Abstract
The optimal treatment for medullary thyroid cancer is total thyroidectomy and central nodal lymphadenectomy at presentation when the primary cancer is small and has not metastasized significantly (1). In the three phenotypes of familial medullary cancer, i.e., familial medullary cancer, multiple endocrine neoplasia (MEN) IIA, and MENIIB, screening of families for patients with a mutation in the RET proto-oncogene and a genetic predisposition for the diseases allows surgery at an even earlier stage (2–4). Unfortunately, not all patients are treated at the optimal time. Some patients with sporadic medullary cancer have extensive local and distant metastases at the time of diagnosis. It is important to define the extent of disease when planning treatment. Other patients who have undergone appropriate surgery are found to have a measurable calcitonin level after the operation. This implies there is residual disease in the thyroid bed or lymph nodes or distant sites. It is helpful if the site or sites of calcitonin production can be identified when they are small and amenable to removal at a reoperation.
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References
Kebebew E, Ituarte PHG, Siperstein AE, et al. Medullary thyroid carcinoma. Clinical characteristics, treatment, prognostic factors, and a comparison of staging systems. Cancer 2000; 88:1139–1148.
Machens A, Niccoli-Sire P, Hoegel J, et al. Early malignant progression of hereditary medullary thyroid cancer. N Engl J Med 2003; 349:1517–1525.
Eng C, Clayton D, Schuffenecker I, et al. The relationship between specific RET proto-oncogene mutations and disease phenotype in multiple endocrine neoplasia type 2. International RET mutation consortium analysis. JAMA 1996; 276:1575–1579.
Cote GJ, Gagel RF. Lessons learned from the management of a rare genetic cancer. N Engl J Med 2003; 349:1566–1568.
Forssell-Aronsson EB, Nilsson O, Bejegard SA, et al. 111In-DTPA-DPhe1-octreotide binding and somatostatin receptor subtypes in thyroid tumors. J Nucl Med 2000; 41:636–642.
Adalet I, Demirkale P, Unal S, et al. Disappointing results with Tc-99m tetrofosmin for detecting medullary thyroid carcinoma metastases comparison with Tc-99m VDMSA and TI-201. Clin Nucl Med 1999; 24:678–683.
Adams BK, Fataar A, Byrne MJ, et al. Pentavalent technetium-99m (V)-DMSA uptake in a pheochromocytoma in a patient with Sipple’s syndrome. J Nucl Med 1990; 31:106–108.
Baulieu JL, Guilloteau D, Delisle MJ, et al. Radioiodinated metaiodobenzylguanidine uptake in medullary thyroid cancer. A French cooperative study. Cancer 1987; 60:2189–2194.
Bockisch A, Brandt-Mainz K, Gorges R, et al. Diagnosis in medullary thyroid cancer with [18F]FDG-PET and improvement using a combined PET/CT scanner. Acta Med Austriaca 2003; 30:22–25.
Adams S, Baum R, Rink T, et al. Limited value of fluorine-18 fluorodeoxyglucose positron emission tomography for the imaging of neuroendocrine tumours. Eur J Nucl Med 1998; 25:79–83.
Brandt-Mainz K, Muller SP, Gorges R, et al. The value of fluorine-18 fluorodeoxyglucose PET in patients with medullary thyroid cancer. Eur J Nucl Med 2000; 27:490–496.
Diehl M, Risse JH, Brandt-Mainz K, et al. Fluorine-18 fluorodeoxyglucose positron emission tomography in medullary thyroid cancer: results of a multicentre study. Eur J Nucl Med 2001; 28:1671–1676.
Szakall S, Jr, Esik O, Bajzik G, et al. 18F-FDG PET detection of lymph node metastases in medullary thyroid carcinoma. J Nucl Med 2002; 43:66–71.
Barrington S, Maisey MN. Skeletal muscle uptake of fluorine-18 FDG: effect of oral diazepam. J Nucl Med 1996; 37:1127–1129.
Cohade C, Mourtzikos KA, Wahl RL. “USA-Fat”: prevalence is related to ambient outdoor temperature-evaluation with 18F-FDG PET/CT. J Nucl Med 2003; 44:1267–1270.
Cook G, Maisey MN, Fogelman I. Normal variants, artefacts and interpretative pitfalls in PET with 18-fluoro-2-deoxyglucose and carbon-11 methionine. Normal variants, artefacts and interpretative pitfalls in PET with 18-fluoro-2-deoxyglucose and carbon-11 methionine. Eur J Nucl Med 1999; 26:1363–1378.
Cook G, Wegner EA, Fogelman I. Pitfalls and artifacts in 18FDG PET and PET/CT oncologic imaging. Semin Nucl Med 2004; 34:122–133.
Gourgiotis L, Sarlis NJ, Reynolds JC, et al. Localization of medullary thyroid carcinoma metastasis in a multiple endocrine neoplasia type 2A patient by 6-[18F]-fluorodopamine positron emission tomography. J Clin Endocrinol Metab 2003; 88:637–641.
Hoegerle S, Altehoefer C, Ghanem N, et al. 18F-DOPA positron emission tomography for tumour detection in patients with medullary thyroid carcinoma and elevated calcitonin levels. Eur J Nucl Med 2001; 28:64–71.
Hoegerle S, Nitzsche E, Altehoefer C, et al. Pheochromocytomas: detection with 18F DOPA whole body PET-initial results. Radiology 2002; 222:507–512.
Ilias I, Yu J, Carrasquillo JA, et al. Superiority of 6-[18F]-fluorodopamine positron emission tomography versus [131I]-metaiodobenzylguanidine scintigraphy in the localization of metastatic pheochromocytoma. J Clin Endocrinol Metab 2003; 88:4083–4087.
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© 2006 Humana Press Inc., Totowa, NJ
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McDougall, I.R. (2006). PET in Medullary Thyroid Cancer. In: Wartofsky, L., Van Nostrand, D. (eds) Thyroid Cancer. Humana Press. https://doi.org/10.1007/978-1-59259-995-0_74
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DOI: https://doi.org/10.1007/978-1-59259-995-0_74
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