Focal Nodular Hyperplasia (FNH) is a benign lesion of the liver, representing a localized overgrowth of normal liver tissue components rather than a true cancerous tumor. It is the second most common benign liver lesion after hemangioma. FNH is typically discovered incidentally during imaging performed for other reasons, as most individuals do not experience symptoms. The condition is most frequently observed in women between the ages of 20 and 50. FNH is not associated with liver disease or cirrhosis and carries virtually no risk of transforming into a malignant tumor.
Defining Focal Nodular Hyperplasia
FNH is characterized as a well-circumscribed mass composed of normal liver cells (hepatocytes), bile duct elements, and specialized liver macrophages (Kupffer cells). These components are present in the lesion but are arranged in an abnormal, nodular pattern, reflecting an increase in cell number in reaction to a stimulus.
The most distinctive anatomical feature of FNH is the central stellate scar, visible in most cases. This scar is a dense core of fibrous tissue from which thin septa radiate outwards, dividing the lesion into smaller nodules. The central scar typically contains malformed, thick-walled arteries and small bile ductules, but lacks the normal portal vein branches. This abnormal organization of vessels and cells distinguishes FNH from the surrounding healthy liver tissue.
FNH lesions are typically solitary, though approximately 20% of cases involve multiple lesions. Most lesions measure between four and eight centimeters in diameter. The presence of all normal liver cell types, including Kupffer cells, is a key feature used in imaging to help differentiate FNH from other masses.
Understanding the Cause and Formation
The formation of FNH is not fully understood, but the prevailing theory centers on a localized vascular anomaly. A pre-existing malformed artery within the liver causes an increase in localized blood flow. This abnormal arterial supply triggers a hyperplastic, regenerative response from the surrounding hepatocytes.
The central scar is thought to form as a reaction to this altered blood flow. The anomalous artery within the scar generates a spoke-wheel pattern of blood flow, which stimulates the growth of fibrous tissue and the proliferation of liver cells.
The role of hormones, particularly oral contraceptives, is debated, but they are not the primary cause of FNH. Hormones like estrogen may act as growth promoters, potentially leading to larger lesions in women who use them. However, FNH lesions occur in men and children, and they are not considered hormone-dependent tumors like some hepatic adenomas.
Diagnosis and Differentiation from Other Liver Masses
Magnetic Resonance Imaging (MRI) is considered the most sensitive and specific modality for confirming FNH, often achieving a specificity of up to 98%. MRI can clearly visualize the characteristic central scar, which appears bright on T2-weighted images and enhances with a contrast agent on delayed scans.
The use of contrast agents is essential, as FNH lesions display a distinct pattern of enhancement. During the arterial phase, the lesion shows intense, homogeneous enhancement due to its rich arterial supply, often described as a “lightbulb” sign. In the later phases, the lesion becomes isointense, meaning it blends in with the surrounding liver tissue.
Differentiation from other hypervascular liver masses, such as Hepatic Adenoma (HA) or Hepatocellular Carcinoma (HCC), is the main medical challenge. Unlike FNH, malignant lesions typically “wash out” the contrast agent in the delayed phases, appearing dark relative to the liver. Specialized contrast agents are taken up by the Kupffer cells in FNH, causing the lesion to appear bright in the delayed phase—a feature absent in most malignant tumors. A liver biopsy is only rarely needed when typical imaging features are absent or when there is persistent uncertainty about the diagnosis.
Management and Long-Term Outlook
Once a definitive diagnosis of FNH is established, the standard approach is conservative management, and no active treatment is typically required. Since FNH is a benign lesion, most individuals are asymptomatic.
Initial follow-up imaging may be performed at six to twelve months to confirm the lesion’s stability. If the lesion remains stable and the diagnosis is certain, further monitoring can often be discontinued. There is no need for lifestyle modification, such as discontinuing oral contraceptives or avoiding pregnancy.
Surgical removal is reserved for rare circumstances, primarily when the lesion is causing symptoms like abdominal pain or when its massive size (typically over 10 cm) poses a risk of compression on adjacent structures. Resection may also be considered if the diagnosis remains uncertain and cannot be definitively distinguished from a malignant tumor or an aggressive adenoma. The overall long-term prognosis for individuals with FNH is excellent.