Objective. We performed this study to investigate the risk factors for postoperative hypocalcemia after total thyroidectomy with central lymph node dissection (CLND). Study Design. This was a single-center prospective study based on 176 consecutive patients who underwent total thyroidectomy for papillary thyroid carcinoma. Setting. Patients were recruited between January 2016 and June 2018. Subjects and Methods. Patients who underwent bilateral (n = 155, bilateral group) and ipsilateral CLND (n = 21) after total thyroidectomy were included. The preoperative and postoperative parathyroid hormone (PTH) and calcium levels were detected. The risk factors for transient hypocalcemia were identified using logistic regression analysis and receiver operating characteristic (ROC) curve analysis. Results. Fifty-one (28.98%) patients developed transient hypocalcemia, and 2 patients (1.14%) developed permanent hypoparathyroidism. There was no difference in the gender ratio or the morbidity of hypocalcemia between the patients who underwent bilateral and ipsilateral CLND. On postoperative day 1, PTH decrease was a risk factor for transient hypocalcemia in the whole cohort (β = 0.043, OR = 1.044, 95% CI 1.023–1.065, p<0.001), bilateral group (β = 0.042, OR = 1.043, 95% CI 1.022–1.064, p<0.001), and female patients (β = 0.049, OR = 1.050, 95% CI 1.026–1.075, p<0.001). Tumor diameter was a risk factor for transient hypocalcemia in female patients (β = 0.499, OR = 1.647, 95% CI 1.003–2.704, p=0.049). The ROC curve analysis illustrated that 65.58%, 71.00%, and 71.00% PTH level reduction had high accuracy in predicting transient hypocalcemia in the whole cohort, bilateral group, and female patients, respectively (AUC = 0.986, 0.987, and 0.987). Conclusion. Asymptomatic female patients with bilateral CLND and a 71.00% PTH level reduction were at a high risk of transient hypocalcemia.

Circular RNAs (circRNAs) are often aberrantly expressed in human tumors and also serve a critical regulatory role in papillary thyroid cancer (PTC). The aim of this study is to investigate the expression pattern and biological role of circVANGL1 in PTC. The results revealed that circVANGL1 was significantly upregulated in human PTC samples. In addition, high circVANGL1 expression was closely associated with adverse clinical parameters of PTC patients. Our in vitro experiments further indicated that the knockdown of circVANGL1 using siRNA obviously repressed migration, proliferation, EMT, and invasion of PTC cells, while opposite effects were induced by its overexpression. We further noted that circVANGL1 could interact with miR-194 directly in PTC, and serve as a ceRNA to regulate ZEB1 function. Moreover, miR-194 inhibition markedly abrogated the effects of circVANGL1 knockdown in PTC cells. Therefore, our results provide convincing evidence that circVANGL1 may exert oncogenic effects in PTC, partly via regulating the miR-194/ZEB1 axis.