Immunohistochemical Markers on Needle Biopsies Are Helpful for the Diagnosis of Focal Nodular Hyperplasia and Hepatocellular Adenoma Subtypes

Bioulac‐Sage, Paulette; Cubel, Gaëlle; Taouji, Saı̈d; Scoazec, Jean‐Yves; Leteurtre, Emmanuelle; Paradis, Valérie; Stürm, Nathalie; Nhieu, Jeanne Tran Van; Wendum, Dominique; Bancel, Brigitte; Ramos, Jeanne; Paraf, F; Paul, M.C. Saint; Michalak, Sophie; Fabrè, Monique; Guettier, Catherine; Bail, Brigitte Le; Zucman‐Rossi, Jessica; Balabaud, Charles

doi:10.1097/pas.0b013e3182653ece

Cited by 115 publications

(100 citation statements)

References 30 publications

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“…24 In view of these morphological challenges, immunohistochemical staining for glutamine synthetase and serum amyloid-associated protein is increasingly being used to confirm the diagnosis. 14 Our results highlight the utility and the pitfalls in interpretation of these stains (Table 5). Glutamine synthetase shows pericentral staining in the normal liver and map-like glutamine synthetase staining in virtually all the cases of focal nodular hyperplasia.…”

Section: Discussionmentioning

confidence: 56%

“…12,13 In focal nodular hyperplasia, there is expansion of the b-catenin-activated centrizonal region, which leads to overexpression in a characteristic geographic map-like pattern. [14][15][16] Diffuse cytoplasmic expression of glutamine synthetase is seen in a small subset of b-cateninactivated hepatocellular adenomas, but the map-like pattern typical of focal nodular hyperplasia is not observed in hepatocellular adenomas. On the other hand, inflammatory hepatocellular adenomas, but not focal nodular hyperplasia, show cytoplasmic staining with antibodies to acute phase reactants, including serum amyloid-associated protein and C-reactive protein.…”

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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: 56%

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confidence: 99%

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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“…While immunohistochemical staining of LFABP, β-catenin, glutamine synthetase, serum amyloid A, and C-reactive protein has proven to be very effective in differentiating between the four subtypes of HCA, it is also useful in the differentiation between HCA and FNH (9,20). In a retrospective, multicenter study in France, Bioulac-Sage et al (20) found that the certainty of biopsy diagnosis of FNH increased from 53% to 87% when additional immunohistochemistry markers and glutamine synthetase immunostaining were used.…”

Section: Implications For Diagnosismentioning

confidence: 99%

Genotype-phenotype correlations in hepatocellular adenoma: an update of MRI findings

Thomeer¹,

Bröker²,

Lussanet³

et al. 2014

Diagn Interv Radiol

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Hepatocellular adenoma (HCA) is a generally benign liver tumor with the potential for malignancy and bleeding. HCAs are categorized into four subtypes on the basis of genetic and pathological features: hepatocyte nuclear factor 1α-mutated HCA, β-catenin-mutated HCA, inflammatory HCA, and unclassified HCA. Magnetic resonance imaging (MRI) plays an important role in the diagnosis, subtype characterization, and detection of HCA complications; it is also used to differentiate HCA from focal nodular hyperplasia. In this review, we present an overview of the genetic abnormalities, oncogenesis, and typical and atypical MRI findings of specific subtypes of HCA using contrast-enhanced MRI with or without hepatobiliary contrast agents (gadobenate dimeglumine and gadoxetate disodium). We also discuss their different management implications after diagnosis.

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“…Currently, liver ultrasound (US) and MRI are the recommended diagnostic imaging tools for characterizing the lesion and subsequent follow-up. Glutamine synthetase is a nitrogen metabolism enzyme with a distribution in the human liver characterized by its strict pericentrolobular localization [25] . It has emerged as a good marker for identification of resected FNH and for differentiating FNH from all other types of hepatocellular nodules developed on normal liver [26] .…”

Section: Focal Nodular Hyperplasiamentioning

confidence: 99%

Differential diagnosis and management of liver tumors in infants

Fernández-Pineda

Cabello-Laureano

2014

WJH

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During the first year of life, most of the liver neoplasms are benign in origin, but some of these histologically benign lesions may be challenging in their management. Although most hepatic hemangiomas can be safely observed until involution is documented, some patients will need treatment due to progressive hepatomegaly, hypothyroidism and/or cardiac failure. Large mesenchymal hamartomas may require extensive hepatic resection and an appropriate surgical plan is critical to obtain good results. For malignant neoplasms such as hepatoblastoma, complete surgical resection is the mainstay of curative therapy. The decision about whether to perform an upfront or delayed resection of a primary liver malignant tumor is based on many considerations, including the ease of resection, surgical expertise, tumor histology and stage, and the likely chemosensitivity of the tumor. This article reviews the initial management of the more common hepatic tumors of infancy, focusing on the differential diagnosis and treatment options.

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Immunohistochemical Markers on Needle Biopsies Are Helpful for the Diagnosis of Focal Nodular Hyperplasia and Hepatocellular Adenoma Subtypes

Cited by 115 publications

References 30 publications

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

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

Genotype-phenotype correlations in hepatocellular adenoma: an update of MRI findings

Differential diagnosis and management of liver tumors in infants

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