Hao Li1,2, Nir Livneh1,3, Snjezana Dogan4, Ashok R Shaha1. 1. Head and Neck Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, USA. 2. Otorhinolaryngology, Tan Tock Seng Hospital, Singapore, Singapore. 3. Otolaryngology, Head and Neck Surgery, Sheba Medical Center, Ramat Gan, Israel. 4. Pathology, Memorial Sloan Kettering Cancer Center, New York, New York, USA.
Abstract
INTRODUCTION: The collision of medullary (MTC) and papillary thyroid carcinoma (PTC) in the same cervical lymph node can occur, but its growth kinetics has not been reported. CASE PRESENTATION: We report a 27-year-old male patient who had collision nodal metastases from PTC and sporadic MTC in the central compartment. This was treated with total thyroidectomy and central neck dissection. The collision nodal metastasis persisted and presented with a single sonographically enlarging central compartmental lymph node postoperatively. The volume of the collision nodal metastasis increased from 226 to 507 mm3 over the first 8 months, from 507 to 572 mm3 over the next 6 months, and from 572 to 762 mm3 over the next 31 months. The calcitonin and carcinoembryonic antigen (CEA) fluctuated in the first 19 months followed by a steady increase at a doubling time of 1.97 and 8.42 years, respectively. Unstimulated thyroglobulin remained at 0.2 ng/mL or lower during the same period while thyrotropin (TSH) was not suppressed. Revision central neck dissection performed 4.5 years later resulted in undetectable serum calcitonin, CEA of 2 ng/mL, and thyroglobulin of 0.1 ng/mL from a preoperative calcitonin of 212 ng/L, CEA of 10 ng/mL, and thyroglobulin of 0.2 ng/mL. Further structural imaging 13.5 months later revealed no evidence of disease. DISCUSSION: The growth kinetics of collision nodal metastasis from PTC and MTC can be similar to conventional PTC and MTC. Furthermore, the growth rate of such collision nodal metastases can be slow. Guided by tumor marker doubling time and regular structural imaging, surgical salvage performed after a period of active surveillance may still result in biochemical and structural remission.
INTRODUCTION: The collision of medullary (MTC) and papillary thyroid carcinoma (PTC) in the same cervical lymph node can occur, but its growth kinetics has not been reported. CASE PRESENTATION: We report a 27-year-old male patient who had collision nodal metastases from PTC and sporadic MTC in the central compartment. This was treated with total thyroidectomy and central neck dissection. The collision nodal metastasis persisted and presented with a single sonographically enlarging central compartmental lymph node postoperatively. The volume of the collision nodal metastasis increased from 226 to 507 mm3 over the first 8 months, from 507 to 572 mm3 over the next 6 months, and from 572 to 762 mm3 over the next 31 months. The calcitonin and carcinoembryonic antigen (CEA) fluctuated in the first 19 months followed by a steady increase at a doubling time of 1.97 and 8.42 years, respectively. Unstimulated thyroglobulin remained at 0.2 ng/mL or lower during the same period while thyrotropin (TSH) was not suppressed. Revision central neck dissection performed 4.5 years later resulted in undetectable serum calcitonin, CEA of 2 ng/mL, and thyroglobulin of 0.1 ng/mL from a preoperative calcitonin of 212 ng/L, CEA of 10 ng/mL, and thyroglobulin of 0.2 ng/mL. Further structural imaging 13.5 months later revealed no evidence of disease. DISCUSSION: The growth kinetics of collision nodal metastasis from PTC and MTC can be similar to conventional PTC and MTC. Furthermore, the growth rate of such collision nodal metastases can be slow. Guided by tumor marker doubling time and regular structural imaging, surgical salvage performed after a period of active surveillance may still result in biochemical and structural remission.
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