Effects of L-thyroxine Replacement Therapy on Carotid Intima-media Thickness in Patients with Primary Hypothyroidism

Çakal, Erman; Turgut, Ahmet Tuncay; Demirbaş, Berrin; Özkaya, Mesut; Çakal, Beytullah; Serter, Rüştü; Aral, Y.

doi:10.1055/s-0028-1085998

Cited by 9 publications

(7 citation statements)

References 25 publications

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“…We can therefore not completely exclude the possibility that the TBRs were higher during TSH suppression because the period of TSH suppression was longer. However, our findings seem to be in contrast to earlier studies showing a decrease in vascular disease with thyroid hormone replacement therapy in (subclinical) hypothyroidism [ 39 , 40 ]. This rather supports a detrimental effect of increased thyroid hormones on arterial inflammation.…”

Section: Discussioncontrasting

confidence: 99%

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

Boswijk

Sanders

Broeders

et al. 2019

Eur J Nucl Med Mol Imaging

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Purpose We aimed to investigate the influence of both hypothyroidism and thyroid-stimulating hormone (TSH) suppression on vascular inflammation, as assessed with 18 F-fluorodeoxyglucose ( 18 F-FDG) positron emission tomography (PET)/computed tomography (CT). Methods Ten thyroid carcinoma patients underwent an 18 F-FDG PET/CT during post-thyroidectomy hypothyroidism and during thyrotropin (TSH) suppression after 131 I (radioiodine) ablation therapy. We analysed the 18 F-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 (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 max p = 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. Electronic supplementary material The online version of this article (10.1007/s00259-019-04292-w) contains supplementary material, which is available to authorized users.

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Section: Discussioncontrasting

confidence: 99%

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

Boswijk

Sanders

Broeders

et al. 2019

Eur J Nucl Med Mol Imaging

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“…Cakal et al have similarly established higher CAIMT in primary hypothyroid patients. 21,22 Their study has also found a positive correlation between lipids, CAIMT, and TSH levels and have concluded that CAIMT is an objective sign of accelerated atherosclerosis in patients with primary hypothyroidism. In contrast to these studies, Delitala et al in their study concluded that thyroid hormone was not associated with carotid artery plaque or increased CAIMT.…”

Section: Comparison Of Parameters After 4 Months Of Levothyroxine Amomentioning

confidence: 94%

Assessment of carotid intima-media thickness in hypothyroidism and the effect of thyroid replacement therapy

et al. 2018

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Background: Carotid artery intima-media thickness (CAIMT) measurement in hypothyroidism will help assess the progression of atherosclerosis and timely intervention may prevent vascular complications.Methods: This study included 30 clinical hypothyroid (CH), 30 subclinical hypothyroid (SCH) and 30 euthyroid. As per procedure, informed consent was taken from the patients in prescribed formats before their participation in the study. Patients were divided into 3 groups of CHs, SCH and Controls after obtaining the thyroid function test values. CAIMT on the right side was measured in the three groups for comparison. Other parameters included age, sex, height, weight, body mass index (BMI), total cholesterol and triglycerides. After 4 months of levothyroxine therapy, CAIMT, total cholesterol and triglycerides were reassessed.Results: The CAIMT was increased in CH and SCH group when compared to euthyroid individuals. The mean CAIMT in CH group was 0.60±0.009cm, in SCH group it was 0.055±0.010 cm and in controls it was 0.047±0.006 cm. After 4 months of levothyroxine therapy, there was no change observed in the mean CAIMT values.Conclusions: CAIMT levels were increased in CH and SCH group when compared to euthyroid group. There was no regression of CAIMT after 4 months of levothyroxine therapy.

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“…Impaired intracellular glucose catabolism and GLUT4 translocation, decreased glycogen synthesis and glucose oxidation, and altered blood flow, have been proposed as underlying mechanisms [25, 26, 90, 93, 94]. Increased intima-media thickness of the common carotid artery has been reported in some studies in patients with overt hypothyroidism [53, 95, 96]. A higher frequency and/or severity of coronary heart disease [4, 97, 98] and an increased ischemic stroke risk [99] have been reported in patients with overt hypothyroidism.…”

Section: Thyroid Disease and Cardiovascular Riskmentioning

confidence: 99%

Lipid Abnormalities and Cardiometabolic Risk in Patients with Overt and Subclinical Thyroid Disease

2011

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Dyslipidemia is a common finding in patients with thyroid disease, explained by the adverse effects of thyroid hormones in almost all steps of lipid metabolism. Not only overt but also subclinical hypo- and hyperthyroidism, through different mechanisms, are associated with lipid alterations, mainly concerning total and LDL cholesterol and less often HDL cholesterol, triglycerides, lipoprotein (a), apolipoprotein A1, and apolipoprotein B. In addition to quantitative, qualitative alterations of lipids have been also reported, including atherogenic and oxidized LDL and HDL particles. In thyroid disease, dyslipidemia coexists with various metabolic abnormalities and induce insulin resistance and oxidative stress via a vice-vicious cycle. The above associations in combination with the thyroid hormone induced hemodynamic alterations, might explain the increased risk of coronary artery disease, cerebral ischemia risk, and angina pectoris in older, and possibly ischemic stroke in younger patients with overt or subclinical hyperthyroidism.

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Effects of L-thyroxine Replacement Therapy on Carotid Intima-media Thickness in Patients with Primary Hypothyroidism

Cited by 9 publications

References 25 publications

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

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

Assessment of carotid intima-media thickness in hypothyroidism and the effect of thyroid replacement therapy

Lipid Abnormalities and Cardiometabolic Risk in Patients with Overt and Subclinical Thyroid Disease

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