A 39-year-old woman presented with a left neck swelling which underwent sonographic evaluation and fine needle aspiration. Cytology demonstrated medullary thyroid carcinoma with positive immunostaining for calcitonin and carcinoembryonic antigen in an adjacent lymph node confirming local spread. Baseline positron emission tomography/computed tomography (PET/CT) and magnetic resonance imaging (MRI) revealed innumerable metastases within both hepatic lobes (Fig. 1). Serum calcitonin was > 2000 pg/ml (normal range < 11.5 pg/ml). Following referral to cancer genetics, germline deoxyribose nucleic acid analysis yielded no mutation in the REarranged during Transfection (RET) proto-oncogene.
The patient was treated with vandetanib to downstage the tumour prior to resection. Vandetanib is an oral small-molecule tyrosine kinase inhibitor that targets vascular endothelial growth factor receptors 2 and 3, RET, and, at higher concentrations, epithelial growth factor receptor. It has been shown to improve progression-free survival and tumour response in patients with unresectable, locally advanced or metastatic disease [9]. Three months later, serum calcitonin nadired at 353 pg/ml. Restaging PET/CT and MRI confirmed some reduction in the volume of metastases but showed significant residual burden of hepatic disease.
Vandetanib was held in anticipation of surgical resection of the primary tumour and within four weeks the serum calcitonin had risen to to 663 pg/ml. Six weeks following Vandetanib cessation, the patient underwent total thyroidectomy and bilateral central neck dissection with a left modified radical neck dissection. The resection specimen revealed a 3-cm tumour with extra thyroidal extension and lymphovascular invasion, with a total 14 out of 43 nodes positive for tumour involvement (American Joint Committee on Cancer staging pT3 pNb1).
On serial monitoring after thyroidectomy, calcitonin steadily increased from 3,131 pg/ml on the fifth postoperative day to 17,764 pg/ml 100 days later, a doubling time of six weeks.
The patient remained asymptomatic and was reticent to restart systemic therapy in consideration of its associated toxicities. However, given the significant rise in tumour markers, a decision was taken to perform embolisation of the hepatic metastases.
TAE was performed in two stages: first the right hepatic lobe followed by the left hepatic lobe eight days later. Both procedures were carried out through 5Fr right femoral access. Using a Mikaelsson catheter, selective catheterisation was performed of the coeliac and superior mesenteric arteries and arteriography performed. The proper hepatic artery was selectively catheterised using a microcatheter and selective arteriography was performed.
During the first procedure, selective right hepatic arteriography revealed a significant disease burden within the right lobe of the liver. The right hepatic artery was embolised with 100-μm microspheres (Embosphere, Merit Medical, Utah, USA). During the second procedure, repeat right hepatic arteriography revealed a small volume of residual disease; therefore, further subselective right hepatic artery embolisation using 100-μm microspheres was performed. This was followed by selective embolisation of the left hepatic artery and of a large accessory left hepatic artery arising from the left gastric artery (Fig. 2). The patient developed mild post-embolisation cholecystitis after the second procedure, settled with conservative methods. She was discharged home well six days later.
While the pre-treatment metastases were relatively occult on CT, a CT one day following the second embolisation procedure showed multiple hypoenhancing foci throughout both hepatic lobes consistent with devascularised metastases (Fig. 3). A follow-up liver MRI four weeks later showed significantly reduced enhancement in the multiple hepatic metastases consistent with radiological treatment response (Fig. 4). The serum calcitonin measured four weeks post procedure was 6,065 pg/mL.