In Europe and North America, hepatocellular adenomas (HCA) occur, classically, in middle-aged woman taking oral contraceptives. Twenty percent of women, however, are not exposed to oral contraceptives; HCA can more rarely occur in men, children, and women over 65 years. HCA have been observed in many pathological conditions such as glycogenosis, familial adenomatous polyposis, MODY3, after male hormone administration, and in vascular diseases. Obesity is frequent particularly in inflammatory HCA. The background liver is often normal, but steatosis is a frequent finding particularly in inflammatory HCA. The diagnosis of HCA is more difficult when the background liver is fibrotic, notably in vascular diseases. HCA can be solitary, or multiple or in great number (adenomatosis). When nodules are multiple, they are usually of the same subtype. HNF1α-inactivated HCA occur almost exclusively in woman. The most important point of the classification is the identification of β-catenin mutated HCA, a strong argument to identify patients at risk of malignant transformation. Some HCA already present criteria indicating malignant transformation. When the whole nodule is a hepatocellular carcinoma, it is extremely difficult to prove that it is the consequence of a former HCA. It is occasionally difficult to identify HCA remodeled by necrosis or hemorrhage. 1. Introduction The diagnosis of hepatocellular adenomas (HCA) may occasionally be difficult for the following reasons.(i)The nodule is discovered in a context different to what we are used to see, such as in men, in women not exposed to oral contraceptives (OC), in older persons, or in children.(ii)The tumor per se may be difficult to identify due to the partial necrosis or to the major remodeling of the tumor leading to the presence of criteria seen mostly in focal nodular hyperplasia (FNH) and/or to difficulties in differentiation from hepatocellular carcinoma (HCC). (iii)The presence of an underlying liver disease such as nonalcoholic steatohepatitis (NASH), vascular disorder, and fibrosis.(iv)HCA, HCC, and FNH or different HCA subtypes can be present in the same patient, some more prone to HCC transformation, with the difficult task, in some cases, to differentiate HCA from HCC.(v)Finally, HCA can be discovered unexpectedly in patients treated for other liver tumors or developed in the context of diseases affecting the liver or other organs. In this paper, we review the clinical/epidemiological context of HCA, based on our experience (personal cases and consult cases); all these cases being classified according
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