This chapter is designed to serve as a guide to clinicians seeking to better understand the role of positron emission tomography (PET) in the management of proven thyroid malignancies as well as providing insights on the role of PET in detecting and characterizing primary thyroid disease processes, both malignant and nonmalignant.

The incidence of thyroid cancer ranges between 4 and 12 cases per 100,000 per year, but it is increasing (1,2). Radiation exposure is one of the risk factors for thyroid cancer. Many aspects in the management of this disease are debated. The use of PET adds an additional topic for debate, but its role in management is becoming increasingly well established. The differentiated cancers, papillary and follicular, constitute approximately 90% of thyroid cancers (3) (Figs. 8.8.1 and 8.8.2). Although differentiated thyroid cancers are highly treatable, they require vigilant follow-up. When indicated, initial therapy consists of a total thyroidectomy and radioiodine ablation therapy (4). Despite this, approximately 20% of patients develop recurrences, most within the first 10 years after diagnosis (1,5). After treatment, patients are monitored clinically, with iodine scans and with measurements of serum thyroglobulin. Serum levels of this protein should be undetectable with effective treatment. An increase in serum thyroglobulin over time is suspicious for recurrent or metastatic disease. In 10% to 15% of patients with an elevated thyroglobulin, a diagnostic iodine-131 (¹³¹I) whole-body scintigraphy (WBS) to localize disease is negative (6). Poorly differentiated or progressively dedifferentiated thyroid cancer cells often lose the ability to concentrate radioactive ¹³¹I. Furthermore, 50 % of these patients, when retreated empirically, will have uptake on posttreatment WBS scan (7), indicating the diagnostic scan was falsely negative. Although false-negative scans could probably be made less frequently by using a higher dose of radioiodine for the scans, this is probably not desirable as “stunning” of the gland could occur, potentially resulting in less-effective treatments. At the same time, these cells often exhibit increased metabolic activity, as evidenced by enhanced glucose uptake (8). The imaging of these poorly differentiated, noniodine-avid metastases and recurrences is problematic. Radioiodine imaging detects well-differentiated recurrences and metastases with a high specificity but only moderate sensitivity. A 2-fluorine-18-fluoro-2-deoxyglucose (¹⁸F-FDG) PET may improve on this sensitivity and has been proposed as a molecular imaging modality for these patients.

For many years, ¹³¹I, ¹²³I, and technetium-99m (^99mTc) pertechnetate have had major roles in evaluating thyroid diseases, both malignant and benign. In areas where ¹²³I costs are not prohibitively high, this tracer has assumed a major role in evaluating the thyroid. Although the positron emitter ¹²⁴I should be able to do most imaging currently done by other isotopes, and perhaps at a higher quality, it is not yet widely available. Further, the dosimetry of ¹²⁴I is somewhat problematic in that there is substantial radiation dose deposited by the positron annihilation events and the long, 4-plus-day half-life, coupled with the considerable fraction of decay events associated with gamma ray emissions, which are not imaginable with PET.

Thus, this chapter concentrates on the radiotracer most commonly used in PET thyroid cancer imaging, FDG. The [¹⁸F]-FDG PET has already been shown to effectively detect various types of cancer by virtue of their increased glucose metabolism (9).