focal nodular hyperplasia

FNH arises from a hyperplastic response of hepatocytes to a congenital arteriovenous malformation, leading to localized hyperperfusion and polyclonal hepatocyte proliferation (unlike hepatic adenoma, which is monoclonal and hormonally driven). Histologically, FNH shows nodules of normal-appearing hepatocytes surrounded by fibrous septa radiating from a central stellate scar containing a large feeding artery, bile ductular proliferation, and chronic inflammation. It is NOT associated with oral contraceptive use (unlike hepatic adenoma), though OCPs may cause it to enlarge slightly. Most cases are asymptomatic and discovered incidentally on imaging; rarely, patients present with vague right upper quadrant discomfort. On imaging, contrast-enhanced CT/MRI shows a hypervascular lesion with rapid arterial enhancement and a central scar that is hypodense on arterial phase but may show delayed enhancement (especially on MRI with hepatobiliary contrast agents like gadoxetate, since FNH contains functioning bile ducts and Kupffer cells, allowing uptake similar to normal liver parenchyma—a key distinguishing feature from adenoma and hepatocellular carcinoma, which lack Kupffer cells/bile ductules and do not take up hepatobiliary contrast in delayed phases). Diagnosis is typically made with imaging alone; biopsy is rarely needed. Management is conservative observation given the benign course, no malignant transformation risk, and low risk of rupture/hemorrhage (contrast with hepatic adenoma, which has higher rupture and malignant transformation risk, especially with large size or OCP use). Surgical resection is reserved for symptomatic lesions or diagnostic uncertainty.