Abstract

A 47-year-old man underwent a total thyroidectomy, central and right lateral neck dissection for a 5 cm right thyroid nodule in May 2002. Pathology revealed papillary thyroid carcinoma of the right nodule with vascular invasion and positive lymph nodes in the right central compartment (10/16 lymph nodes positive) and right lateral compartment (9/19 lymph nodes positive). In September 2002, he received radioactive iodine ablation with 146.7 mCI of I-131 after surgery with post-therapy I-131 scan showing thyroid bed uptake as well as uptake suspicious for residual lymph node metastases in the right lateral cervical lymph node region. On 6-month follow-up in July 2003, his stimulated thyrolobulin (Tg) levels were elevated at 251 ng/ml with negative Tg antibodies. A pretherapy scan did not show any uptake. He was subsequently treated 200 mCI of I-131 in August 2003 and post-therapy scan showed two foci of uptake in right lower neck consistent with residual lymph node metastases. Subsequent to this treatment, his stimulated Tg level was elevated to 4,734 ng/ml with negative Tg antibodies. Additional tests at this time including MRI neck, CT scan of head, neck, abdomen, and pelvis and FDG-PET showed FDG-positive lymph nodes in the right lateral neck and a 3 cm mass in the left thyroid bed. A bone scan done at this time was negative. He underwent a modified radical neck dissection in which 8 out of 21 lymph nodes were positive for papillary thyroid carcinoma. After surgical debulking, he was treated with 431.5 mCI of I-131 following a radioiodine dosimetry protocol. His post-therapy scan showed abnormal tracer uptake in left lateral neck region without anatomic correlate on cross-sectional imaging. He continued to have elevated Tg levels on thyroid hormone suppression with no obvious source on various imaging studies. In June 2007, PET-CT showed a new nasopharyngeal mass and a 3 mm right apex lung nodule. A stimulated Tg at this time was 661 ng/ml. He received radiation therapy (surgical debulking was not possible) to this nasopharyngeal mass without an improvement in Tg levels. His PET/CT in 2008 showed new sclerotic lesions in the right superior pubic ramus and body of the sternum. His Tg was 80 ng/ml on levothyroxine suppression, stimulated Tg was 1,138 ng/ml and a diagnostic I-131 scan was negative. He was followed conservatively for a few months at which time suppressed Tg levels continued to rise and his lung nodule grew to more than 1 cm in size. He was started on an experimental treatment protocol with sunitinib in May 2009. He completed 11 monthly cycles of sunitinib in June 2010 at which time his Tg had risen to 1,039 ng/ml and PET/CT showed stable pelvic and sternal lesions but a new occipital bone lesion and new bilateral subpleural lung metastases had developed. He was withdrawn from the sunitinib protocol for progressive disease and started on monthly zoledronic acid infusions for his bone metastases. The occipital bone lesion was surgically resected and treated with external beam radiotherapy. A repeat PET/CT in August 2011 showed an increase in size of his pelvic and sternal lytic lesions. He received radiotherapy to these lesions and enrolled in phase-2 study with lenvatinib. Zoledronic acid was discontinued and he began therapy with monthly subcutaneous denosumab for his bone metastases. His last imaging showed stable lung and bone disease.

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