P3.S379: Focal Nodular Hyperplasia Mimicking Relapse in Wilms Survivor

Introduction: The liver is a common site for the development of benign and malignant masses, both primary and metastatic. Focal Nodular Hyperplasia (FNH) is the one of the most common benign liver lesions, second only to hepatic hemangiomas. Reports have identified an increased incidence of benign liver lesions, FNH in particular, in cancer survivors who underwent chemotherapy or radiation therapy. FNH is seen in only 0.02% of the general pediatric population, but its frequency increases to 0.45% in patients with a history of treatment for malignancy. The challenge upon identifying liver lesions in patients with a prior history of malignancy, is how to differentiate oncologic recurrence from benign lesions in a way that minimizes unnecessary treatment and potential related morbidity. We present a patient with a history of Wilms Tumor who was found on routine surveillance to have multifocal liver masses that we hope can provide insight into the evaluation of liver masses in patients with a history of malignancy.

Case Description: The patient was diagnosed with Stage III Diffuse Anaplastic Wilms Tumor of the left kidney at age 3. She was treated with nephrectomy, total abdomen radiation and chemotherapy via revised regimen UH-1, with no major complications. 3-year surveillance abdominal ultrasound identified a liver lesion. Follow up MRI revealed 5 hepatic masses with arterial hyperenhancement fading to background during portal and delayed phases. CT showed the lesions to homogenously hyperenhance relative to the liver on late arterial phase and did not reveal extrahepatic lesions. Liver biopsy was negative for recurrent Wilms Tumor. This combination of radiologic and pathologic findings suggested that the lesions were FNH-like in etiology. On serial imaging, the hepatic lesions persisted with mild interval enlargement on CT; consistent with FNH, and the patient maintains oncologic remission.

Discussion: The pathophysiology of FNH is not well understood, but some suggest that circulatory disturbances caused by chemotherapy may cause this hepatic hyperplasia. In our patient with history of aggressive Stage III Wilms Tumor, multifocal liver lesions like these prompted significant family stress and interventional radiology biopsy of the lesions. Uncommon imaging features of FNH, including multiplicity as in our patient, are more common in patients with previous malignancy. Early hyperenhancement fading to background can serve as a favorable indicator on imaging of these lesions. Invasive biopsies may be unnecessary in cases such as ours if imaging is consistent with FNH.

Conclusion: Imaging surveillance is a critical component of cancer survivorship and identification of relapse is the first priority. An index of suspicion for mimickers of relapse with the correct findings and clinical picture can minimize the need for more invasive diagnostics. With the right imaging findings, close interval imaging may be a viable alternative to invasive biopsy.