[Morphomolecular subtyping of hepatocellular adenoma].

Abstract

Hepatocellular adenomas (HCAs) are rare benign hepatocellular neoplasia that typically occur in a non-cirrhotic liver in young women on contraceptive therapy or in metabolic liver disease. HCAs may be subtyped radiologically and histologically, controlled under discontinuation of contraceptives, and resected in the case of malignant transformation potential or an HCA size of more than 5 cm.Histologically, HCAs present as well-differentiated hepatocellular neoplasms, which in contrast to focal nodular hyperplasia (FNH) lack portal tract-like structures. Prognostically relevant morphomolecular HCA subtypes have been described. HNF1A-inactivated HCAs often show a prominent steatosis and loss of L‑FABP. Inflammatory HCAs (IHCAs) are characterized morphologically by a prominent inflammatory infiltrate and ectatic sinusoids and show a positive immune reaction with antibodies against serum amyloid A and CRP. In contrast to other HCAs, β‑catenin-activated HCAs due to CTNNB1 mutation in exon 3 occur relatively more frequently in men (for example after intake of anabolic steroids) and have a significantly increased risk of transformation in a hepatocellular carcinoma (HCC) in comparison to CTNNB1 mutations in exons 7 and 8. CTNNB1 mutations may also occur in IHCAs (b-IHCA). Sonic hedgehog-activated HCAs show increased ASS1 expression and have a high risk of rupture and bleeding.Concerning differential diagnosis, it is important to distinguish HCAs from FNH, which cover a clinically similar patient group, and from highly differentiated HCC, which occur more frequently in men at an increased patient age and in chronic liver disease.