1.
Low-normal thyroid function and the pathogenesis of common cardio-metabolic disorders.
van Tienhoven-Wind, LJ, Dullaart, RP
European journal of clinical investigation. 2015;(5):494-503
Abstract
BACKGROUND Subclinical hypothyroidism may adversely affect the development of cardiovascular disease (CVD). Less is known about the role of low-normal thyroid function, that is higher thyroid-stimulating hormone and/or lower free thyroxine levels within the euthyroid reference range, in the development of cardio-metabolic disorders. This review is focused on the relationship of low-normal thyroid function with CVD, plasma lipids and lipoprotein function, as well as with metabolic syndrome (MetS), chronic kidney disease (CKD) and nonalcoholic fatty liver disease (NAFLD). MATERIALS AND METHODS This narrative review, which includes results from previously published systematic reviews and meta-analyses, is based on clinical and basic research papers, obtained via MEDLINE and PubMed up to November 2014. RESULTS Low-normal thyroid function could adversely affect the development of (subclinical) atherosclerotic manifestations. It is likely that low-normal thyroid function relates to modest increases in plasma total cholesterol, LDL cholesterol and triglycerides, and may convey pro-atherogenic changes in lipoprotein metabolism and in HDL function. Most available data support the concept that low-normal thyroid function is associated with MetS, insulin resistance and CKD, but not with high blood pressure. Inconsistent effects of low-normal thyroid function on NAFLD have been reported so far. CONCLUSIONS Observational studies suggest that low-normal thyroid function may be implicated in the pathogenesis of CVD. Low-normal thyroid function could also play a role in the development of MetS, insulin resistance and CKD, but the relationship with NAFLD is uncertain. The extent to which low-normal thyroid function prospectively predicts cardio-metabolic disorders has been insufficiently established so far.
2.
Visfatin plasma concentrations in patients with hyperthyroidism and hypothyroidism before and after control of thyroid function.
Ozkaya, M, Sahin, M, Cakal, E, Yuzbasioglu, F, Sezer, K, Kilinc, M, Imrek, SS
Journal of endocrinological investigation. 2009;(5):435-9
Abstract
Alterations in thyroid function are associated with changes in body weight, metabolism, and low-grade inflammation. In several studies, plasma levels of visfatin were found to be associated with body mass index, diabetes, and metabolic syndrome. In our study we aimed to evaluate visfatin levels according to thyroid dysfunction. The study cohort comprised 56 Hashimoto thyroiditis patients with hypothyroidism (43.94+/-14.27 yr), 56 Graves patients with hyperthyroidism (45.87+/-13.28 yr), and 56 euthyroid healthy subjects (45.23+/-7.11 yr) as a control group. In addition, we evaluated the effect of therapy on plasma visfatin levels in 16 hypothyroid and in 25 hyperthyroid patients. Markedly low visfatin levels were found in hyperthyroid patients [9.44 (8.07- 10.8) ng/ml] compared with the hypothyroid [49.93 (40.72- 59.1) ng/ml] and control groups [38.6 (30.6-46.6) ng/ml] (p<0.001, p<0.001). Plasma visfatin levels in patients with hypothyroidism decreased significantly following treatment [58.58 (10.21-190.7) ng/ml vs 40.00 (10.01-102.6) ng/ml; p=0.001]. Plasma visfatin levels increased significantly after antithyroid therapy in patients with hyperthyroidism [7.86 (1.02-19.23) ng/ml vs 12.63 (3.48-110.9) ng/ml; p<0.001]. There were negative correlations between visfatin levels with free T3 (r=-0.719, p<0.001), and free T4 (r=-0.716, p<0.001) levels. There was a positive correlation between visfatin and TSH levels (r=0.701, p<0.001). There was a negative correlation between delta visfatin levels with delta free T3, delta free T4 (r=-0.686, p<0.001; r=-0.624, p<0.001). Visfatin thus seems to be regulated by thyroid hormones. While the influence of thyroid dysfunction on adipocytokine production and release is still poorly understood, the results of our study suggest that the effects of hyper- and hypothyroidism on various metabolic parameters may be partly mediated by visfatin.
3.
Selenium substitution has no direct effect on thyroid hormone metabolism in critically ill patients.
Angstwurm, MW, Schopohl, J, Gaertner, R
European journal of endocrinology. 2004;(1):47-54
Abstract
BACKGROUND In severe illness, plasma selenium levels are decreased; a decreased activity of the selenoenzyme 5'-deiodinase has been hypothesized to contribute to low tri-iodothyronine (T3) levels in non-thyroidal illness (NTI) syndrome in these patients. OBJECTIVE To analyse the influence of selenium substitution on thyroid hormone metabolism in patients with severe sepsis. DESIGN A prospective, randomized, controlled study at the medical internal intensive care unit of the University of Munich. Results are for 41 consecutive patients with severe sepsis with an APACHE II score >15. Patients received either sodium selenite (500 microg/day for the first 3 days, reducing to 250 and then 125 microg/day every 3 days) or a placebo. RESULTS At study entry, APACHE II score and demographics were identical in both groups. The mean levels of TSH, free tri-iodithyronine and total T3, as well as plasma selenium and selenium-dependent peroxidase (GSH-Px) activity, were decreased. Plasma selenium and GSH-Px activity were normalized on days 3, 7 and 14 in patients receiving selenium (n=21), but remained below normal in the control patients. Patients receiving selenium had a better clinical outcome and thyroid hormone levels normalized earlier. Thyroid hormone levels increased in patients who showed clinical improvement, independent of selenium levels or selenium substitution. CONCLUSIONS Selenium substitution in patients with NTI improves morbidity, but has no direct effect on the free and total thyroid hormones. In severely ill patients, decreased deiodinase activity due to low plasma selenium levels seems unlikely. After clinical revival, TSH and then the thyroidal hormones normalize independently of selenium substitution.