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ObjectiveMethodsResultsConclusionThe aim of this study was to investigate changes in heart rate variability (HRV) and QT dispersion (QTd) in patients with differentiated thyroid cancer at different TSH suppression levels.The study included 125 DTC patients, who had been on TSH suppression treatment (TSHST) for at least 1 year. The patients were categorized into three groups: patients with TSH < 0.1 mIU/L (n:30), those with TSH 0.1 to 0.5 mIU/L (n:56), and those with TSH 0.5 to 2 mIU/L (n:39). The first two groups were classified as suppression groups, and the last as replacement (control) group. All patients underwent 12-lead electrocardiogram (ECG) recording and 24-hour rhythm holter echocardiography analysis.The HRV results derived from a 24-hour rhythm holter did not exhibit any significant difference (p < 0.05). In dispersion evaluations, the QTd was significantly longer in the suppression groups (groups 1 and 2), than in the replacement group (group 3) (p < 0.001 and p:0.002, respectively). The same was found for corrected QT dispersion (QTcd) (p < 0.001 and p: 0.008, respectively). In multivariate linear regression analysis, TSH was found to affect QTd (β = -0.299; p = 0.002) and QTcd (β = -0.300; p = 0.002) values independently.In this study, it was shown that in patients with DTC receiving TSHST, QT dispersion prolonged as the TSH suppression level increased. Especially in high-risk DTC patients, evaluation of QTd may be useful in terms of evaluating cardiovascular risk and regulating TSHST level. [ABSTRACT FROM AUTHOR]

It has demonstrated that there is a connection between chronic TSH suppressive treatment and the reduction of bone mineral density (BMD) or the development of osteoporosis in patients with differentiated thyroid cancer (DTC). The aim of the study was to determine the effect of vitamin D3 supplementation on BMD and the development of osteoporosis in patients with DTC. Two hundred four (204) patients with a diagnosis of DTC were included. All patients received thyroid hormone replacement therapy along with vitamin D (5000IU/day). Data including age, gender, body mass index, smoking, menopausal status, family history of osteoporosis, and postoperative duration were collected. The serum levels of TSH, calcium, 25-OH-vitamin D, and parathyroid hormone measurements and BMD by using dual-energy X-ray absorptiometry were performed on whole patients. The mean age of patients was 56.20±9.31 years. With osteoporosis, 22 of the patients were female (10.8%) and 1 was male (0.5%). Twenty one (21) females with OP were postmenopausal state. There was a statistically significant difference between osteoporosis and age, menopausal status, and family history of osteoporosis, but not for the other factors. Although there was no statistically significant difference between osteoporosis and the levels of TSH and vitamin D, most patients with osteoporosis had TSH<0.5 mIU/mL (n=18) and vitamin D<30 ng/mL (n=16). Age and family history of osteoporosis were identified as independent predictive factors for developing osteoporosis. Vitamin D may be considered as a supplemental and supportive treatment in patients with thyroid cancer for preventing cancer recurrence and osteoporosis. [ABSTRACT FROM AUTHOR]

Surgery—with or without postoperative radioiodine—is the standard of care for most patients with differentiated thyroid carcinoma (DTC). Thyroid hormone replacement therapy is the mainstay of long-term medical management. Patients treated with total thyroidectomy and some who undergo lobectomy alone require thyroid hormone therapy to restore euthyroidism with normal serum thyroid-stimulating hormone (TSH) levels. Because TSH acts as a growth factor for thyroid follicular cells (including those that are neoplastic), it can potentially affect the onset and/or progression of follicular-cell derived thyroid cancer. For this reason, some patients are placed on thyroid hormone therapy at doses that suppress secretion of TSH (suppression therapy). This mini-review looks at the potential benefits and risks of this practice in patients diagnosed with DTC. Aggressive TSH-suppressive therapy is of little or no benefit to the vast majority of patients with DTC. Practice guidelines, therefore, recommend a graded algorithm in which the potential benefits of suppression are weighed against the associated cardiovascular and skeletal risks. Large randomized controlled studies are needed to confirm the presumed oncological benefits of TSH-suppression and its causal role in adverse cardiac, skeletal, and quality of life effects and to assess the efficacy of TSH normalization in reversing or reducing these effects. [ABSTRACT FROM AUTHOR]