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• W2997472303 abstract "HomeRadioGraphicsVol. 40, No. 1 PreviousNext Gastrointestinal ImagingFree AccessInvited Commentary on “Hyperintense Liver Masses at Hepatobiliary Phase Gadoxetic Acid–enhanced MRI”Neeraj LalwaniNeeraj LalwaniAuthor AffiliationsDepartment of Radiology, Wake Forest University and Baptist Health Winston-Salem, North CarolinaNeeraj LalwaniPublished Online:Dec 13 2019https://doi.org/10.1148/rg.2020190200MoreSectionsPDF ToolsImage ViewerAdd to favoritesCiteTrack CitationsPermissionsReprints ShareShare onFacebookTwitterLinked In It is my pleasure to comment on the insightful article by Fujita et al (1) in this issue of RadioGraphics. This article can be considered a ready reckoner for all hyperintense lesions that are seen during the hepatobiliary phase (HBP) of gadoxetic acid–enhanced MRI.Gadoxetic acid is a hepatocyte-specific contrast agent and can help better characterize hepatic lesions. It is transported by anion-transporting polypeptides (OATPs), which are present in functional hepatocytes. Any hepatic lesion with preserved expression of OATP can take up gadoxetic acid and appear hyperintense during the HBP. On the other hand, lesions without functioning hepatocytes or without expression of OATP appear hypointense during the HBP. It is noteworthy that the HBP is an intracellular-dominant phase, and hepatic lesions usually appear hyperintense during the extracellular phase of imaging performed with any other contrast agent.The uptake of gadoxetic acid during the HBP has been classically described in association with focal nodular hyperplasia (FNH) (2); for years, scholars believed that all hyperintense lesions seen during the HBP are FNH. As imaging evolved, researchers found that hyperintensity during the HBP could be observed with variegated hepatic lesions and correlated with preserved OATP expression. OATP expression can be seen in either functional hepatocytes or tumor cells of hepatic origin. Occasionally, a lesion may also appear hyperintense during the HBP owing to peritumoral retention of gadoxetic acid, retention of gadoxetic acid in the extracellular space, or biliary enhancement in the tumor. Fujita et al (1) have provided a comprehensive review of hyperintense hepatic lesions during the HBP and describe the relevant associated differential diagnoses, histopathologic and molecular features, and imaging findings. The characterization of hepatic lesions remains crucial in clinical practice, and knowledge of the entities discussed in this review will facilitate optimal patient management.Fujita et al first outline the characteristics of gadoxetic acid, with emphasis on the kinetic features and transport mechanisms of this agent and the clinical implications for its use in the assessment of hepatocellular carcinoma (HCC). Gadoxetic acid–enhanced examinations can enable improved detection of small (≤2 cm) HCCs (3) and better diagnosis of borderline hepatic nodules such as early (ie, low-grade) HCCs and high-grade dysplastic nodules (4). It is crucial to understand that assessment of nonperipheral washout should be performed during only the portal venous phase (PVP) of gadoxetic acid examinations, because only the PVP corresponds to an extracellular-dominant phase in these studies. Neither the transitional phase (TP) (after the PVP but before the HBP, or 2–5 minutes after the injection) nor the HBP can be relied on to demonstrate washout, although the HBP is more sensitive for the detection of smaller HCCs. This article also includes, in a tabulated format, valuable summaries of the pros and cons of gadoxetic acid.Fujita et al (1) classify hepatic lesions according to the types of cells or compartments (ie, spaces) that take up gadoxetic acid. The uptake by hyperplastic hepatocytes is seen in FNH, FNH-like lesions, and nodular regenerative hyperplasia (NRH), whereas gadoxetic acid is taken up by the neoplastic cells (with preserved OATP) in adenoma and HCC. Lesions such as hemangiomas and cholangiocarcinomas demonstrate uptake in the extracellular space, whereas lesions such as intraductal papillary neoplasm of the bile duct (IPNB) and lymphoma exhibit uptake (ie, accumulation) in the biliary tract.Fujita et al (1) define difficult and complex terms in simple language; for example, hyperplastic hepatocytes are lucidly described as normal functioning hepatocytes and abnormal bile ducts that do not communicate with the surrounding biliary system. Most of the important and clinically relevant entities and differential diagnoses are discussed from a clinical and practical standpoint.These authors