TY - JOUR
T1 - TSH suppression aggravates arterial inflammation — an 18F-FDG PET study in thyroid carcinoma patients
AU - Boswijk, Ellen
AU - Sanders, Karin J. C.
AU - Broeders, Evie P. M.
AU - de Ligt, Marlies
AU - Vijgen, Guy H. E. J.
AU - Havekes, Bas
AU - Mingels, Alma M. A.
AU - Wierts, Roel
AU - van Marken Lichtenbelt, Wouter D.
AU - Schrauwen, Patrick
AU - Mottaghy, Felix M.
AU - Wildberger, Joachim E.
AU - Bucerius, Jan
N1 - Funding Information:
This study was financially supported in part by the Stichting de Weijerhorst (E.Bo., J.E.W., J.B.). M.d.L. was funded by a Diabetes Fonds Project Grant (2012.00.1525). W.D.v.M.L. was funded by EU FP7, project DIABAT (HEALTH-F2-2011-278373), and by the Dutch Organization for Scientific Research (NWO-ZonMw 91209037).
Publisher Copyright:
© 2019, The Author(s).
PY - 2019/7
Y1 - 2019/7
N2 - 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.
AB - 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.
KW - Positron emission tomography (PET)
KW - Thyroid disease
KW - Atherosclerosis
KW - Inflammation
KW - TSH suppression
KW - POSITRON-EMISSION-TOMOGRAPHY
KW - ENDOTHELIAL FUNCTION
KW - METABOLIC-ACTIVITY
KW - WALL INFLAMMATION
KW - GLUCOSE-TRANSPORT
KW - HORMONE
KW - RISK
KW - ATHEROSCLEROSIS
KW - INSULIN
KW - HYPERTHYROIDISM
U2 - 10.1007/s00259-019-04292-w
DO - 10.1007/s00259-019-04292-w
M3 - Article
C2 - 30859432
SN - 1619-7070
VL - 46
SP - 1428
EP - 1438
JO - European Journal of Nuclear Medicine and Molecular Imaging
JF - European Journal of Nuclear Medicine and Molecular Imaging
IS - 7
ER -