Abstract

PurposeWe aimed to investigate the influence of both hypothyroidism and thyroid-stimulating hormone (TSH) suppression on vascular inflammation, as assessed with F-18-fluorodeoxyglucose (F-18-FDG) positron emission tomography (PET)/computed tomography (CT).MethodsTen thyroid carcinoma patients underwent an F-18-FDG PET/CT during post-thyroidectomy hypothyroidism and during thyrotropin (TSH) suppression after I-131 (radioiodine) ablation therapy. We analysed the F-18-FDG uptake in the carotids, aortic arch, ascending, descending, and abdominal aorta to investigate the effects of thyroid hormone status on arterial inflammation. Target-to-background ratios (TBRs) corrected for blood pool activity were established for all arterial territories. Results were further compared to euthyroid historic control subjects.ResultsIn general, there was a trend towards higher vascular TBRs during TSH suppression than during hypothyroidism (TBRmax all vessels=1.6 and 1.8, respectively, p=0.058), suggesting a higher degree of arterial inflammation. In concurrence with this, we found increased C-reactive protein (CRP) levels after levothyroxine treatment (CRP=2.9mg/l and 4.8mg/l, p=0.005). An exploratory comparison with euthyroid controls showed significant higher TBRs during TSH suppression for the carotids, aortic arch, thoracic descending aorta, and when all vascular territories were combined (TBR(max)p=0.013, p=0.016, p=0.030 and p=0.018 respectively).ConclusionsArterial inflammation is increased during TSH suppression. This finding sheds new light on the underlying mechanism of the suspected increased risk of cardiovascular disease in patients with TSH suppression.

Original languageEnglish
Pages (from-to)1428-1438
Number of pages11
JournalEuropean Journal of Nuclear Medicine and Molecular Imaging
Volume46
Issue number7
DOIs
Publication statusPublished - Jul 2019

Keywords

  • Positron emission tomography (PET)
  • Thyroid disease
  • Atherosclerosis
  • Inflammation
  • TSH suppression
  • POSITRON-EMISSION-TOMOGRAPHY
  • ENDOTHELIAL FUNCTION
  • METABOLIC-ACTIVITY
  • WALL INFLAMMATION
  • GLUCOSE-TRANSPORT
  • HORMONE
  • RISK
  • ATHEROSCLEROSIS
  • INSULIN
  • HYPERTHYROIDISM

Cite this