assert that the presence of intense homogeneous arterial enhancement and iso- or hyperintensity during the HBP clenches the diagnosis of FNH because most hypervascular hepatic lesions show hypointensity during the HBP; this finding is very useful in practice. However, they overemphasize the imaging features of central scars in FNH, as the hyperintense scars typically seen on T2-weighted MR images can be absent in 23% of cases (5) and may not enhance. On the other hand, a central scar can also be present in 25%–56% of fibrolamellar HCCs and retain contrast material during the delayed phase, contrary to classic belief (5). FNH-like lesions are commonly associated with alcoholic liver cirrhosis and demonstrate imaging features that are similar to those of FNH.Hepatocellular adenoma (HCA) demonstrates hypointensity during the HBP conventionally; this observation facilitates the differentiation of HCA from FNH. Nevertheless, the diagnostic accuracy of gadoxetic acid–enhanced MRI in the differentiation of HCA from FNH is reportedly high and overestimated (6,7). Previously categorized telangiectatic FNH, which may show strong hyperintensity on T2-weighted MR images, lacks a central scar, demonstrates persistent contrast enhancement on delayed MR images, and is now described as a variant of inflammatory HCA (I-HCA) (8). Fujita et al (1) follow the classification of HCAs described by the Bordeaux group, in which HCA is categorized into four subtypes: β-catenin activated (B-HCA), I-HCA, hepatocyte nuclear factor 1α mutated (H-HCA), and unclassified (U-HCA). B-HCAs have been shown to have higher premalignancy potential (9). Research findings (10,11) have shown that about 10% of I-HCAs might contain mutations involving the β-catenin gene. Therefore, the issue of whether B-HCA should be considered a separate entity or simply a genetic mutation that can be present in any HCA remains controversial. The HCAs that take up gadoxetic acid and appear hyperintense and/or isointense during the HBP may harbor mutations of the β-catenin gene. Hence, the uptake of gadoxetic acid by HCAs during the HBP is clinically important because such HCAs have a higher propensity to develop malignancies. Overall, the sole finding of a hyperintense lesion during the HBP is neither a sign of benignity nor diagnostic of FNH, and the correlation of this finding with other MRI features is mandatory before a clinical decision can be made.Fujita et al (1) briefly touch on hedgehog-activated adenoma, which was previously considered a type of U-HCA and accounts for 4% of all HCAs. These HCAs have a higher tendency to bleed (7). However, an additional heterogeneous subgroup of HCAs that might demonstrate higher malignancy potential and was not covered in this article includes androgen-associated adenomas, pigmented adenomas, and myxoid adenomas. Pigmented and myxoid adenomas are characterized by heavy lipofuscin and abundant myxoid material content, respectively (12,13). Moreover, it has been suggested that pigmentation and β-catenin activation may be manifestations of the malignant transformation process in any histologic subtype of HCA (13).Current histopathologic and genetic classifications of HCAs do not encompass the newer heterogenous HCA groups, and, thus, an expanded system based on identifiable risk factors has been proposed. These risk factors may include exposure to hormones (estrogen or androgens) or preexisting parenchymal disease (glycogen storage disease) (13). On the basis of this classification, estrogen-induced HCAs include H-HCAs (40% of cases), I-HCAs (50% of cases), and U-HCAs (10% of cases). Similarly, androgen-related HCAs are H-HCAs (10% of cases), I-HCAs (20% of cases), and U-HCAs (70% of cases). Among the HCAs associated with glycogen storage disease, 70% are I-HCAs and the rest are U-HCAs. The majority (60%) of HCAs associated with no identifiable risk factors are unclassified, with the rest of them being equally distributed among H-HCAs and I-HCAs (7). Myxoid-type adenomas consist of H-HCAs exclusively and are described as protein kinase A–associated adenomas in this identifiable risk factor–based classification system. It is interesting that pigmentation and β-catenin activation are indicators of potential malignant transformation and can be seen with any of these subtypes (7). The imaging findings of these heterogeneous HCA subgroups have not been described, and this may explain why they are excluded in this article.Generally, OATP expression is downregulated as neovascularization evolves during hepatocarcinogenesis. Nonetheless, about 10%–15% of HCCs may retain OATP expression and appear