI 25, ENDOREM, Guerbet, France) were provided as a stable aqueous colloid with an iron concentration of 11.2 mg/ml. It was diluted at a dosage of 15 mmol/kg body weight in 100 ml 5% glucose and administered intravenously. The solution was slowly
infused over 35 min. Imaging was started 15 min after the end of infusion. Following imaging sequences with the same parameters were used before and after SPIO administration: breath-hold T1-weighted spoiled gradient-echo (TR = 170 ms, TE = 6 ms, FA = 70), T2-weighted fast spin-echo (turbo spin-echo) (TR = 6000 ms, TE = 85 ms), both sequences were acquired using 14 – 16 sections and a thickness of 8 mm. The matrix was 145 256 (phase encoding frequency encoding). On T2-weighted pre-SPIO images, lesions were hardly visible being hypo-isointense relative to liver parenchyma, on post-SPIO images no improvement in lesion detection was observed. The central portion of adenoma in the right liver lobe revealed high signal on both pre- and post-SPIO images. On T1-weighted images, high signal lesions revealed signal loss on post-SPIO images compared to pre-SPIO images (Figs. 1 and 2). Hyperintense central portion of the lesion in the posterior segment of the right liver lobe on T2-weighted images did not reveal signal
Fig. 1. MRI at the level of hepatic dome. (a) T1-weighted spoiled gradient-echo (TR = 170 ms, TE = 6 ms, FA = 70) image reveals two hyperintense lesions in the lateral segment of the left liver lobe (Segment 2) and in the anterior segment of the right liver lobe (Segment 4a) (arrows), which remain hyperintense on (b) fat-suppressed spoiled gradient-echo image with the same parameters. (c) T2-weighted fast spin-echo image (TR = 6000 ms, TE = 85 ms) at the same level reveals no visible lesions. (d) On post-SPIO T1-weighted spoiled gradient-echo image with pre-SPIO, parameters reveals signal loss of the lesions (arrows).
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Fig. 2. MRI at a more caudal section. (a) T1-weighted spoiled gradient-echo (TR = 170 ms, TE = 6 ms, FA = 70) image reveals two additional hyperintense lesions in the right lobe of the liver together with the lesion is Segment 2 (arrows), the lesion in the posterior segment of the right liver lobe reveals hypointense center (short arrow). (b) On T1-weighted fat-suppressed spoiled gradient-echo image with the same parameters, hyperintense signal of the lesions persists. (c) On T2-weighted fast spin-echo image (TR = 6000 ms, TE = 85 ms), no lesion can be visualized except the center portion of the lesion in the posterior segment of the right liver lobe, which is hyperintense relative to liver (arrow). (d) On post-SPIO T1-weighted spoiled gradient-echo image with pre-SPIO parameters, signal loss of the lesions is revealed (arrows). (e) T2-weighted post-SPIO image reveals no visible lesions, except the hyperintense center of the lesion in the posterior segment of the right liver lobe (arrow).
change after SPIO administration (Fig. 2). Imaging findings were consistent with multiple hepatic adenomatosis and the patient was referred to surgery for the resection of the subcapsular adenomas. The lateral segment of the left liver lobe (Segment 2) and the posterior segment of the right liver
lobe (Segment 7) were resected. Histopathology of the lesions was consistent with adenomas. There was no evidence of hemorrhage on histopathology specimen of the lesion in Segment 2, but the lesion in Segment 7 of the right liver lobe revealed intratumoral hemorrhage.
