PURPOSE: Whole body Positron Emission Tomography (PET) was used to evaluate the existence of cancer cells. However, PET had limitations in identifying thyroid cancer cells because of their slow progression, and evidence regarding its accuracy in finding thyroid cancer cells is insufficient. Therefore, we investigated the usefulness of PET for evaluation of patients with thyroid nodules by studying the relationships between PET and thyroid ultrasonography. METHODS: We evaluated 4,627 patients who had undergone PET from January 2007 to October 2011 and selected 370 patients who had undergone thyroid ultrasonography. We compared and analyzed the amount of thyroid SUVmax of PET, the pattern of glucose uptake, and findings of thyroid ultrasonography based on their size, shape, location, and FNAC. RESULTS: Of 370 patients, 197 (53.2%) subjects were found to have thyroid nodules, and 211 (57.0%) subjects had higher sugar metabolism, regardless of having thyroid nodules. No statistical correlations were observed among nodule size, nodule location,and higher sugar metabolism, however, noticeable relationships were observed between the shape of the cells on thyroid ultrasonography and FDG uptake of PET. In cases of papillary thyroid cancer, there was higher FDG uptake, compared to benign lesions in particular, SUVmax of the papillary thyroid cancer showed a significantly elevated level of FDG uptake. CONCLUSION: Despite its limited usefulness in identifying the characteristics of thyroid nodules being benign or malignant, PET is appropriate for evaluation of the malignancy of thyroid cells
Diagnosis* ; Electrons* ; Glucose ; Humans ; Metabolism ; Positron-Emission Tomography* ; Thyroid Gland* ; Thyroid Neoplasms ; Thyroid Nodule* ; Ultrasonography

OBJECTIVE: To investigate the expression and clinical significance of EphA2 and E cadherin proteins in papillary thyroid carcinoma tissues, and to explore the relationship between them. METHOD: Using immunohistochemical SP/PV method, we detected the expression of EphA2 and E cadherin in tumors of 43 papillary thyroid carcinomas, 11 thyroid adenoma and 10 normal thyroid tissues, then studied their relationships with clinic pathological factors. RESULT: The total positive rates of EphA2 and E cadherin expression were 58. 14% and 32. 56% in papillary thyroid carcinoma tissues, 18. 18% and 81. 81% in thyroid adenoma.tissues and they were 10. 00% and 100. 00% in normal thyroid tissues respectively. The positive expression of EphA2 in carcinoma tissues was higher than in the thyroid adenoma tissues and normal thyroid tissues (P<0. 05) and the positive expression of E cadherin in carcinoma tissues was lower than that in the thyroid adenoma tissues and normal thyroid tissues (P<0. 05). The positive expression of EphA2 and E cadherin was associated with lymph node metastasis and histological grade (P<0. 05), but it was not associated with all the clinic-pathological factors including age, sex and the tumor size (P>0. 05). In papillary thyroid carcinoma tissues, the expression of EphA2 was negatively correlated with the expression of E cadherin protein (r= -0. 416, P<0. 01). CONCLUSION EphA2 and E cadherin may be involved in carcinogenesis and development of papillary thyroid carcinoma.
Adenoma ; metabolism ; pathology ; Antigens, CD ; Cadherins ; metabolism ; Carcinoma ; metabolism ; pathology ; Carcinoma, Papillary ; Humans ; Lymphatic Metastasis ; Receptor, EphA2 ; metabolism ; Thyroid Cancer, Papillary ; Thyroid Gland ; metabolism ; Thyroid Neoplasms ; metabolism ; pathology

