A reappraisal of risk factors for early hypocalcemia after parathyroidectomy in dialysis patients.

We aimed to identify risk factors for early hypocalcemia after parathyroidectomy in patients with secondary hyperparathyroidism. We retrospectively enrolled 106 of 120 consecutive patients with secondary hyperparathyroidism who underwent parathyroidectomy between January 2019 and July 2021. Perioperative laboratory parameters, preoperative computerized tomography (CT) images, and postoperative histology were evaluated. Parathyroid calcification was defined as hyperdense regions with a density of > 130 Hounsfield Units on CT images of the parathyroid. Subtotal parathyroidectomy, total parathyroidectomy without auto-transplantation, or total parathyroidectomy with auto-transplantation were performed in the present study. Postoperative hypocalcemia was defined as a serum calcium concentration < 2.1 mmol/L within 4 days of surgery. The participants were categorized according to the presence (n = 33) or absence (n = 73) of postoperative hypocalcemia. The demographics, comorbidities, and surgical details were similar in the two groups. Multivariate analysis showed that the preoperative alkaline phosphatase activity, serum intact parathyroid hormone and calcium concentrations, and parathyroid calcification were independent risk factors for postoperative hypocalcemia (all P < 0.05). Receiver operating characteristic analysis generated areas under the curves for preoperative alkaline phosphatase, intact parathyroid hormone, and parathyroid calcification of 0.82, 0.80, and 0.70, respectively (all P < 0.05). Cut-off values for preoperative alkaline phosphatase (> 242.9 IU/L) and intact parathyroid hormone (> 2,104 pg/mL) were found to be predictive of postoperative hypocalcemia. High preoperative alkaline phosphatase activity and serum intact parathyroid hormone concentration and low serum calcium are associated with higher risks of postoperative hypocalcemia. Calcification of the parathyroid may represent a novel radiologic means of predicting postoperative hypocalcemia.

Prognostic value analysis of mutational and clinicopathological factors in non-small cell lung cancer.

INTRODUCTION: Targeting activating oncogenic driver mutations in lung adenocarcinoma has led to prolonged survival in patients harboring these specific genetic alterations. The prognostic value of these mutations has not yet been elucidated. The prevalence of recently uncovered non-coding somatic mutation in promoter region of TERT gene is also to be validated in lung cancer. The purpose of this study is to show the prevalence, association with clinicalpathological features and prognostic value of these factors. METHODS: In a cohort of patients with non-small cell lung cancer (NSCLC) (n = 174, including 107 lung adenocarcinoma and 67 lung squamous cell carcinoma), EGFR, KRAS, HER2 and BRAF were directly sequenced in lung adeoncarcinoma, ALK fusions were screened using FISH (Fluorescence in situ Hybridization).TERT promoter region was sequenced in all of the 174 NSCLC samples. Associations of these somatic mutations and clinicopathological features, as well as prognostic factors were evaluated. RESULTS: EGFR, KRAS, HER2, BRAF mutation and ALK fusion were mutated in 25.2%, 6.5%, 1.9%, 0.9% and 3.7% of lung adenocarcinomas. No TERT promoter mutation was validated by reverse-sided sequencing. Lung adenocarcinoma with EGFR and KRAS mutations showed no significant difference in Disease-free Survival (DFS) and Overall Survival (OS). Cox Multi-variate analysis revealed that only N stage and HER2 mutation were independent predictors of worse overall survival (HR = 1.653, 95% CI 1.219-2.241, P = 0.001; HR = 12.344, 95% CI 2.615-58.275, P = 0.002). CONCLUSIONS: We have further confirmed that TERT promoter mutation may only exist in a very small fraction of NSCLCs. These results indicate that dividing lung adenocarcinoma into molecular subtypes according to oncogenic driver mutations doesn't predict survival difference of the disease.