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Focal nodular hyperplasia (FNH) is a benign hepatic lesion classified as a non-neoplastic hamartomatous hyperplasia of hepatocytes, bile ductules, and vascular structures. It is characterized by disorganized liver tissue, typically with no risk of malignant transformation.

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https://www.youtube.com/watch?v=fN3Yflcxl0Q

Etiopathogenesis

• Believed to result from localized vascular anomalies, particularly anomalous arteries that induce hyperplastic changes in the surrounding liver parenchyma.
• Not associated with oral contraceptive use, unlike hepatic adenoma.

Epidemiology

• Most commonly affects women aged 20–50 years.
• Often asymptomatic, though some patients may present with right upper quadrant discomfort or hepatomegaly.
• Found incidentally during imaging for unrelated indications.
• Multiple lesions are present in ~20% of cases.

Pathology

• Composed of normal hepatocytes, bile ductules, Kupffer cells, and fibrous stroma.
• A central stellate scar with radiating fibrous septa is seen in ~50% of cases.
• No true capsule, calcification, hemorrhage, or necrosis (unlike hepatic adenomas).

![Hepatic haemangioma and focal nodular hyperplasia: a | Liver ultrasonography of hepatic haemangioma (HH) showed a homogeneous hyperechogenic nodule (arrow). b | MRI with the injection of gadolinium chelate of HH with hyperintensity on T2-weighted imaging and peripheral discontinuous and progressive centripetal enhancement from arterial to portal venous phases.  c | The main histological features (in red) and pathophysiological mechanisms (in blue) of focal nodular hyperplasia (FNH) are represented. d | Histology of FNH with a central fibrous scar, a central dystrophic artery and regenerative hepatocellular nodules. e | Map-like pattern of glutamine synthetase, a target gene of the Wnt–β-catenin pathway, at immunohistochemistry in a FNH sample. f | MRI with the injection of gadolinium chelate of an FNH showing a homogeneous nodule without capsule and arterial phase hyperenhancement except for the central scar that harbours a progressive enhancement on portal venous and late phases.

Nault, JC., Paradis, V., Ronot, M. et al. Benign liver tumours: understanding molecular physiology to adapt clinical management. Nat Rev Gastroenterol Hepatol 19, 703–716 (2022). https://doi.org/10.1038/s41575-022-00643-5](attachment:15896692-0e72-4f1d-bc2d-c2b9e299c453:41575_2022_643_Fig1_HTML.webp)

Hepatic haemangioma and focal nodular hyperplasia: a | Liver ultrasonography of hepatic haemangioma (HH) showed a homogeneous hyperechogenic nodule (arrow). b | MRI with the injection of gadolinium chelate of HH with hyperintensity on T2-weighted imaging and peripheral discontinuous and progressive centripetal enhancement from arterial to portal venous phases.  c | The main histological features (in red) and pathophysiological mechanisms (in blue) of focal nodular hyperplasia (FNH) are represented. d | Histology of FNH with a central fibrous scar, a central dystrophic artery and regenerative hepatocellular nodules. e | Map-like pattern of glutamine synthetase, a target gene of the Wnt–β-catenin pathway, at immunohistochemistry in a FNH sample. f | MRI with the injection of gadolinium chelate of an FNH showing a homogeneous nodule without capsule and arterial phase hyperenhancement except for the central scar that harbours a progressive enhancement on portal venous and late phases.

Nault, JC., Paradis, V., Ronot, M. et al. Benign liver tumours: understanding molecular physiology to adapt clinical management. Nat Rev Gastroenterol Hepatol 19, 703–716 (2022). https://doi.org/10.1038/s41575-022-00643-5

Radiology