Management of hepatocellular adenoma: Solitary-uncomplicated, multiple and ruptured tumors

Toso, Christian; Majno, Pietro; Andrés, Axel; Rubbia‐Brandt, Laura; Berney, Thierry; Bühler, Léo H.; Morel, Philippe; Mentha, Gilles

doi:10.3748/wjg.v11.i36.5691

Cited by 40 publications

(31 citation statements)

References 27 publications

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“…This risk can therefore only be estimated from the pathological records of operated patients. In surgical series of more than 20 patients [11,12,14,15,16,17,18,19,20,21,22,23,24,25,26,27], the proportion of HA with malignant transformation is 5% and this figure appears very reproducible over time (table 1). One has to realize that it is only a rough estimate of the risk of malignancy of HA for two reasons:…”

Section: Risk Of Malignant Transformation Of Hamentioning

confidence: 87%

Malignant Transformation of Liver Adenoma: An Analysis of the Literature

Farges

Dokmak²

2010

Dig Surg

102

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As adenoma in other locations, hepatic adenoma (HA) may transform into hepatocellular carcinoma (HCC) and hepatocyte dysplasia is most probably the intermediate step between both conditions. Malignant HA may appear as microscopic or macroscopic areas of HCC within the HA. These areas are typically well differentiated and without vascular extension or satellite nodules. AFP measurements are not reliable as they are usually normal. The risk of malignant transformation of HA cannot be reliably quantified yet. Several series are concordant to show that approximately 5% of patients whose HA have been resected had pathological evidence of HCC within their HA. This figure however does not take into account fully transformed HA where evidence of the preexisting benign lesion might have disappeared. The risk of malignant transformation is correlated with the diameter of the HA and it is very unusual when it is <5 cm and the same holds true for patients with multiple HA. These results suggest that small HA could be safely observed as they are also at low risk of bleeding. These conclusions might not apply to male patients who are at lower risk of HA, except in specific conditions, but appear to be at a much higher risk of malignant changes.

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Section: Risk Of Malignant Transformation Of Hamentioning

confidence: 87%

Malignant Transformation of Liver Adenoma: An Analysis of the Literature

Farges

Dokmak²

2010

Dig Surg

102

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“…Surgery remains the main treatment to avoid these complications [16,17,18]. Currently the main characteristic to guide treatment remains the size of the nodule with excision for nodules ≥5 cm and surveillance for nodules <5 cm [3,10].…”

Section: Investigation Of Hca Subtypesmentioning

confidence: 99%

Subtype Classification of Hepatocellular Adenoma

2010

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Hepatocellular adenomas (HCA) are rare benign tumours occurring mainly in women under oral contraceptives. HCA bleed frequently and transform rarely into hepatocellular carcinoma. Identification of genes recurrently mutated in HCA and good genotype/phenotype correlations provided the basis of a pathomolecular classification of different HCA subgroups, characterized using immunohistochemical markers. HNF1A-mutated HCA: Biallelic-inactivating mutations of HNF1A gene are identified in 35–40% of HCA. HNF1α-inactivated HCA display characteristic pathological features, including marked steatosis. The expression of FABP1 (which is a HNF1A target gene) is downregulated and the absence of L-FABP expression diagnosed this subgroup. β-Catenin-mutated HCA: β-catenin mutations leading to activation of the Wnt/β-catenin pathway represented 10–15% of HCA. They are characterized by overexpression of glutamine synthetase and aberrant nuclear β-catenin staining. These β-catenin-activated HCA are at greater risk of malignant transformation; they are difficult to differentiate from well-differentiated HCC. Inflammatory HCA (50%): These are defined by the presence of inflammatory infiltrates, sinusoidal dilatation and thick-walled arteries. Small in-frame deletions that target the binding site of gp130 for IL-6 have been reported in 60% of inflammatory HCA. There is an overexpression of the inflammatory proteins serum amyloid A and C-reactive protein in tumour hepatocytes both at mRNA and protein levels. Inflammatory HCA occurred more frequently in patients with high body mass index; they can be also mutated for β-catenin and therefore are probably at risk of HCC. Unclassified HCA: Less than 10% of HCA do not express any of the above-mentioned phenotypic markers. Taking into account noticeable differences between the HCA subgroups, in terms of clinical and prognostic features, phenotyping may become an important tool for HCA management strategy.

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“…Review of the literature reveals that approximately 30% of cases are complicated by hemorrhage [1,5]. It has been suggested that adenomas greater than 5 cm in diameter should be resected as they are at increased risk of bleeding, though bleeding has also been reported with smaller lesions [6,7]. The risk of malignant transformation to hepatocellular carcinoma is 5-10% [1,5].…”

Section: Discussionmentioning

confidence: 99%

Orthotopic Liver Transplantation for Hepatic Adenoma in a Patient with Portal Vein Agenesis

Sibulesky¹,

Taner²,

Willingham³

et al. 2009

TOTRANSJ

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Congenital portal vein agenesis, known as the Abernathy malformation, was first described in 1793. It is associated with focal nodular hyperplasia and adenomas due to abnormal hepatic regeneration secondary to abnormal or absent flow to the liver. We report a case of a 25-year-old Caucasian female with a complicated medical history including idiopathic membranoproliferative glomerulonephritis, hypertension, hyperlipidemia, Sweet's syndrome, acute febrile neutrophilic dermatosis, who incidentally was diagnosed with multiple liver nodules, the largest 14 cm in diameter, arising at the junction of the left and right hepatic lobes. She was also noted to have a congenital absence of the portal vein. There was no evidence of cirrhosis or portal hypertension. Liver function tests and -fetoprotein were within normal limits. A biopsy of the largest mass revealed hepatocellular adenoma. Because of the size, location, and multiplicity of the lesions, we elected to proceed with orthotopic liver transplantation. She subsequently underwent deceased donor liver transplantation using the piggyback technique. Despite dividing the portal vein shunt after completion of the caval anastomosis and minimizing the portal vein clamp time, her spleen spontaneously ruptured, for which splenectomy was performed. The patient did well postoperatively with good liver function.

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Management of hepatocellular adenoma: Solitary-uncomplicated, multiple and ruptured tumors

Cited by 40 publications

References 27 publications

Malignant Transformation of Liver Adenoma: An Analysis of the Literature

Malignant Transformation of Liver Adenoma: An Analysis of the Literature

Subtype Classification of Hepatocellular Adenoma

Orthotopic Liver Transplantation for Hepatic Adenoma in a Patient with Portal Vein Agenesis

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