Gadoxetic acid, a hepatobiliary-specific contrast medium used for MRI, is becoming increasingly important in the detection and characterization of hepatic mass lesions. This medium is taken up by functioning hepatocytes, and the liver parenchyma is strongly enhanced in the hepatobiliary phase (HBP), during which hepatic mass lesions without functioning hepatocytes commonly show hypointensity. However, some hepatic mass lesions show hyperintensity in the HBP. Focal nodular hyperplasia (FNH) and FNH-like lesions show hyperintensity in the HBP owing to the uptake of gadoxetic acid by hyperplastic normal hepatocytes. The tumor cells of some types of hepatocellular adenoma (eg, β-catenin–acti-vated type, inflammatory type) and hepatocellular carcinoma (eg, green hepatoma) can show uptake of gadoxetic acid. Retention of gadoxetic acid in the extracellular space can cause hyperintensity of fibrotic tumors or hemangiomas during the HBP owing to the extracellular contrast agent characteristics of gadoxetic acid. During the HBP, peritumoral retention is observed in some tumors, such as hepatocellular carcinomas, gastrointestinal stromal tumors, and neuroendocrine tumors. Gadoxetic acid is excreted into the bile; therefore, biliary tract enhancement can be observed in the cystic components of intraductal papillary neoplasms of the bile duct. Intratumoral bile ducts can be observed in malignant lymphomas. Knowledge of these specific mechanisms, which can cause hyperintensity during the HBP depending on the pathologic or molecular background, is important not only for precise imaging-based diagnoses but also for understanding the pathogenesis of hepatic mass lesions.
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