Hepatic adenomatosis occurs predominantly in women during the 4 th and 5 th decades of life (1). Hepatic adenomatosis is rare, although its real frequency could be underestimated because many patients are asymptomatic. Hepatic adenomatosis is defined as the presence of multiple adenomas (arbitrarily > 10) involving both lobes of the liver. Patients with glycogen storage disease or with a history of steroid intake are not considered to have liver adenomatosis (1, 2).Although the exact aetiology of hepatic adenomatosis is still unclear, congenital or acquired hepatic vascular abnormalities, mutations of the hepatocyte nuclear factor 1alpha (HNF1A) gene, and non-alcoholic fatty liver disease have been proposed as potential causes for the development of hepatic adenomatosis (1, 2). Hepatocellular adenomas in patients with hepatic adenomatosis may be of the inflammatory, HNF-1alpha-mutated, or beta-catenin-mutated subtypes, and as a consequence may show variable imaging findings.We describe the magnetic resonance imaging (MRI) findings in a 39-year-old woman presenting with non-alcoholic fatty liver disease and hepatic adenomatosis characterized by the inflammatory subtype of hepatic adenomas. minimal or no signal drop-off on chemical shift sequences. On T1-weighted in-phase images, lesions were isointense or mildly hyperintense compared to liver parenchyma (Fig. 1). On fat suppressed T1-weighed images, due to liver steatosis, lesions were markedly hyperintense (Fig. 2). One lesion measuring 8 cm demonstrated an irregular central T1-and T2-weighted hypointense area. Case reportA 39-year-old female with unremarkable previous medical history was referred for MRI after detecting a large liver mass during routine ultrasound examination. Patient had taken oral contraceptives for 12 years. Physical examination showed slight overweight (body mass index 29). The laboratory evaluations and blood biochemistry profile showed elevated C-reactive protein (11,4 mg/dl; normal value < 0,5), alkaline phosphatase (417 U/L, normal values 27-126) and γ-glutamyltransferase (101 U/L, normal values 5-43) levels. Hepatitis B surface antigen, anti-hepatitis B surface antibody and anti-hepatitis C antibody were negative.Serum alpha-fetoprotein (AFP), carcinoembryonic antigen (CEA) and carbohydrate antigenic determinant (CA) 19-9 were normal. On MRI, liver parenchyma showed marked signal drop-off on T1-weighted out-ofphase images and corresponded to steatosis of the liver parenchyma. Multiple, approximately 14, well-delineated focal liver lesions with variable size (1-10 cm diameter) involving both liver lobes were noted. Lesions were diffusely hyperintense on T2-weighted images, with higher signal intensity in the periphery of the lesion (Fig. 1) We report a case with the inflammatory subtype of hepatic adenomatosis in a 39-year-old woman with liver steatosis. the magnetic resonance imaging features using extracellular gadolinium chelates and hepatocytetargeted contrast agents are described.

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