Focal nodular hyperplasia (FNH) is one of the benign tumors of the liver after hepatic hemangioma, accounting for 8% of primary tumors of the liver, with a prevalence of about 0.9% in the population. FNH is usually asymptomatic and has no malignant potential. It is believed that FNH is a proliferative response of the liver parenchyma to congenital arteriovenous malformations rather than a tumor in the true sense of the word. Some investigators have also suggested that the development of FNH may be related to estrogen. The vast majority of patients with FNH have no clinical symptoms, and less than 1/3 of patients have mild epigastric pain or abdominal masses, usually occurring incidentally during caesarean surgery or physical examination. Ultrasound, CT, MRI and angiography can help to characterize and localize the lesion, but they all have certain limitations, and their combined application can improve the diagnosis rate. Ultrasound: FNH usually appears as mild hypoechoic or isoechoic, rarely hyperechoic, often with lobulated contours and hypoechoic corona, while the internal echogenicity of the mass is evenly distributed and may be somewhat linearly enhanced with clear margins and no envelope, and the stellate scar is mildly hyperechoic. Color Doppler flow imaging (CDFI) shows a thick artery in the center of the lesion radiating in all directions, and high arterial flow velocity and low resistance are characteristic of FNH. 85% to 90% of FNH ultrasonography shows early enhancement in the arterial phase, radiating perfusion in the central artery of the lesion in all directions, and uniform hyper-echoic lesions in the late arterial phase. The late arterial lesion is uniformly hyperechoic, the portal phase and sinus phase are slightly hyperechoic or isoechoic, and the central scar is hypoechoic in both the arterial and portal phases. CT: hypo- or iso-dense occupancy on plain scan, and in 1/3 of patients, a hypo-dense stellate scar is seen in the center of the mass; 89% to 100% of lesions show rapid, significant, and uniform enhancement in the arterial phase after enhancement, and the central scar is hypo- or slightly hyperdense; most lesions in the delayed phase are iso-dense, and the central scar may be iso- or hyperdense. MRI: except for the scar, the signal is homogeneous, the signal is equal or slightly low in T1WI, and equal or slightly high in T2WI; there are two typical dynamic enhancement patterns after Gd-DTPA injection: (1) FNH without scar is significantly enhanced in the arterial phase, and mild to moderate enhancement or equal or slightly low signal in the portal and delayed phases; (2) FNH with scar is significantly enhanced in the arterial phase (no enhancement of the scar), and mild to moderate enhancement or equal or slightly low signal in the portal phase. Atypical images of FNH include multiple foci, pseudo-envelope, no scar, hemorrhage, and inhomogeneous enhancement. A central scar is seen in approximately 50% of patients with a low signal in the T1-weighted phase and high signal in the T2-weighted phase. Superparamagnetic material, the target cells are Kuffer cells and hepatocytes, respectively. These contrast agents can be used to confirm hepatocyte-derived lesions, when Kuffer cells within the FNH lesion take up the contrast agent to reduce the signal intensity in the T2-weighted phase. Angiography: FNH shows a multivessel mass exhibiting a central arterial blood supply and radiolucent perfusion to the periphery, with uniform staining in the hepatic parenchymal phase and a filling defect in the portal venous phase; the lesion does not invade the portal vein and there is no vascular leakage or arteriovenous fistula. Nuclear examination: 99mTc sulfur gel scintigraphy was used, and 50%-70% of FNH showed sulfur gel concentration, which can be distinguished from hepatocellular carcinoma and hepatic adenoma without Kuffer cells. Treatment It is a benign lesion without malignant tendency, and complications are rare. The following consensus has been formed for its management: observation and follow-up of FNH is safe, and surgery should be avoided once the diagnosis is clear; surgical resection should be performed only if the tumor growth or tissue diagnosis is unclear. Minimally invasive treatment methods including arterial embolization, radiofrequency ablation and high intensity focused ultrasound can be used for FNH with clear diagnosis and clinical symptoms. For a few cases with huge masses or multifocal FNH causing liver failure, liver transplantation can be considered. For FNH found incidentally during dissection, the decision to take surgery at the same time should be based on the size and location of the mass, the patient’s condition and the experience of the operator. In asymptomatic FNH, it is best to perform only a simple liver tissue biopsy. The risk of pregnancy and complications of FNH is inconclusive, and prophylactic resection is not necessary in women who wish to become pregnant.
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