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Table 1 Observations, mechanism, typical imaging features and prevalence of iso- or hyperintensity signal characteristics on hepatobiliary phase

From: Spectrum of liver lesions hyperintense on hepatobiliary phase: an approach by clinical setting

Observations Mechanisms Typical imaging features Prevalence of iso- or hyperintensity
Non-cirrhotic patients
Focal nodular hyperplasia Overexpression of OATP1B3; suggested also an increase in well-differentiated bile ducts Iso- or hyperintensity; hyperintense rim on HBP 97%
Hepatocellular adenomas Overexpression of OATP1B3 Iso- or hyperintensity 83%, 19%, 0% and 0% of β-catenin, inflammatory, HNF1α inactivated, and unclassified HCAs, respectively
Fat sparing in steatotic liver Preserved or even increased parenchymal function compared to the background steatotic liver Homogeneous iso- or hyperintensity Nearly always (no specific data available)
Primary or secondary vascular disorders
FNH-like nodule Equal or overexpression of OATP1B3 Iso- or hyperintensity; hyperintense rim on HBP 100%
Oncologic patients
FNH-like nodule Equal or overexpression of OATP1B3 Iso- or hyperintensity; hyperintense rim on HBP 100%
Metastases Retention in fibrotic stroma; aberrant expression of OATP1B3 Targetoid appearance No specific data available
Cholangiocarcinoma Retention in fibrotic stroma Targetoid enhancement 42–57%
Cirrhotic patients
Hepatocellular Carcinoma Overexpression of OATP1B3 Homogeneous hyperintensity, mosaic pattern, nodule-in-nodule appearance or peritumoral hyperintensity 8.8–14%
Regenerative or low-grade dysplastic nodules Overexpression of OATP1B3 Homogeneous iso- or hyperintensity No specific data available
Multiacinar regenerative nodules Overexpression of OATP1B3 Hyperintense rim on HBP No specific data available
Periportal hyperintensity Possible regenerative changes of periportal hepatocytes Bandlike hyperintense areas along the portal tracts 3%