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Objective The current guidelines recommend that potassium iodide be given in the immediate preoperative period for patients with Graves’ disease who are undergoing thyroidectomy. Nonetheless, the evidence behind this recommendation is tenuous. The purpose of this study is to clarify the benefits of preoperative iodine administration from published comparative studies. Data Sources We searched PubMed, Embase, Cochrane, and CINAHL from 1980 to June 2018. Review Methods Studies were included that compared preoperative iodine administration and no premedication before thyroidectomy. For the meta-analysis, studies were pooled with the random-effects model. Results A total of 510 patients were divided into the iodine (n = 223) and control (n = 287) groups from 9 selected studies. Preoperative iodine administration was significantly associated with decreased thyroid vascularity and intraoperative blood loss. Significant heterogeneity was present among studies. We found no significant difference in thyroid volume or operative time. Furthermore, the meta-analysis showed no difference in the risk of postoperative complications, including vocal cord palsy, hypoparathyroidism/hypocalcemia, and hemorrhage or hematoma after thyroidectomy. Conclusion Preoperative iodine administration decreases thyroid vascularity and intraoperative blood loss. Nonetheless, it does not translate to more clinically meaningful differences in terms of operative time and postoperative complications.

Aberrant lipid metabolism provides bioenergetic, biosynthetic, and redox supplies to cancer cells. Previous studies have reported differential lipid profiling in thyroid malignancies. Sterol regulatory element-binding protein 1 (SREBP1), encoded by the SREBF1 gene, is a master regulator of cellular lipid homeostasis. The clinical and functional significance of SREBP1 in thyroid cancer is not well understood. Here, we showed that SREBP1 expression is significantly upregulated in invasive thyroid cancer than in normal thyroid tissue or benign thyroid nodules. High tumoral SREBP1 expression was associated with extrathyroidal extension, advanced disease stage, and shorter disease-specific survival in patients with differentiated thyroid cancer. SREBP1 overexpression significantly increased the oxygen consumption rate, filopodia formation, and migratory and invasive capacities of thyroid cancer cells. Knockdown of SREBF1 or treatment with an SREBP1 activation inhibitor fatostatin had the opposite effect. RNA-Seq analysis showed that modulation of SREBP1 expression was accompanied by corresponding changes in the expression of epithelial-mesenchymal transition markers and CYR61/CTGF. SREBP1-facilitated cell invasion could be abrogated by treatment with a YAP inhibitor such as verteporfin or genetic silencing of CYR61 or CTGF. In summary, SREBP1 upregulation can be used as a prognostic indicator for thyroid cancer, and SREBP1 overexpression is involved in cancer invasiveness, at least partly, through upregulation of CYR61/CTGF via the Hippo-YAP pathway.