Metabolic reprogramming of cancer cell is one of essential hallmarks of cancer. Otto Warburg first demonstrated that cancer cells utilized more glucose and enhanced glycolytic pathway in the presence of oxygen in 1926. Scientific observations of basic and clinical research in several decades supported that cancer-specific metabolism can be an emerging target for treatment of cancer. Metabolic reprogramming is regulated by both oncogenic signaling and tumor suppressor genes associated with critical signaling pathways in metabolism. These changes provided energy, substrates for cell growth and proliferation, favoring microenvironment, and important for redox balancing for cancer cells. Recent advance of several tools for evaluation comprehensive metabolic profiles of cancer cells provided us to identification of metabolic Achilles' heel of cancers including thyroid cancer. This approach can be a useful strategy for advance in treatment of cancer patients.
Genes, Tumor Suppressor ; Glucose ; Heel ; Humans ; Metabolism* ; Metabolome ; Oxidation-Reduction ; Oxygen ; Thyroid Gland* ; Thyroid Neoplasms*

Primary thyroid cancers including papillary, follicular, poorly differentiated, and anaplastic carcinomas show substantial differences in biological and clinical behaviors. Even in the same pathological type, there is wide variability in the clinical course of disease progression. The molecular carcinogenesis of thyroid cancer has advanced tremendously in the last decade. However, specific inhibition of oncogenic pathways did not provide a significant survival benefit in advanced progressive thyroid cancer that is resistant to radioactive iodine therapy. Accumulating evidence clearly shows that cellular energy metabolism, which is controlled by oncogenes and other tumor-related factors, is a critical factor determining the clinical phenotypes of cancer. However, the role and nature of energy metabolism in thyroid cancer remain unclear. In this article, we discuss the role of cellular energy metabolism, particularly mitochondrial energy metabolism, in thyroid cancer. Determining the molecular nature of metabolic remodeling in thyroid cancer may provide new biomarkers and therapeutic targets that may be useful in the management of refractory thyroid cancers.
Carcinogenesis ; Carcinoma ; Disease Progression ; Energy Metabolism* ; Iodine ; Mitochondria ; Oncogenes ; Phenotype ; Thyroid Gland* ; Thyroid Neoplasms ; Biomarkers

BACKGROUND: Thyroid dysfunction is associated with cardiovascular diseases. However, the role of thyroid function in lipid metabolism remains partly unknown. The present study aimed to investigate the causal association between thyroid function and serum lipid metabolism via a genetic analysis termed Mendelian randomization (MR). METHODS: The MR approach uses a genetic variant as the instrumental variable in epidemiological studies to mimic a randomized controlled trial. A two-sample MR was performed to assess the causal association, using summary statistics from the Atrial Fibrillation Genetics Consortium (n = 537,409) and the Global Lipids Genetics Consortium (n = 188,577). The clinical measures of thyroid function include thyrotropin (TSH), free triiodothyronine (FT3) and free thyroxine (FT4) levels, FT3:FT4 ratio and concentration of thyroid peroxidase antibodies (TPOAb). The serum lipid metabolism traits include total cholesterol (TC) and triglycerides, high-density lipoprotein, and low-density lipoprotein (LDL) levels. The MR estimate and MR inverse variance-weighted method were used to assess the association between thyroid function and serum lipid metabolism. RESULTS: The results demonstrated that increased TSH levels were significantly associated with higher TC (β = 0.052, P = 0.002) and LDL (β = 0.041, P = 0.018) levels. In addition, the FT3:FT4 ratio was significantly associated with TC (β = 0.240, P = 0.033) and LDL (β = 0.025, P = 0.027) levels. However, no significant differences were observed between genetically predicted FT4 and TPOAb and serum lipids. CONCLUSION Taken together, the results of the present study suggest an association between thyroid function and serum lipid metabolism, highlighting the importance of the pituitary-thyroid-cardiac axis in dyslipidemia susceptibility.
Lipid Metabolism/genetics* ; Mendelian Randomization Analysis ; Thyroid Function Tests ; Thyroid Gland ; Thyrotropin ; Thyroxine ; Triiodothyronine

