Hepatic adenomas (HAs) are rare benign tumors of the liver and comprise 2% of all liver tumors with an annual incidence of 3-4/100,000 per year in Europe and North America. These tumors may be clinically silent or present with abdominal pain. Although rare, the most important complications associated with this tumor is haemorrhage and malignant transformation to hepatocellular carcinoma. The reported risk of malignant transformation is believed to be 4.2%. We present an extremely rare case report of a young woman on the oral contraceptive pill (OCP) with malignant transformation of a hepatic adenoma complicated additionally by tumor rupture and intraperitoneal bleed. This article therefore highlights the need to carefully evaluate any liver lesion in a young female on the OCP to be a possible adenoma and if confirmed to be so, to consider the potential risks associated with it as well as the need for follow-up imaging in order to avoid life threatening complications.

OBJECTIVE: Steatohepatitic hepatocellular carcinoma (SH-HCC) is a newly proposed concept, which shows histological features of steatohepatitis in HCC lesions, and it is strongly associated with metabolic syndrome (MS) and steatosis/steatohepatitis in non-cancerous lesions. Recently, a substantial number of HCC associated with MS were reported to have developed from pre-existing inflammatory hepatocellular adenoma (HCA). To elucidate the characteristic features of SH-HCC, we clinicopathologically investigated strictly diagnosed SH-HCC and non-SH-HCC (standard HCC).
METHODS: This was a retrospective multicenter study. A clinicopathological investigation was undertaken to compare 62 cases with SH-HCC features to 31 age- and sex-matched standard HCC cases, including an immunohistochemical study using markers for classification of HCA and diagnosis of HCC.
RESULTS: The characteristic features of SH-HCC compared with standard HCC include a higher rate of complications of MS, more frequent non-alcoholic fatty liver disease as an underlying liver disease, and HCC development in non-cirrhotic liver. The rate of solitary tumors showed no difference between the two groups, but the median diameter of the main tumor was greater in SH-HCCs (45 mm/20 mm, P = 0.01). The HCCs were mostly moderately differentiated, and the patterns were mainly trabecular in both groups. Positive findings for serum amyloid A and C-reactive proteins, classification markers of inflammatory HCA, were significantly higher in cancerous lesions of SH-HCC cases (50%/13%, P < 0.01 and 42%/16%, respectively; P = 0.01).
CONCLUSIONS: We confirmed that SH-HCC was strongly associated with MS and NAFLD, and found that classification markers of inflammatory HCA were significantly higher in SH-HCC. Further studies are needed to elucidate the relationship between SH-CCC and HCA for understanding the carcinogenic pathways in these diseases.

Rapid advances in molecular and anatomic pathology have greatly improved our understanding of hepatocellular adenomas. Principle among them is a clinically relevant, histology-based classification that identifies hepatic adenomas at greatest risk for malignant transformation. This new classification system has led to general consensus on the major subtypes of hepatic adenomas. However, controversy remains regarding how to incorporate less common types of hepatic adenomas into the classification system and how to incorporate adenoma subtyping into clinical care. This article provides an in-depth review of how adenomas are classified, with a focus on the current rationale, the consensus, and controversies.

UNASSIGNED: β-Catenin-activated hepatocellular adenomas have an elevated risk of harboring foci of hepatocellular carcinoma. Inflammatory adenomas also have an increased propensity for malignant transformation and are associated with a systemic inflammatory syndrome. Patients with these two adenoma subtypes benefit from excision. We assessed whether β-catenin-activated and inflammatory adenomas could be identified using a limited immunohistochemical panel.
UNASSIGNED: Forty-six adenomas were assessed by morphology and β-catenin, serum amyloid A, and glutamine synthetase immunostains.
UNASSIGNED: Morphologic examination produced a morphologic working diagnosis of inflammatory adenoma in 25 (54%) of 46 cases, β-catenin-activated adenoma in three (7%) of 46 cases, and 18 (39%) of 46 cases of other adenomas. After immunohistochemical staining, the morphologic diagnosis was confirmed in 15 (33%) of 46 and changed in 20 (43%) of 46, for a final distribution of 16 (35%) of 46 inflammatory adenomas, four (9%) of 46 β-catenin-activated adenomas, seven (15%) of 46 β-catenin-activated inflammatory adenomas, and 19 (41%) of 46 other adenomas.
UNASSIGNED: Inflammatory and β-catenin-activated adenomas were readily identified by immunostaining patterns. These findings reinforce the necessity of immunohistochemistry in classifying adenomas, as assessing morphology alone often provided inaccurate subclassification. β-Catenin-activated and inflammatory adenomas can be accurately diagnosed using only a limited panel of widely available immunostains.