Fact-sheet: Focal nodular hyperplasia


Updated on 10/26/2022 at 4:11 PM

Note : 0/10

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Definition

Nodular proliferation of normal hepatocytes
Around a central scar
Containing a feeding artery from which spoke-wheel vessels arise
Benign and Common: Prevalence 0.9%
Association with hemangiomas in 20% of cases
Macroscopically:

  • Well-defined nodule
  • Similar to the adjacent parenchyma
  • Central fibrous scar
  • Fibrous septa radiating from the scar, dividing the lesion into nodules
  • The margins of FNH are well-defined, often lobulated, and one of the characteristic features is the absence of a capsule
  • Hemorrhage or necrosis is exceptional

Microscopically:

  • Well-defined hepatocellular nodules centered on a central scar
  • Normal hepatocytes that may be focally atrophic or, more rarely, hypertrophic
  • The central scar consists of connective tissue with a few foci of myxoid deposits
  • It always contains abnormal vessels of variable caliber
  • Rarely, fatty infiltration is present

Clinical features

Female >>> Male (8/1).
20-50 years.
Usually an incidental finding.
Otherwise, pain or abdominal mass.

Laboratory findings

Possible elevation of GGT (20%)

Ultrasound

Lesion usually homogeneous, hypoechoic or isoechoic

Central scar: thin hyperechoic band

Central vascularity (RI < hepatic artery RI), with peripheral vessels

Contrast-enhanced ultrasound:

  • Rapid centrifugal filling
  • Complete homogeneous enhancement during the portal and late phases, except for the central stellate area.

CT

  • Before injection: isodense or slightly hypodense lesion
  • Hypervascularity during the arterial phase, then isodense on the delayed phase
  • Homogeneity
  • Rounded or often lobulated contour
  • Central component: hypodense stellate image enhancing on the delayed phase. Central arteries during the arterial phase.
  • No capsule

MRI

Reference examination

5 diagnostic criteria (Se=80%, Sp>98%):

  • Isosignal or slight T1 hyposignal with isosignal or slight T2 hypersignal
  • Central stellate area with T2 hypersignal
  • Homogeneous lesion apart from the central area
  • Intense, homogeneous, transient arterial enhancement followed by isosignal during the portal and delayed phases
  • Absence of capsule

After administration of a hepatobiliary contrast agent, during the hepatobiliary phase (Gd-BOPTA 1h30, Gd-EOB-DTPA 20 min): delayed enhancement (96% accuracy).

Vascular intervention

Angiography, now obsolete: central arterial supply continuing into peripheral branches in a spoke-wheel pattern

Differential diagnosis

Fibrolamellar carcinoma:

  • young patients (10 to 40 years, mean: 23 years)
  • no sex predilection
  • occurs in a healthy liver in 95% of cases
  • no identified risk factor
  • AFP usually normal or near-normal
  • better prognosis than HCC
  • single, large lesion (5 to 20 cm), well-defined but not encapsulated (≠ HCC)
  • neoplastic eosinophilic cells arranged in trabeculae separated by collagenous fibrous tissue, forming a nodule with a central fibrous core
  • more rarely: satellite "daughter" nodular lesions or multiple disseminated nodular lesions
  • punctate calcifications present near the central scar
  • capsular retraction
  • rare vascular invasion
  • slow growth