Diffusely increased 18F-FDG thyroid radionuclide uptake is not always hyperthyroidism

Case description

A 25-year-old woman who was otherwise overtly healthy and asymptomatic without any history of medical illnesses or chronic medications had volunteered for a research study on brown fat. She underwent whole-body ¹⁸F-FDG PET/MR imaging according to a standard protocol. This unexpectedly revealed abnormally increased FDG uptake (SUVmax=6.84) over the anterior neck strangely reminiscent of typical radionuclide (^99m Tc or ¹³¹I) thyroid scans of hyperthyroidism (figure 1A,B). What is the diagnosis, and how would you confirm it?

Figure 1

¹⁸F-FDG-PET scans showing diffusely increased radionuclide uptake by the thyroid gland as shown in the coronal section (A) and the sagittal section (B).

Answer: A prescan screening thyroid function test revealed a serum-free thyroxine (FT4) of 10.0 pmol/L (RI: 8–20) and serum thyroid-stimulating hormone (TSH) of 4.28 mIU/L (RI: 0.45–4.50). An invaluable clue came from a thyroid function test performed 7 months earlier: FT4=13.2 pmol/L (RI: 8–20) and TSH=2.43 (RI: 0.45–4.50). This implied a progressive decline in FT4 associated with a reciprocal increase in TSH. Thyroid ultrasonography was done next, which revealed a general heterogeneous echotexture with parenchymal hypoechogenicity consistent with thyroiditis (figure 2). Corroborating the ultrasound scan, the nonenhanced T2-weighted MR images that were simultaneously acquired during the PET-MRI fusion scan revealed high and inhomogeneous signal intensities within the thyroid parenchyma suggestive of a diagnosis of Hashimoto thyroiditis (figure 3). Serum antithyroid peroxidase autoantibody exceeded 1000 IU/mL (normal <50 IU/mL), while serum antithyroglobulin autoantibody was 33.55 IU/mL (normal <4.1 IU/mL). Despite the relatively ‘normal’ thyroid function tests, the evidence was supportive of an actively evolving thyroid autoimmunity consistent with early Hashimoto’s thyroiditis. Short ACTH stimulation test excluded concomitant hypocortisolism, a crucial step to avoid precipitating addisonian crisis during L-thyroxine initiation in those with unsuspected adrenalitis from autoimmune polyglandular syndrome. She was prescribed L-thyroxine at 25 μg/day. The dose was doubled 2 years later, which optimised her energy level and body weight. At a 4-year follow-up visit, she remained euthyroid with serum FT4 of 12.5 pmol/L (RI: 8–16), FT3 of 4.7 pmol/L (RI: 3.5–6.0) and TSH of 1.54 mIU/L (RI: 0.45–4.50).

Figure 2

Thyroid ultrasound scan revealing a gland with heterogeneous echotexture with diffuse hypo-echogenicity in bilateral lobes consistent with thyroiditis.

Figure 3

MRI of thyroid of the same patient, showing non-enhanced T2-weighted coronal (A) and sagittal (B) images with inhomogeneous high signal intensities within the thyroid parenchyma supportive of Hashimoto thyroiditis.