Magnetic resonance imaging of a small vessel hepatic hemangioma in a cirrhotic patient with histopathologic correlation Sara Lewis, Badr Aljarallah, Anshu Trivedi, Swan N. Thung PII: DOI: Reference:

S0899-7071(15)00050-9 doi: 10.1016/j.clinimag.2015.02.007 JCT 7783

To appear in:

Journal of Clinical Imaging

Received date: Revised date: Accepted date:

13 November 2014 9 January 2015 5 February 2015

Please cite this article as: Lewis Sara, Aljarallah Badr, Trivedi Anshu, Thung Swan N., Magnetic resonance imaging of a small vessel hepatic hemangioma in a cirrhotic patient with histopathologic correlation, Journal of Clinical Imaging (2015), doi: 10.1016/j.clinimag.2015.02.007

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ACCEPTED MANUSCRIPT Magnetic resonance imaging of a small vessel hepatic hemangioma in a cirrhotic patient with histopathologic correlation.

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Case Report

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Authors: Sara Lewis MD1, Badr Aljarallah MD2, Anshu Trivedi MD3, Swan N. Thung MD3

Institution: 1

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Department of Radiology, Body MRI

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Department of Medicine

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Department of Pathology Icahn School of Medicine at Mount Sinai

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One Gustave Levy Place

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Division of Liver Pathology, The Lillian and Henry Stratton - Hans Popper

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New York, NY 10029

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Corresponding author: Sara Lewis, MD Icahn School of Medicine at Mount Sinai Department of Radiology One Gustave Levy Place New York, NY 10029 Email: [email protected] Tel: (212) 241-0712 Financial Support: None.

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Abstract

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The authors report and discuss a rare case of a small vessel hepatic hemangioma in a 59-

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year-old female patient with liver cirrhosis, which was pre-procedurally characterized as indeterminate due to its atypical magnetic resonance imaging (MRI) features. This

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manuscript reviews the MRI features of an unusual lesion with pathologic correlation,

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emphasizes the importance of accurate characterization of liver lesions in the cirrhotic liver, and discusses the role of percutaneous biopsy. We believe this is the first reported

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case of a small vessel hepatic hemangioma in a cirrhotic liver with imaging and

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histopathologic correlation.

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Keywords: Small vessel hepatic hemangioma; indeterminate liver lesion; cirrhosis; MRI

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Clinical and laboratory assessment A 59 year old female presented to her gastroenterologist for evaluation of epigastric abdominal pain. The pain was described as dull, mild to moderate in severity, without relationship to food intake and or position, and lasting several months in duration. She was initially treated for gastroesophageal reflux (GERD) with no improvement in symptoms. Past medical history was negative for liver disease or malignancy. Past surgical history was positive for appendectomy and oophorectomy for benign disease. Routine colonoscopy was significant only for a hyperplastic polyp. Physical exam revealed an obese patient with a body mass index (BMI) of 32. The physical exam was positive for minimal tenderness at the

ACCEPTED MANUSCRIPT right upper quadrant. Laboratory assessment revealed mildly elevated AST (53 U/L), ALT (68 U/L) and GGT (178 U/L). Hepatitis B and C serologies were negative. Alphafetoprotein

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(AFP) was normal (5.9 ng/mL).

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Imaging Evaluation

The patient was referred for abdominal ultrasound at an outside hospital. The sonographer

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performing the first abdominal ultrasound examination was not able to comprehensively

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assess the right lobe of the liver due to technical limitations (i.e. obese patient). Therefore, the patient was referred to abdominal MRI. She subsequently underwent non-contrast MRI

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at outside hospital demonstrating a 2.3 cm heterogeneous nodule in the right hepatic lobe. The patient then presented to our institution for further characterization of the lesion and

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background liver parenchyma.

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The MRI examination was performed on a 1.5T GE Optima MR450w (GE Healthcare, Wausheka, WI, USA) using a torso phased array coil (32 channel). The imaging protocol included coronal and axial SSFSE, GRE T1-weighted in and out of phase imaging, fat suppressed FSE T2WI, axial respiratory triggered DWI with multiple b-values (50, 400, 800) and pre and post contrast enhanced T1WI using axial breath-hold 3D T1 fatsuppressed spoiled gradient recalled echo sequence (LAVA). Post contrast was performed following the dynamic intravenous injection of weight based gadolinium based contrast agent followed by a 20 mL saline flush (2 mL/sec) with a power injector using 3 time points: late arterial, portal venous and late venous phases. Gadolinium based contrast agent

ACCEPTED MANUSCRIPT used for this patient was 9 mL gadobutrol (Gadavist, Bayer Healthcare Pharmaceuticals). Fixed delay technique (20 seconds) was used to acquire dynamic post contrast phase

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images. The portal venous and late venous phases were performed 60 and 180 seconds

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after the administration of contrast material.

