[1] DAVIES L, WELCH H G. Current thyroid cancer trends in the United States[J]. Head Neck Surg, 2014,140(4):317-322. [2] NATH M C, ERICKSON L A. Aggressive variants of papillary thyroid carcinoma:hobnail, tall cell, columnar,and solid[J]. Adv Anat Pathol, 2018,25(3):172-179. [3] FREUDENTHAL B, WILLIAMS G R. Thyroid stimulating hormone suppression in the long-term follow-up of differentiated thyroid cancer[J]. Clin Oncol, 2017,29(5):325-328. [4] BRABANT G. Thyrotrppin suppresive therapy in thyroid carcinoma:what are the targots?[J]. Clin Endocrinol Metab, 2008,93(3):1167-1169. [5] SAWKA A M, BRIERLEY J D, EZZAT S, et al. Managing newly diagnosed thyroid cancer[J]. CMAJ, 2014,186 (4):269-275. [6] 张雅婧,高再荣. PET/CT 在 “Tg 阳性碘-131 扫描阴性”分化型甲状腺癌中的临床应用进展[J]. 中国医疗器械信息,2015,17(4):8-12. [7] JIN P, FENG H, OUYANG W, et al. Radiation dose rates of differentiated thyroid cancer patients after 131I therapy[J]. Radiat Environ Biophys, 2018,57(2):169. [8] 刘燕霞,张勇军. 促甲状腺激素抑制治疗对分化型甲状腺癌患者甲状腺功能的影响[J]. 中国现代医生,2019,57(17):24-27. [9] KLEIN HESSELINK E N, KLEIN HESSELINK M S, de BOCK G H, et al. Long-term cardiovascular mortality in patients with differentiated thyroid carcinoma:An observational study[J]. Clin Oncol, 2013,31(32):4046-4053. [10] COLLET T H, GUSSEKLOO J, BAUER D C, et al. Subclinical hyperthyroidism and the risk of coronary heart disease and mortality[J]. Arch Intern Med, 2012, 172(10) : 799-809. [11] 杨柳,靳水,吴彬彬,等. 促甲状腺素抑制治疗对分化型甲状腺癌患者术后左室收缩同步性的影响[J]. 中国实用医刊,2018,45(21):16-19. [12] 王海英. 甲状腺功能亢进症和心律失常[J].现代电生理学杂志,2019,26(1):32-35. [13] DELITALA A P. Subclinical hyperthyroidism and the cardiovascular disease[J]. Horm Metab Res, 2017,49(10) : 723-731. [14] VILCHEZ J A L, PEREZ-CUELLAR M, MARIN F, et al. sST2 levels are associated with all-cause mortality in anticoagulated patients with atrial fibrillation[J]. Eur J Clin Invest, 2015,45(9) :899-905. [15] HWANG H S, CHO J S, HONG Y A, et al. Vascular calcification and left ventricular hypertrophy in hemodialysis patients:interrelationship and clinical impacts[J]. Int J Med Sci, 2018,15(6):557-563. [16] KIM Y I, SHIN H W, CHUN Y S, et al. CST3 and GDF15 ameliorate renal fibrosis by inhibiting fibroblast growth and activation[J]. Biochem Biophys Res Commun, 2018,500(2):288-295. [17] SHARMA U C, POKHAREL S, van BRAKEL T J, et al. Galectin-3 marks activated macrophages in failure-prone hypertrophied hearts and contributes to cardiac dysfunction[J]. Circulation, 2004,110(19):3121-3128. [18] LIU Y H, d′AMBROSIO M, LIAO T D, et al. N-acetyl-seryl-aspartyllysyl-proline prevents cardiac remodeling and dysfunction induced by Galectin-3, a mammalian adhesion /growth-regulatory lectin[J]. Am J Physiol Heart Circ Physiol, 2009,296 (2):H404- H412. [19] HU H J, ZHANG C, TANG Z H, et al. Regulating the Warburg effect on metabolic stress and myocardial fibrosis remodeling and atrial intracardiac waveform activity induced by atrial fibrillation[J]. Biochem Biophys Res Commun, 2019,516(3):653-660. |