1.
Intravenous thiamine for septic shock: A meta-analysis of randomized controlled trials.
Qian, X, Zhang, Z, Li, F, Wu, L
The American journal of emergency medicine. 2020;(12):2718-2722
Abstract
INTRODUCTION The efficacy of intravenous thiamine to treat septic shock remains controversial. We conduct a systematic review and meta-analysis to explore the impact of intravenous thiamine on treatment efficacy of septic shock. METHODS We have searched PubMed, EMbase, Web of science, EBSCO, and Cochrane library databases through June 2020 and included randomized controlled trials (RCTs) assessing the effect of intravenous thiamine on septic shock. This meta-analysis was performed using the random-effect model. RESULTS Four RCTs were included in the meta-analysis. Overall, compared with control group in patients with septic shock, intravenous thiamine revealed no substantial impact on mortality (odd ratio [OR] = 0.87; 95% confidence interval [CI) = 0.62 to 1.21; P = 0.40), lactate change (standard mean difference [SMD] = 0.04; 95% CI = -0.28 to 0.35; P = 0.82), Sequential Organ Failure Assessment (SOFA) change (SMD = 0.02; 95% CI = -0.18 to 0.21; P = 0.87), intensive care unit (ICU) stay (SMD = -0.02; 95% CI = -0.33 to 0.30; P = 0.90) or renal replacement therapy (OR = 0.47; 95% CI = 0.07 to 3.15; P = 0.43). CONCLUSIONS Intravenous thiamine showed no benefit over placebo in treating patients with septic shock.
2.
Protective Effect of Folic Acid on Oxidative DNA Damage: A Randomized, Double-Blind, and Placebo Controlled Clinical Trial.
Guo, X, Cui, H, Zhang, H, Guan, X, Zhang, Z, Jia, C, Wu, J, Yang, H, Qiu, W, Zhang, C, et al
Medicine. 2015;(45):e1872
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Abstract
Although previous reports have linked DNA damage with both transmissions across generations as well as our own survival, it is unknown how to reverse the lesion. Based on the data from a Randomized, Double-blind, Placebo Controlled Clinical Trial, this study aimed to assess the efficacy of folic acid supplementation (FAS) on DNA oxidative damage reversal.In this randomized clinical trial (RCT), a total of 450 participants were enrolled and randomly assigned to 3 groups to receive folic acid (FA) 0.4 mg/day (low-FA), 0.8 mg/day (high-FA), or placebo (control) for 8 weeks. The urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) and creatinine (Cr) concentration at pre- and post-FAS were measured with modified enzyme-linked immunosorbent assay (ELISA) and high-performance liquid chromatography (HPLC), respectively. A multivariate general linear model was applied to assess the individual effects of FAS and the joint effects between FAS and hypercholesterolemia on oxidative DNA damage improvement. This clinical trial was registered with ClinicalTrials.gov, number NCT02235948.Of the 438 subjects that received FA fortification or placebo, the median (first quartile, third quartile) of urinary 8-OHdG/Cr for placebo, low-FA, and high-FA groups were 58.19 (43.90, 82.26), 53.51 (38.97, 72.74), 54.73 (39.58, 76.63) ng/mg at baseline and 57.77 (44.35, 81.33), 51.73 (38.20, 71.30), and 50.65 (37.64, 76.17) ng/mg at the 56th day, respectively. A significant decrease of urinary 8-OHdG was observed after 56 days FA fortification (P < 0.001). Compared with the placebo, after adjusting for some potential confounding factors, including the baseline urinary 8-OHdG/Cr, the urinary 8-OHdG/Cr concentration significantly decreased after 56 days FAS [β (95% confidence interval) = -0.88 (-1.62, -0.14) and P = 0.020 for low-FA; and β (95% confidence interval) = -2.68 (-3.42, -1.94) and P < 0.001 for high-FA] in a dose-response fashion (Ptrend < 0.001). Test of interaction between hypercholesterolemia and FA supplementation on urinary 8-OHdG reduction was significant (P = 0.001).The present study demonstrates that FA fortification is independently linked to the reduction of urinary 8-OHdG/Cr in a dose-related pattern, which suggests that FA is beneficial to protect against oxidative damage to DNA. This effect is apparently stronger in those with hypercholesterolemia. The authors provide a new insight into the prevention and reversal of oxidative DNA damage.