We took advantage of the reported genotype/phenotype classification to analyze our surgical series of hepatocellular adenoma (HCA). The series without specific known etiologies included 128 cases (116 women). The number of nodules varies from single, <5, and >5 in 78, 38, and 12 cases, respectively. The resection was complete in 95 cases. We identified 46 HNF1␣-inactivated HCAs (44 women), 63 inflammatory HCAs (IHCA, 53 women) of which nine were also ␤-catenin-activated, and seven ␤-catenin-activated HCAs (all women); six additional cases had no known phenotypic marker and six others could not be phenotypically analyzed. Twenty-three of 128 HCAs showed bleeding. No differences were observed in solitary or multiple tumors in terms of hemorrhagic manifestations between groups. In contrast, differences were observed between the two main groups. Steatosis (tumor), microadenomas (resected specimen), and additional benign nodules were more frequently observed in HNF1␣-inactivated HCAs (P < 0.01) than in IHCAs. Body mass index > 25, peliosis (tumor), and steatosis in background liver were more frequent in IHCA (P < 0.01). After complete resection, new HCAs in the centimetric range were more frequently found during follow-up (>1 year) in HNF1␣-inactivated HCA. After incomplete resection (HCA left in nonresected liver), the majority of HCA remained stable in the two main groups and even sometimes regressed. Six patients of 128 developed hepatocellular carcinoma (HCC) (all were ␤-catenin-activated, whether inflammatory or not). Conclusion: There were noticeable clinical differences between HNF1␣-inactivated HCA and IHCA; there was no increased risk of bleeding or HCC related to the number of HCAs; ␤-cateninactivated HCAs are at higher risk of HCC. As a consequence, we believe that management of HCA needs to be adapted to the phenotype of these tumors. (HEPATOLOGY 2009;50:481-489.)

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Hepatocellular adenomas (HCAs) are a group of benign tumors forming three molecular pathological subgroups: (1) hepatocyte nuclear factor 1␣ (HNF-1␣)-inactivated, (2) ␤-catenin-activated, and (3) inflammatory. Some HCAs present both ␤-catenin activation and inflammation. We analyzed magnetic resonance imaging (MRI) data for correlations between features on imaging and pathological classification of HCAs. We included 50 cases for which pathology specimens were classified into three groups based on immunohistochemical staining. Two characteristic MRI profiles were identified corresponding to HNF-1␣-inactivated and inflammatory HCAs. Fifteen HCAs were HNF-1␣-inactivated. The corresponding lesions showed (1) diffuse signal dropout on T1-weighted chemical shift sequence due to steatosis, (2) isosignal or slight hypersignal on T2-weighted (T2W) images, and (3) moderate enhancement in the arterial phase, with no persistent enhancement in the portal venous and delayed phases. For the diagnosis of HNF-1␣-inactivated HCA, the positive predictive value of homogeneous signal dropout on chemical shift images was 100%, the negative predictive value was 94.7%, the sensitivity was 86.7%, and the specificity was 100%. Twenty-three HCAs were inflammatory and showed (1) an absence or only focal signal dropout on chemical shift sequence; (2) marked hypersignal on T2W sequences, with a stronger signal in the outer part of the lesions, correlating with sinusoidal dilatation areas; and (3) strong arterial enhancement, with persistent enhancement in the portal venous and delayed phases. Marked hypersignal on T2W sequences associated with delayed persistent enhancement had a positive predictive value of 88.5%, a negative predictive value of 84%, a sensitivity of 85.2%, and a specificity of 87.5% for the diagnosis of inflammatory HCA. Conclusion: HNF-1␣-mutated HCAs and inflammatory HCAs were associated with specific MRI patterns related to diffuse fat repartition and sinusoidal dilatation, respectively. (HEPATOLOGY 2008;48:808-818.) H epatocellular adenoma (HCA) is a rare type of benign monoclonal liver neoplasm, occurring mostly in young women using oral contraceptives. Several molecular features associated with HCA have recently been described (for review, see Rebouissou et al. 1 ).Biallelic-inactivating mutations of the TCF1 gene inactivating hepatocyte nuclear factor 1␣ (HNF-1␣) have been identified in 35% to 50% of HCAs. 2-4 Furthermore, HCAs harboring HNF-1␣ mutations have been shown to display repressed gluconeogenesis, together with activa-