TSH suppression aggravates arterial inflammation - an ¹⁸F-FDG PET study in thyroid carcinoma patients.

Abstract

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). 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. In general, there was a trend towards higher vascular TBRs during TSH suppression than during hypothyroidism (TBR_max 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 (TBR_maxp = 0.013, p = 0.016, p = 0.030 and p = 0.018 respectively). 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.