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3. Discussion Hepatic adenomas are benign neoplasms of the liver. They are composed of sheets and cords of hepatocytes, fat, and Kupfer cells. These benign liver tumors are common among females and are associated with several conditions such as oral contraceptive and anabolic steroid use, Type I glycogen storage disease, and diabetes mellitus. Hepatic adenomas are hypervascular and they may cause life-threatening hemorrhage [4]. Unlike solitary liver adenomas, hepatic adenomatosis does not have sex-based predominance. The etiology of hepatic adenomatosis is not clear. Although hepatic adenomatosis is reported to have same etiologic factors, some investigations revealed no regression of lesions after steroid or estrogen withdrawal. Patients with hepatic adenomatosis refer to physicians with upper quadrant pain due to subcapsular location of adenomas. Liver function tests reveal abnormal values most of the time because of multiplicity the lesions [1– 3]. Like in solitary adenomas, hemorrhage is the main complication of hepatic adenomatosis and malignant transformation to HCC has been sporadically reported [3,4]. Imaging findings of hepatic adenomatosis are not different from solitary adenomas [1 – 3]. MRI findings of hepatic adenomas have been described in larger series. On T1-weighted images, hepatic adenomas are isointense with the liver parenchyma or can reveal high signal or heterogeneously high and low signal intensity. High signal on T1-weighted images is attributed to hemorrhage, glycogen, or fat deposition of the lesion [4,7]. Several other malignant liver lesions have high signal intensity on T1-weighted images. Hemorrhagic liver metastases of any primary, melanoma, or multiple myeloma metastases are hyperintense on T1-weighted images. These lesions can have low signal on T2-weighted images or are isointense with the liver on T2-weighted fat-suppressed images [8]. HCC has been reported to have high signal on T1-weighted images due to intratumoral fat or protein content. Fat content of the lesions can be demonstrated on T1-weighted out-of-phase gradientecho images with a signal loss compared to in-phase gradientecho images [8]. In our case, T1-weighted fat-suppressed images ruled out the fat component of the lesions and absence of signal loss and high signal on T1-weighted fat-suppressed images was related to glycogen content or hemorrhagic composition of the lesions. On histopathology, there was no evidence of intratumoral bleeding, except one lesion in the posterior segment of the right liver lobe, with low signal or isointense with the liver parenchyma on T1- and high signal on T2-weighted images centrally. The signal intensity of this lesion was consistent with hyperacute stage of hemorrhage, which may have occurred in our case. Serial gadolinium-enhanced images can characterize focal liver lesions [5]. Hepatic adenomas are hypervascular and reveal increased contrast enhancement on early arterial phase with a washout on intermediate and late images. HCC or hypervascular metastases can have same early enhancement
pattern, in these cases, clinical history is important [5]. In our case, dynamic enhancement pattern could not be evaluated due to hyperintensity of the lesions on T1-weighted images. RES-specific contrast agent SPIO has been used to characterize focal liver lesions. It was taken up by Kupfer cells and decreases signal intensity of the liver on both T1- and T2weighted images. Hepatocellular adenoma and focal nodular hyperplasia (FNH) have been reported to reveal uptake of SPIO due to their Kupfer cell content and reveal signal loss on T1- and T2-weighted images. Malignant lesion do not take up SPIO, and reveal high signal on both T1- and T2-weighted images relative to liver parenchyma. T2- and proton-weighted images are used routinely to evaluate focal liver lesions before and after SPIO application [5,6]. T1-weighted images are used to assess blood pool effect of SPIO, which is characterized by increased signal intensity on T1-weighted images. Hemangiomas reveal uptake of SPIO due to their vascular content and have high signal on T1-weighted mages [5]. In our case, high signal of multiple hepatic adenomas on T1weighted images altered the interpretation of contrast enhancement dynamics of the lesions. T1-weighted images did better in evaluating the signal loss of the lesions after SPIO, since the lesions were more hyperintense than the liver parenchyma on T1-weighted images. FNH has to be considered in differential diagnosis if the lesions reveal SPIO uptake. However, FNH seldom reveals hyperintense signal on T1-weighted images, and multiplicity of lesions has been sporadically reported [3]. In conclusion, we described a case of hepatic adenomatosis, their signal on T1-weighted images hindered the interpretation of contrast enhancement of the lesions on T1-weighted images. The signal loss on T1-weighted images after SPIO application was a distinctive imaging feature of the lesions. References [1] Brummet D, Burton EM, Sabio H. Hepatic adenomatosis: rapid sequence MR imaging following gadolinium enhancement: a case report. Pediatr Radiol 1999;29:231 – 4. [2] Choi BI, Han JK, Kim SH, Han MC. MRI findings in liver adenomatosis. Gastrointest Radiol 1991;16:234 – 6. [3] Grazioli L, Federle MP, Ichikawa T, Balzano E, Nalesnik M, Madariaga J. Liver adenomatosis: clinical histopathologic, and imaging findings in 15 patients. Radiology 2000;216:395 – 402. [4] Chung KY, Mayo-Smith WW, Saini S, Rahmouni A, Golli M, Mathieu D. Hepatocellular adenoma: MR imaging features with pathologic correlation. AJR, Am J Roentgenol 1995;165:303 – 8. [5] Semelka RC, Helmberger TKG. Contrast agents for MR imaging of the liver. Radiology 2001;218:27 – 38. [6] Grandin C, Van Beers BE, Robert A, Gigot J-F, Geubel A, Pringot J. Benign hepatocellular tumors: MRI after superparamagnetic iron oxide administration. J Comput Assisted Tomogr 1995;19:412 – 8. [7] Paulson EK, McClellan JS, Washington K, Spritzer CE, Meyers WC, Baker ME. Hepatic adenoma: MR characteristics and correlation with pathologic findings. AJR, Am J Roentgenol 1994;163:113 – 6. [8] Kelekis NL, Semelka RC, Woosley JT. Malignant lesions of the liver with high signal intensity on T1-weighted MR images. J Magn Reson Imaging 1996;6:291 – 4.