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Abstract
PurposeWe 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).MethodsTen 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.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 = 2.9 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).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.
Highlights
Patients with differentiated thyroid carcinoma (DTC) are commonly subjected to both ends of the thyroid hormone spectrum as a result of their therapy [10, 11]
We aimed to investigate the influence of thyroid function on vascular inflammation, as assessed with 18F-FDG positron emission tomography (PET) / computed tomography (CT)
We were able to show that vascular to-background ratios (TBRs), as a measure for arterial inflammation, are higher under thyroid-stimulating hormone (TSH)-suppressive medication than during hypothyroidism, indicating a negative impact of TSH suppression on atherosclerosis
Summary
Patients with differentiated thyroid carcinoma (DTC) are commonly subjected to both ends of the thyroid hormone spectrum as a result of their therapy [10, 11]. Patients are left hypothyroid before adjuvant radioactive iodine (I131) ablation to facilitate uptake of radioactive iodine in the remaining thyroid tissue. Since DTC cells express TSH receptors, high TSH levels will stimulate potential residual malignant tissue proliferation, and iodine uptake, increasing the effect of I131 ablation [10, 11]. Patients are subscribed long-term levothyroxine treatment to induce a state of TSH suppression to prevent further stimulation of possible residual malignant tissue [10,11,12]. Recent guidelines emphasize a personalized approach, weighing individual risk of recurrent disease against the risk of adverse effects of TSH suppression [10,11,12,13]
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