Hepatocellular adenoma management and phenotypic classification: the Bordeaux experience.
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 >or=5 in 78, 38, and 12 cases, respectively. The resection was complete in 95 cases. We identified 46 HNF1alpha-inactivated HCAs (44 women), 63 inflammatory HCAs (IHCA, 53 women) of which nine were also beta-catenin-activated, and seven beta-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 HNF1alpha-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 HNF1alpha-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 beta-catenin-activated, whether inflammatory or not).


CONCLUSIONS
There were noticeable clinical differences between HNF1alpha-inactivated HCA and IHCA; there was no increased risk of bleeding or HCC related to the number of HCAs; beta-catenin-activated 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.
Bioulac-Sage
Paulette
P
Service d'Anatomie Pathologique, Hôpital Pellegrin, Centre Hospitalier Universitaire Bordeaux, Bordeaux, France. Paulette.bioulac-sage@chu-bordeaux.fr
Laumonier
Hervé
H
Couchy
Gabrielle
G
Le Bail
Brigitte
B
Sa Cunha
Antonio
A
Rullier
Anne
A
Laurent
Christophe
C
Blanc
Jean-Frédéric
JF
Cubel
Gaelle
G
Trillaud
Hervé
H
Zucman-Rossi
Jessica
J
Balabaud
Charles
C
Saric
Jean
J
D018248:Adenoma, Liver Cell / Q000145:classification* / Q000209:etiology / Q000378:metabolism / Q000601:surgery; D000328:Adult; D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D050556:Fatty Acid-Binding Proteins / Q000378:metabolism; D005260:Female; D051538:Hepatocyte Nuclear Factor 1-alpha / Q000378:metabolism; D006801:Humans; D008113:Liver Neoplasms / Q000145:classification* / Q000209:etiology / Q000378:metabolism / Q000601:surgery; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D000685:Serum Amyloid A Protein / Q000378:metabolism; D055815:Young Adult; D051176:beta Catenin / Q000378:metabolism
D050556:Fatty Acid-Binding Proteins; D051538:Hepatocyte Nuclear Factor 1-alpha; D000685:Serum Amyloid A Protein; D051176:beta Catenin; D002097:C-Reactive Protein