Predictive correction of serum sodium concentration with formulas derived from the Edelman equation in patients with severe hyponatremia

Abstract Severe hyponatremia can cause life-threatening cerebral edema. Treatment comprises rapid elevation of serum sodium concentration; however, overcorrection can result in osmotic demyelination. This study investigated potential factors, including predictive correction based on the Edelman equation, associated with appropriate correction in 221 patients with a serum sodium concentration ≤ 120 mEq/L who were admitted to a hospital in Nagoya, Japan. Appropriate correction was defined as an elevation in serum sodium concentration in the range of 4–10 mEq/L in the first 24 h and within 18 mEq/L in the first 48 h after the start of the correction. Appropriate corrections were made in 132 (59.7%) of the 221 patients. Multivariate analysis revealed that predictive correction with an infusate and fluid loss formula derived from the Edelman equation was associated with appropriate correction of serum sodium concentration (adjusted odds ratio, 7.84; 95% confidence interval, 2.97–20.64). Relative without its use, the predictive equation results in a lower proportion of undercorrection (14.3% vs. 48.0%, respectively) and overcorrection (1.0% vs. 12.2%, respectively). These results suggest that predictive correction of serum sodium concentrations using the formula derived from the Edelman equation can play an essential role in the appropriate management of patients with severe hyponatremia

Edoxaban versus warfarin in patients with atrial fibrillation

Contains fulltext : 125374.pdf (publisher's version ) (Open Access)BACKGROUND: Edoxaban is a direct oral factor Xa inhibitor with proven antithrombotic effects. The long-term efficacy and safety of edoxaban as compared with warfarin in patients with atrial fibrillation is not known. METHODS: We conducted a randomized, double-blind, double-dummy trial comparing two once-daily regimens of edoxaban with warfarin in 21,105 patients with moderate-to-high-risk atrial fibrillation (median follow-up, 2.8 years). The primary efficacy end point was stroke or systemic embolism. Each edoxaban regimen was tested for noninferiority to warfarin during the treatment period. The principal safety end point was major bleeding. RESULTS: The annualized rate of the primary end point during treatment was 1.50% with warfarin (median time in the therapeutic range, 68.4%), as compared with 1.18% with high-dose edoxaban (hazard ratio, 0.79; 97.5% confidence interval [CI], 0.63 to 0.99; P<0.001 for noninferiority) and 1.61% with low-dose edoxaban (hazard ratio, 1.07; 97.5% CI, 0.87 to 1.31; P=0.005 for noninferiority). In the intention-to-treat analysis, there was a trend favoring high-dose edoxaban versus warfarin (hazard ratio, 0.87; 97.5% CI, 0.73 to 1.04; P=0.08) and an unfavorable trend with low-dose edoxaban versus warfarin (hazard ratio, 1.13; 97.5% CI, 0.96 to 1.34; P=0.10). The annualized rate of major bleeding was 3.43% with warfarin versus 2.75% with high-dose edoxaban (hazard ratio, 0.80; 95% CI, 0.71 to 0.91; P<0.001) and 1.61% with low-dose edoxaban (hazard ratio, 0.47; 95% CI, 0.41 to 0.55; P<0.001). The corresponding annualized rates of death from cardiovascular causes were 3.17% versus 2.74% (hazard ratio, 0.86; 95% CI, 0.77 to 0.97; P=0.01), and 2.71% (hazard ratio, 0.85; 95% CI, 0.76 to 0.96; P=0.008), and the corresponding rates of the key secondary end point (a composite of stroke, systemic embolism, or death from cardiovascular causes) were 4.43% versus 3.85% (hazard ratio, 0.87; 95% CI, 0.78 to 0.96; P=0.005), and 4.23% (hazard ratio, 0.95; 95% CI, 0.86 to 1.05; P=0.32). CONCLUSIONS: Both once-daily regimens of edoxaban were noninferior to warfarin with respect to the prevention of stroke or systemic embolism and were associated with significantly lower rates of bleeding and death from cardiovascular causes. (Funded by Daiichi Sankyo Pharma Development; ENGAGE AF-TIMI 48 ClinicalTrials.gov number, NCT00781391.)