BACKGROUND AND OBJECTIVES: Selenium is an important trace element for thyroid hormone metabolism, and its deficiency can cause hypothyroidism. Serum selenium concentration is the best biomarker to reflect selenium intake and reserve, although other markers can reflect. Therefore, we preliminarily assessed serum and urine selenium concentrations in patients with thyroid disease compared to those of a healthy population. We also investigated the correlation between serum and urine selenium concentration, thyroid hormone and urinary iodine concentration (UIC). MATERIALS AND METHODS: A total of 97 patients (32 men, 65 women, 52.4±14.7 years) with benign thyroid nodules or thyroid dysfunction who visited the Samsung Medical Center between 2008 and 2013 were included. Data for 175 healthy subjects provided by Lee et al. were used as the control. Serum T3, free T4, and thyroid stimulating hormone (TSH) were measured using commercialized RIA or IRMA kits. Serum/urine selenium and UIC were measured by inductively coupled plasma-mass spectrometry (ICP-MS). RESULTS: Median serum selenium concentration was 110 µg/L (95% CI, 73-156). Median urine selenium concentration was 66.3 µg/gCr (95% CI, 28.7-283.5). Compared to 175 healthy subjects (serum 84 µg/L [95% CI, 30-144], urine 34.5 µg/gCr [95% CI, 0.8-107.2]), serum and urine selenium concentrations of patients with thyroid disease were significantly higher than those of healthy subjects (p<0.001). Serum selenium concentration was significantly correlated with urine selenium concentration after log transformation (r=0.88, p=0.022), but was not significantly correlated with UIC, T3, free T4 and TSH. CONCLUSION: Selenium concentrations of patients with thyroid disease were significantly higher than those of healthy subjects. Serum selenium concentration was significantly correlated with urine selenium concentration.
Female ; Healthy Volunteers ; Humans ; Hypothyroidism ; Iodine ; Male ; Metabolism ; Selenium* ; Spectrum Analysis ; Thyroid Diseases* ; Thyroid Gland* ; Thyroid Nodule ; Thyrotropin

BACKGROUND AND OBJECTIVES: Selenium is an important trace element for thyroid hormone metabolism, and its deficiency can cause hypothyroidism. Serum selenium concentration is the best biomarker to reflect selenium intake and reserve, although other markers can reflect. Therefore, we preliminarily assessed serum and urine selenium concentrations in patients with thyroid disease compared to those of a healthy population. We also investigated the correlation between serum and urine selenium concentration, thyroid hormone and urinary iodine concentration (UIC). MATERIALS AND METHODS: A total of 97 patients (32 men, 65 women, 52.4±14.7 years) with benign thyroid nodules or thyroid dysfunction who visited the Samsung Medical Center between 2008 and 2013 were included. Data for 175 healthy subjects provided by Lee et al. were used as the control. Serum T3, free T4, and thyroid stimulating hormone (TSH) were measured using commercialized RIA or IRMA kits. Serum/urine selenium and UIC were measured by inductively coupled plasma-mass spectrometry (ICP-MS). RESULTS: Median serum selenium concentration was 110 µg/L (95% CI, 73-156). Median urine selenium concentration was 66.3 µg/gCr (95% CI, 28.7-283.5). Compared to 175 healthy subjects (serum 84 µg/L [95% CI, 30-144], urine 34.5 µg/gCr [95% CI, 0.8-107.2]), serum and urine selenium concentrations of patients with thyroid disease were significantly higher than those of healthy subjects (p<0.001). Serum selenium concentration was significantly correlated with urine selenium concentration after log transformation (r=0.88, p=0.022), but was not significantly correlated with UIC, T3, free T4 and TSH. CONCLUSION: Selenium concentrations of patients with thyroid disease were significantly higher than those of healthy subjects. Serum selenium concentration was significantly correlated with urine selenium concentration.
Female ; Healthy Volunteers ; Humans ; Hypothyroidism ; Iodine ; Male ; Metabolism ; Selenium* ; Spectrum Analysis ; Thyroid Diseases* ; Thyroid Gland* ; Thyroid Nodule ; Thyrotropin

