Pathological diagnosis of liver cell adenoma and focal nodular hyperplasia: Bordeaux update

Bioulac‐Sage, Paulette; Balabaud, Charles; Bédossa, Pierre; Scoazec, Jean‐Yves; Chiche, Laurence; Dhillon, Amar P.; Ferrell, Linda D.; Paradis, Valérie; Roskams, Tania; Wanless, Ian R.; Zucman‐Rossi, Jessica

doi:10.1016/j.jhep.2006.12.007

Cited by 170 publications

(115 citation statements)

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“…Similar overlap of histological features has been reported in other studies. 6 Nodular architecture, fibrous bands, and ductular reaction were seen in nearly all focal nodular hyperplasia cases. Inflammatory hepatocellular adenoma also showed a nodular architecture in 7% and incomplete fibrous bands in one-fourth of the cases.…”

Section: Discussionmentioning

confidence: 97%

“…6 On the other hand, inflammatory Staining patterns in focal nodular hyperplasia and adenoma hepatocellular adenoma is a benign hepatocellular neoplasm that is often surgically resected due to risk of hemorrhage and/or neoplastic transformation. 6 Hence the distinction between focal nodular hyperplasia and inflammatory hepatocellular adenoma has a direct impact on patient management. Our series confirms that morphological overlap between focal nodular hyperplasia and inflammatory hepatocellular adenoma makes this distinction difficult on histological grounds.…”

Section: Discussionmentioning

confidence: 99%

“…2,4,5 Based on imaging features, clonality results, and gene expression studies, these so-called 'telangiectatic focal nodular hyperplasia' are now classified as inflammatory (or telangiectatic) hepatocellular adenoma. [6][7][8][9][10] This variant of adenoma is one of the four subtypes recognized in the recent World Health Organization classification: 11 hepatocyte nuclear factor 1a-inactivated, b-catenin-activated, inflammatory, and unclassified. The inflammatory (or telangiectatic) subtype of hepatocellular adenoma is characterized by sinusoidal dilatation, hemorrhage, inflammation, and ductular reaction.…”

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confidence: 99%

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Diagnostic utility and limitations of glutamine synthetase and serum amyloid-associated protein immunohistochemistry in the distinction of focal nodular hyperplasia and inflammatory hepatocellular adenoma

et al. 2014

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Inflammatory hepatocellular adenoma can show overlapping histological features with focal nodular hyperplasia, including inflammation, fibrous stroma, and ductular reaction. Expression of serum amyloidassociated protein in inflammatory hepatocellular adenoma and map-like pattern of glutamine synthetase in focal nodular hyperplasia can be helpful in this distinction, but the pitfalls and limitations of these markers have not been established. Morphology and immunohistochemistry were analyzed in 54 inflammatory hepatocellular adenomas, 40 focal nodular hyperplasia, and 3 indeterminate lesions. Morphological analysis demonstrated that nodularity, fibrous stroma, dystrophic blood vessels, and ductular reaction were more common in focal nodular hyperplasia, while telangiectasia, hemorrhage, and steatosis were more common in inflammatory hepatocellular adenoma, but there was frequent overlap of morphological features. The majority of inflammatory hepatocellular adenomas demonstrated perivascular and/or patchy glutamine synthetase staining (73.6%), while the remaining cases had diffuse (7.5%), negative (3.8%), or patchy pattern of staining (15%) that showed subtle differences from the classic map-like staining pattern and was designated as pseudo map-like staining. Positive staining for serum amyloid-associated protein was seen in the majority of inflammatory hepatocellular adenomas (92.6%) and in the minority of focal nodular hyperplasia (17.5%). The glutamine synthetase staining pattern was map-like in 90% of focal nodular hyperplasia cases, with the remaining 10% of cases showing pseudo map-like staining. Three cases were labeled as indeterminate and showed focal nodular hyperplasia-like morphology but lacked map-like glutamine synthetase staining pattern; these cases demonstrated a patchy pseudo map-like glutamine synthetase pattern along with the expression of serum amyloid-associated protein. Our results highlight the diagnostic errors that can be caused by variant patterns of staining with glutamine synthetase and serum amyloid-associated protein in inflammatory hepatocellular adenoma and focal nodular hyperplasia.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Diagnostic utility and limitations of glutamine synthetase and serum amyloid-associated protein immunohistochemistry in the distinction of focal nodular hyperplasia and inflammatory hepatocellular adenoma

et al. 2014

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“…The histological features and classification of hepatic adenomas have recently been expertly reviewed. 1 The association of hepatic adenomas with different risk factors suggests that they may be a heterogeneous group at the molecular level. To date, mutations in the TCF1 gene (also known as HNF1-a) 2 as well as dysregulation of the b-catenin pathway 3,4 have been the best characterized molecular lesions in these tumors, and, in fact, appear to be mutually exclusive in most cases.…”

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confidence: 99%

“…5 In contrast, those with b-catenin (CTNNB1) mutations are less likely to show fatty change, are more likely to show a pseudoglandular growth pattern and are more likely to show cytological atypia as well as hepatocellular carcinoma. 5 In this study, we sought to fully characterize hepatic adenomas that underwent clear malignant degeneration (1) to document additional cases of this rarely reported event and (2) to investigate the possibility that the background hepatic adenoma in those cases that develop malignant degeneration may contain the equivalent of 'high grade dysplasia,' that is, histological features that may be useful in predicting the development of carcinoma. In this regard, others have reported areas of dysplasia in hepatic adenomas based on fine needle aspirates, raising the possibility of identifying histological precursors to cancer adjacent to the actual cancer foci in these hepatic adenomas.…”

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confidence: 99%

Malignant transformation of hepatic adenomas

et al. 2008

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Hepatic adenomas are benign neoplasms of the liver that occur in several well-defined clinical settings, but principally that of excess hormone exposure. They have a small but poorly characterized risk of malignant degeneration. The clinical presentation and pathological findings were reviewed for all hepatic adenomas resected between January 1, 2003 and July 1, 2006. Immunohistochemistry for p53, b-catenin and a-fetoprotein (AFP) were performed on those cases with malignant transformation and exon 3 of b-catenin was amplified and sequenced. A total of 17 hepatic adenomas were resected and 3 showed malignant transformation. All three cases were in women with an age range of 23-33 years. The clinical presentations were vague abdominal pain. Histologically, the malignant transformation occurred within otherwise typical hepatic adenomas. Two of three cases showed patchy atypia throughout the hepatic adenoma. The hepatocellular carcinoma arose as distinct nodules directly within the adenomas, effectively ruling out synchronous lesions. The hepatocellular carcinomas were unifocal in two cases and multifocal in one case with the greatest dimensions of the hepatocellular carcinoma being 2.5, 2.2, and 1 cm. Immunostains for AFP and b-catenin were negative in both the hepatic adenomas and areas of hepatocellular carcinoma. p53 immunostaining was positive within the areas of malignant transformation in one case. No mutations or deletions were seen in exon 3 of the b-catenin gene for either the adenomas or the carcinoma. In conclusion, two of the cases that developed hepatocellular carcinomas showed cytological atypia in the background adenoma. The hepatocellular carcinomas arose as distinct nodules within the adenomas. No common molecular pathway of hepatocellular carcinogenesis was observed by examining AFP, b-catenin, and p53 immunostains and no b-catenin mutations or deletions were found.

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