ArticleEJNMMI research2026
Assessing vascular inflammation during continuous TSH suppression in differentiated thyroid cancer: a longitudinal [
Article in EJNMMI research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThyroid hormone imbalance has been linked to cardiovascular effects, including atrial fibrillation and cardiac hypertrophy. More recently, studies also suggest higher arterial inflammation during TSH-suppressive therapy. We therefore examined whether continuous TSH suppression is associated with longitudinal increases in arterial inflammation and progression of vascular calcification.
resultsWe retrospectively analyzed 51 patients with differentiated thyroid cancer who underwent two [18F]FDG PET/CT scans, both performed under continuous TSH suppression, after initial treatment with thyroidectomy and radioiodine ablation. The interval between scans was 4.6 ± 4.2 years. A region of interest (ROI) was placed in the carotid artery, aortic arch, ascending-, descending-, and abdominal aorta to extract standard uptake values (SUVs). Blood pool activity of the superior cava vein was used for target-to-background ratio (TBR). We found that FDG uptake (TBRmax) was higher on the follow-up PET/CT in the carotid arteries and aortic arch (mean TBRmax ± SD: 1.55 ± 0.28, 1.78 ± 0.31 vs. 1.39 ± 0.29, 1.65 ± 0.28, respectively; both p < 0.05). No significant differences were seen in the ascending-, descending-, or abdominal aorta, nor when all arterial segments were combined (all p > 0.05). No relevant correlation was observed between interscan interval and TBRmax. Additionally, calcified plaque (CP) scores were derived from the CT component for each arterial site. CP score was markedly higher at follow-up scan in all arteries and correlated moderately with the interscan interval (p < 0.05). A weak, non-significant inverse trend was found between FDG uptake and CP score (p = 0.09).
conclusionsContinuous TSH suppression was associated with modest increases in arterial FDG uptake at certain sites. The lack of a significant correlation between interscan interval and FDG uptake suggests non-linear remodeling rather than steadily increasing inflammation. These findings highlight the need for prospective studies and suggest that individualized TSH suppression strategies, along with cardiovascular risk assessment, may be warranted.
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