The liver demonstrated abnormal morphology, including enlargement of the hilar

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periportal space and a nodular contour, suspicious for cirrhosis. Diffuse loss of signal was

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present throughout the liver on T1 opposed phase images compared to T1 in phase, consistent with diffuse hepatic steatosis. There was a 2.2 cm heterogeneous lesion in

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segment 8 of the liver demonstrating peripheral T2 hyperintensity and a central Y-shaped area of brighter T2 hyperintensity (Fig. 1). A thin rim of perilesional sparing of fat

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deposition was present in the adjacent liver parenchyma. The lesion demonstrated

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diffusion restriction in its peripheral portion with signal loss in the Y-shaped central area on high b-value images (Fig 2). The lesion demonstrated thick, nearly continuous,

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peripheral rim enhancement on arterial phase images that exceeded enhancement of the abdominal aorta. The lesion persistently enhanced on portal venous and late phase images, with no washout (Fig. 3). The Y-shaped area of greater T2 hyperintensity did not enhance. Surrounding transient hepatic enhancement was noted. The central Y-shaped area demonstrated attenuation of signal on high b-value images and high signal on corresponding ADC images, consistent with T2 shine through. The hepatic vessels were patent, and a branch of the right anterior portal vein extended directly to the lesion. No biliary distention was noted peripheral to the lesion. There was no overlying capsular

ACCEPTED MANUSCRIPT retraction or bulging. No additional liver lesion or retroperitoneal lymphadenopathy was

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present.

Pathologic Assessment: The patient underwent uneventful percutaneous CT guided liver

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biopsy 28 days after MRI. The core liver biopsy specimen contains atypical vascular lesion. It consists of clusters of small vessels or capillaries lined by bland but somewhat plump

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endothelial cells with regular round to oval nuclei and fibrotic background (Figures 4A and

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4B). Mitotic figures are absent. Endothelial cells of the vascular lesion are strongly positive for CD34 (Figure 4C), negative for P53, and demonstrate low replication rate (~1%) on Ki-

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67 immunostain. These findings are consistent with small vessel hepatic hemangioma. The non-lesional liver shows micronodular cirrhosis with broad hypocellular fibrous septa and

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moderate macrovesicular steatosis; suggestive of non-alcoholic and/or alcoholic

Discussion

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steatohepatitis induced liver disease (Figure 4D).

Hepatic hemangiomas are the most common benign liver lesion and are believed to be hamartomatous in origin. The prevalence of these lesions ranges from 1-20%, with a female predominance1-3. Cavernous hemangiomas are the most commonly encountered subtype of hepatic hemangioma. Small vessel hemangiomas, as we describe in our case report, represent a distinct pathologic entity and are very rare4. This type of vascular lesion has been reported under different names, such as adult capillary hemangioma and small vessel hepatic hemangioma4-6. The incidence of small vessel hemangiomas is not known.

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Overall, hepatic hemangiomas are most commonly asymptomatic and detected incidentally.

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Hemangiomas may be single or multiple, with multiple lesions reported in 9-22% of

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patients7-9. There is a paucity of literature evaluating the natural history of hepatic

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hemangiomas. The majority of lesions remain stable in size, although growth of lesions has been reported in up to 12.7%9. Significant growth of hepatic hemangiomas is believed to be

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very uncommon. Recurrence following complete resection of giant hemangiomas, however,

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has been reported10. Complications are rare, and large lesions may become symptomatic due to compression upon adjacent structures, rupture or hemorrhage11. Because hepatic

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hemangiomas are frequent, commonly asymptomatic, associated with minimal complications, these lesions usually do not require tissue confirmation or surgical

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resection.

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MR imaging is currently the most accurate modality for diagnosis and characterization of liver lesions. Compared with CT imaging, MRI has superior soft tissue contrast resolution, multiparametric capability and lacks ionizing radiation7. Furthermore, MR imaging has been shown as the optimized imaging modality for diagnosing all subtypes of hepatic hemangiomas, with a reported sensitivities greater than 84% and specificities greater than 90%12,13. Most hepatic hemangiomas are easily distinguished from malignant hepatic tumors using cross sectional imaging including multiphase CT or MRI given characteristic features. Hemangiomas are typically round or lobulated and markedly hyperintense on conventional T2 images. T2 SSFSE images using a long TE are used to discriminate

ACCEPTED MANUSCRIPT hemangioma from cyst: hemangiomas are only mildly hyperintense whereas cysts are markedly hyperintense14. On post-contrast imaging, these lesions demonstrate

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discontinuous, globular, peripheral nodular enhancement with complete or incomplete

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centripetal progression and persistent enhancement8,15. Smaller hemangiomas are often

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equal that of the adjacent abdominal aorta16.

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homogeneously hypervascular. The enhancement of the enhancing components should

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The imaging differential diagnosis for the lesion in our case included hepatocellular carcinoma (HCC), intrahepatic cholangiocarcinoma (ICC), metastasis or atypical

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hemangioma. HCC is the most common primary liver cancer for which cirrhosis is a strong risk factor (i.e. approximately 80% of HCCs arise cirrhotic livers)17,18. The presence of

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arterial enhancement within a cirrhotic nodule usually indicates a progressed HCC17. The

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combination of arterial enhancement, portal venous washout and delayed pseudocapsular enhancement is highly specific for HCC, especially for lesions > 2 cm, enabling confident

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imaging diagnosis to be made 19,20. However, not all HCCs demonstrate this enhancement pattern. Small lesions and distinct HCC subtypes may show variable enhancement patterns, with overlap in appearance with cirrhotic nodules (regenerative and dysplastic nodules), benign and malignant liver lesions. In a recent series by Kim et al, 57% of hypervascular HCCs < 1cm did not show washout21. In addition, the scirrhous subtype of HCC, representing

Magnetic resonance imaging of a small vessel hepatic hemangioma in a cirrhotic patient with histopathologic correlation.

The authors report and discuss a rare case of a small vessel hepatic hemangioma in a 59-year-old patient with liver cirrhosis, which was pre-procedura...
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