Objective To evaluate the safety and efficacy of potassium and magnesium supplement with potassium aspartate and magnesium aspartate injection in gastrointestinal surgery patients during absolute fasting．Methods A multicenter randomized controlled clinical trial was conducted in 111 patients after gastrointestinal surgery. For trial group，56 patients were given potassium aspartate and magnesium aspartate injection （Panangin®） in half of the total potassium replenished dose and the rest half of the potassium replenished dose was given in 10% potassium chloride injection．For control group，55 patients were given 10% potassium chloride injection for the total dose of potassium replenished．Such treatments maintained five consecutive days after surgical operation．Clinical observations were performed until patients were discharged from the hospitals．Results Before the intervention，there were no significant differences for the baseline between two groups （P＞0.05）．There was no significant difference for the serum potassium level between two groups （P＞0.05） after intervention．The amount of urinary potassium （mmol/24 h） for patients in the trial group was significantly lower than that in the control group during treatment after operation．The serum magnesium level of control group was much lower than that of control group （P＜0.05）. In the clinical observation process，no drug-related adverse event was observed．Conclusions The supplementary effect of potassium and magnesium for potassium aspartate and magnesium aspartate injection in patients with gastrointestinal surgery during absolute fasting is significant，and superior to potassium chloride injection for potassium supplement．Potassium aspartate and magnesium aspartate injection is a safe and appropriate choice for patients with potassium depletion．
ObjectiveTo screen pathogenic gene mutations of Gitelman syndrome (GS).MethodsPatients with GS diagnosed and treated in the Department of Endocrinology and Metabolism, West China Hospital of Sichuan University from January 2015 to December 2020 and their family members were included. The pathogenic genes were screened by second-generation sequencing combined with first-generation validation.ResultsA total of 15 GS patients were included. Gene analysis of patients indicated SLC12A3 gene mutation, including 9 cases of compound heterozygous mutation and 6 cases of heterozygous mutation. A total of 12 reported pathogenic sites and 8 new pathogenic mutations were found. Among the newly discovered pathogenic mutations, four were missense mutations (c.539C>A, p.T180K; c.1077C>G, p.N359K; c.1967C>T, p.P656L; and c.2963T>C, p.I988T), one was frame shift mutation caused by single base deletion (c.2543delA, p.D848fs), one was nonsense mutation (c.2129C>A, p.S710X), one was large fragment deletion (exon 7-8 partial coding sequence deletion), and one was coding sequence deletion and abnormal base sequence insertion (IVS7-1 to c.976 deletion GCGGACATTTTTG insertion into ACCGAAAATTTT).ConclusionIn this study, 8 new gene mutations leading to GS were found, and the exact pathogenesis of GS remains to be further confirmed.