Published in:
Open Access
01-07-2019 | Thyroid Disease | Original Article
TSH suppression aggravates arterial inflammation — an 18F-FDG PET study in thyroid carcinoma patients
Authors:
Ellen Boswijk, Karin J. C. Sanders, Evie P. M. Broeders, Marlies de Ligt, Guy H. E. J. Vijgen, Bas Havekes, Alma M. A. Mingels, Roel Wierts, Wouter D. van Marken Lichtenbelt, Patrick Schrauwen, Felix M. Mottaghy, Joachim E. Wildberger, Jan Bucerius
Published in:
European Journal of Nuclear Medicine and Molecular Imaging
|
Issue 7/2019
Login to get access
Abstract
Purpose
We aimed to investigate the influence of both hypothyroidism and thyroid-stimulating hormone (TSH) suppression on vascular inflammation, as assessed with 18F-fluorodeoxyglucose (18F-FDG) positron emission tomography (PET)/computed tomography (CT).
Methods
Ten thyroid carcinoma patients underwent an 18F-FDG PET/CT during post-thyroidectomy hypothyroidism and during thyrotropin (TSH) suppression after 131I (radioiodine) ablation therapy. We analysed the 18F-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.
Results
In 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 = 2.9 mg/l and 4.8 mg/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 (TBRmaxp = 0.013, p = 0.016, p = 0.030 and p = 0.018 respectively).
Conclusions
Arterial 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.