hyperintense during the HBP, which has been associated with the activation of β-catenin and hepatocyte nuclear factor 4α. These HCCs usually demonstrate characteristic histopathologic and biologic behavior, follow a less aggressive pattern, and are associated with lower recurrence rates after treatment. About 20% of HCCs may develop in noncirrhotic livers (5). FNH may closely mimic such HCCs at gadoxetic acid–enhanced MRI, as both of these tumors can show arterial hyperenhancement and hyperintensity during the HBP. In such cases, Fujita et al recommend correlating the findings with apparent diffusion coefficient images and CT findings. A classic washout pattern at CT and low apparent diffusion coefficient values can suggest a diagnosis of HCC.Hepatic lesions with a fibrotic or necrotic component may retain gadoxetic acid in the extracellular space during the HBP; this gadoxetic acid retention is similar to the delayed contrast enhancement seen with use of routine contrast agents. The most common types of lesions that display this retention include cholangiocarcinoma and certain metastases with extensive fibrous stroma. Such retention is often seen at the center of lesions with a higher fibrous concentration and maintained peripheral hepatocytes, giving rise to a targetoid appearance. It is interesting that the targetoid appearance can also be seen during other phases and with other MRI sequences and classified accordingly as targetoid diffusion restriction, targetoid dynamic enhancement, or a targetoid TP or HBP appearance. Occasionally, atypical HCCs also can exhibit targetoid features. Fujita et al (1) also correlated the mixed hypointensity of colorectal metastases with OATP overexpression, which is associated with a worse progression-free survival rate. Therefore, mixed hypointensity of colorectal metastases can function as a radiogenomic marker and predict poor long-term survival. Rarely, rapidly enhancing or high-flow hemangioma also can represent a diagnostic dilemma at gadoxetic acid–enhanced MRI. Marked hyperintensity on heavily T2-weighted MR images, high apparent diffusion coefficient values, and signal intensity following blood pooling can help in making the correct diagnosis.Occasionally, a rim of hyperplastic hepatocytes may surround a tumor and demonstrate pseudoretention of contrast material during the HBP. Fujita et al classify this phenomenon as peritumoral retention. Peritumoral retention has been described with HCCs and other tumors such as metastases from gastrointestinal stromal or neuroendocrine tumors. Similarly, hyperintensity can also be seen owing to contrast material accumulation in compressed or distorted biliary ducts at the periphery of a tumor.Although the Fujita et al article (1) is well written and provides extensive practical guidelines for diagnosing hyperintense hepatic lesions seen during the HBP, the differential diagnosis of FNH, B-HCA, and early, or low-grade, HCC (with retained OATP expression) remains challenging. These authors propose that FNH may (rarely) demonstrate microscopic fat; however, this proposal is likely based on an isolated case report and remains controversial (14). The presence of microscopic fat indicates either H-HCA or low-grade HCC. HCA often demonstrates intense arterial enhancement that persists through the venous and equilibrium phases, whereas FNH is often not easily observed during the venous and equilibrium phases. HCC classically demonstrates washout, regardless of arterial enhancement. Moreover, FNH is not easily discernible on T2-weighted MR images. It would have been helpful for Fujita et al to include a tabulated comparison of these three lesions, with key imaging findings and practical pearls, which may help in differentiating these entities at gadoxetic acid–enhanced MRI.I believe that MRI with gadoxetic acid enhancement can sometimes be confusing and complicate the overall picture, although it can be a sensitive tool for identifying an obscured metastasis that is not otherwise detectable with use of other sequences or imaging modalities. In addition, a compromised arterial phase at gadoxetic acid–enhanced MRI can represent a significant diagnostic challenge if it occurs with altered perfusion, as seen with background cirrhosis or portal venous thrombosis. A combination of apparent diffusion coefficient values, dynamic and/or T2-weighted MRI sequences, and correlation with prior or follow-up CT and/or non–gadoxetic acid–enhanced MRI findings can be helpful in making confident diagnoses.I congratulate Fujita et al for their highly informative and well-illustrated review and thank them for sharing many