Thyroglobulin is the most important and abundant protein in thyroid follicles and has been widely studied as a tumor marker of thyroid cancer recurrence and persistence. Tg is considered the material basis of thyroid hormone synthesis and does not participate in the regulation of thyroid hormone synthesis and secretion. This review summarizes the recent progress in the research of thyroid hormone synthesis and secretion regulation via a negative feedback regulation mechanism by the thyroid-hypothalamus-pituitary axis. Thyroglobulin can negatively regulate the synthesis of thyroid hormone by thyroid follicular cells and antagonize the positive regulation of thyrotropin TSH. The function of thyroid follicular cells is presumably a result of Tg and TSH interaction, and a follicular cycle model is proposed to explain the causes of follicular heterogeneity in glands. We also discuss the prospects and clinical significance of studies into the negative feedback regulation mechanism of the thyroid-hypothalamus-pituitary axis and compare two theories for this mechanism.
Feedback, Physiological ; Humans ; Hypothalamo-Hypophyseal System ; physiology ; Neoplasm Recurrence, Local ; Thyroglobulin ; metabolism ; Thyroid Gland ; physiology ; Thyroid Hormones ; metabolism ; Thyrotropin ; metabolism

The changes of thyroid hormones are expected in patients with chronic renal failure(CRF) because the kidney plays an important role in metabolism and excretion of thyroid hormones. In spite of many studies about this issue, there have not been full consensus about the nature and mechanism of thyroid hormone changes. We undertook the present study to reveal the dialysis effects on these hormones. We measured basal levels of serum total T3 (T3), total T4(T4), free T4(FT4), reverse T3(rT3) and TSH, and then calculated the ratio of T3/T4, rT3/T3 and rT3/T4. The following groups were identifed : Group I-10 cases of normal controls, Group II-18 cases of pre-dialysis or treated conservatively, Group III-20 cases treated by maintenance hemodialysis(HD), Group IV-18 cases treated by continuous ambulatory peritoneal dialysis(CAPD). Patients from group II, III and IV revealed significantly decreased levels of T3 and T4, and increased ratio of rT3/T4 in comparison to the control group(P<0.05). Especially, CAPD group revealed significantly increased levels of T4 and FT4 in comparison to HD group(P<0.05). In the long-term dialysis group(>36months), the mean concentrations of free T4 levels revealed signifcantly decreased in comparison to the short-term dialysis group(P<0.05). Thyroid dysfunction are observed in CRF patients with partial recovery after dialysis therapy. Especially, CAPD achieves significantly improved thyroid dysfunction compared to HD, but further study would be necessary.
Consensus ; Dialysis ; Humans ; Kidney ; Kidney Failure, Chronic* ; Metabolism ; Peritoneal Dialysis* ; Peritoneal Dialysis, Continuous Ambulatory ; Renal Dialysis* ; Thyroid Gland* ; Thyroid Hormones

Thyroid cancer is one of the most common malignancies of endocrine organs, and its incidence rate has increased steadily over the past several decades. Most differentiated thyroid tumors derived from thyroid epithelial cells exhibit slow-growing cancers, and patients with these tumors can achieve a good prognosis with surgical removal and radioiodine treatment. However, a small proportion of patients present with advanced thyroid cancer and are unusually resistant to current drug treatment modalities. Thyroid tumorigenesis is a complex process that is regulated by the activation of oncogenes, inactivation of tumor suppressors, and alterations in programmed cell death. Mitochondria play an essential role during tumor formation, progression, and metastasis of thyroid cancer. Recent studies have successfully observed the mitochondrial etiology of thyroid carcinogenesis. This review focuses on the recent progress in understanding the molecular mechanisms of thyroid cancer relating to altered mitochondrial metabolism.
Carcinogenesis ; Cell Death ; Epithelial Cells ; Humans ; Incidence ; Metabolism* ; Mitochondria ; Neoplasm Metastasis ; Oncogenes* ; Prognosis ; Quality Control* ; Thyroid Gland* ; Thyroid Neoplasms*