valuable tips and appropriate guidelines. I hope that this commentary complements their excellent work and adds value for readers.References1. Fujita N, Nishie A, Asayama Y, et al. Hyperintense liver masses at hepatobiliary phase gadoxetic acid–enhanced MRI: imaging appearances and clinical importance. RadioGraphics 2020;40(1):72–94. Link, Google Scholar2. Kacl GM, Hagspiel KD, Marincek B. Focal nodular hyperplasia of the liver: serial MRI with Gd-DOTA, superparamagnetic iron oxide, and Gd-EOB-DTPA. Abdom Imaging 1997;22(3):264–267. Crossref, Medline, Google Scholar3. Kierans AS, Kang SK, Rosenkrantz AB. The diagnostic performance of dynamic contrast-enhanced MR imaging for detection of small hepatocellular carcinoma measuring up to 2 cm: a meta-analysis. Radiology 2016;278(1):82–94. Link, Google Scholar4. Kim BR, Lee JM, Lee DH, et al. Diagnostic performance of gadoxetic acid–enhanced liver MR imaging versus multidetector CT in the detection of dysplastic nodules and early hepatocellular carcinoma. Radiology 2017;285(1):134–146. Link, Google Scholar5. Gaddikeri S, McNeeley MF, Wang CL, et al. Hepatocellular carcinoma in the noncirrhotic liver. AJR Am J Roentgenol 2014;203(1):W34–W47. Crossref, Medline, Google Scholar6. Glockner JF, Lee CU, Mounajjed T. Inflammatory hepatic adenomas: characterization with hepatobiliary MRI contrast agents. Magn Reson Imaging 2018;47:103–110. Crossref, Medline, Google Scholar7. Ponnatapura J, Kielar A, Burke LMB, et al. Hepatic complications of oral contraceptive pills and estrogen on MRI: controversies and update—adenoma and beyond. Magn Reson Imaging 2019;60:110–121. Crossref, Medline, Google Scholar8. Attal P, Vilgrain V, Brancatelli G, et al. Telangiectatic focal nodular hyperplasia: US, CT, and MR imaging findings with histopathologic correlation in 13 cases. 2003;228(2):465–472. Google Scholar9. Garcia-Buitrago MT. Beta-catenin staining of hepatocellular adenomas. Gastroenterol Hepatol (N Y) 2017;13 (12):740–743. Medline, Google Scholar10. van Aalten SM, Thomeer MG, Terkivatan T, et al. Hepatocellular adenomas: correlation of MR imaging findings with pathologic subtype classification. Radiology 2011;261(1):172–181. Link, Google Scholar11. Grazioli L, Federle MP, Brancatelli G, Ichikawa T, Olivetti L, Blachar A. Hepatic adenomas: imaging and pathologic findings. RadioGraphics 2001;21(4):877–892; discussion 892–894. Link, Google Scholar12. Mounajjed T, Yasir S, Aleff PA, Torbenson MS. Pigmented hepatocellular adenomas have a high risk of atypia and malignancy. Mod Pathol 2015;28(9):1265–1274. Crossref, Medline, Google Scholar13. Torbenson M. Hepatic Adenomas: classification, controversies, and consensus. Surg Pathol Clin 2018;11(2):351–366. Crossref, Medline, Google Scholar14. Stanley G, Jeffrey RB Jr, Feliz B. CT findings and histopathology of intratumoral steatosis in focal nodular hyperplasia: case report and review of the literature. J Comput Assist Tomogr 2002;26(5):815–817. Crossref, Medline, Google ScholarArticle HistoryPublished online: Dec 13 2019Published in print: Jan 2020 FiguresReferencesRelatedDetailsAccompanying This ArticleHyperintense Liver Masses at Hepatobiliary Phase Gadoxetic Acid–enhanced MRI: Imaging Appearances and Clinical ImportanceDec 13 2019RadioGraphicsRecommended Articles Hyperintense Liver Masses at Hepatobiliary Phase Gadoxetic Acid–enhanced MRI: Imaging Appearances and Clinical ImportanceRadioGraphics2019Volume: 40Issue: 1pp. 72-94Liver MR Imaging in Children: Current Concepts and TechniqueRadioGraphics2016Volume: 36Issue: 5pp. 1517-1532Morphomolecular Classification Update on Hepatocellular Adenoma, Hepatocellular Carcinoma, and Intrahepatic CholangiocarcinomaRadioGraphics2022Volume: 42Issue: 5pp. 1338-1357Focal Nodular Hyperplasia and Focal Nodular Hyperplasia–like LesionsRadioGraphics2022Volume: 42Issue: 4pp. 1043-1061Benign Hepatocellular Nodules: Hepatobiliary Phase of Gadoxetic Acid–enhanced MR Imaging Based on Molecular BackgroundRadioGraphics2016Volume: 36Issue: 7pp. 2010-2027See More RSNA Education Exhibits A Nodule by Any Other Name: A Pictorial Review of FNH and FNH-like Lesions on MRIDigital Posters2020Don't Get Washed Out: Atypical Manifestations of Hepatocellular CarcinomaDigital Posters2019Pediatric Focal Nodular Hyperplasia: Imaging Features and Diagnostic DifficultiesDigital Posters2019 RSNA Case Collection Focal nodular hyperplasia of the liverRSNA Case Collection2020Focal nodular hyperplasiaRSNA Case Collection2020Radioembolization of Liver Metastasis RSNA Case Collection2020 Vol. 40, No. 1 Metrics Altmetric Score PDF download" @default.
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