The effects of melatonin administration on disease severity and sleep quality in children with atopic dermatitis: A randomized, double-blinded, placebo-controlled trial.

BACKGROUND: The aim of this clinical trial was to determine the effects of melatonin administration on disease severity and sleep quality in children diagnosed with atopic dermatitis (AD). METHODS: This randomized, double-blinded, placebo-controlled trial was conducted by recruiting 70 patients, aged 6-12 years, who had been diagnosed with AD. Study participants were randomly allocated into two intervention groups to receive either 6 mg/d melatonin supplements or placebo (n = 35 each group) for 6 weeks. Severity of disease was assessed using the scoring atopic dermatitis (SCORAD) and objective SCORAD indices. Sleep quality was evaluated by completing the Children's Sleep Habits Questionnaire (CSHQ). RESULTS: Following 6 weeks of intervention, melatonin supplementation significantly improved SCORAD index (ß -3.55; 95% CI, -6.11, -0.98; P = 0.007), objective SCORAD index (ß -3.23; 95% CI, -5.08, -1.38; P = 0.001), serum total IgE levels (ß -153.94 ku/L; 95% CI, -260.39, -47.49; P = 0.005), and CSHQ scores (ß -2.55; 95% CI, -4.34, -0.75; P = 0.006). However, melatonin had no significant impact on pruritus scores, high-sensitivity C-reactive protein (hs-CRP), sleep-onset latency, total sleep time, weight, and BMI compared with placebo. CONCLUSIONS: Overall, melatonin supplementation had beneficial effects on disease severity, serum total IgE levels, and CSHQ among children diagnosed with AD.

Selenium supplementation lowers insulin resistance and markers of cardio-metabolic risk in patients with congestive heart failure: a randomised, double-blind, placebo-controlled trial.

This study was carried out to evaluate the effects of Se supplementation on metabolic profiles in patients with congestive heart failure (CHF). This randomised double-blind, placebo-controlled trial was performed among fifty-three subjects with CHF, aged 45-85 years old. Subjects were randomly allocated into two groups to take either 200 µg/d of Se as Se yeast (n 26) or placebo (n 27) for 12 weeks. Metabolic profiles were assessed at baseline and at the end of trial. Compared with the placebo, Se supplementation led to significant reductions in serum insulin (-18·41 (sd 27·53) v. +13·73 (sd 23·63) pmol/l, P<0·001), homoeostatic model of assessment for insulin resistance (-1·01 (sd 1·61) v. +0·55 (sd 1·20), P<0·001) and a significant increase in quantitative insulin sensitivity check index (QUICKI) (+0·007 (sd 0·03) v. -0·01 (sd 0·01), P=0·007). In addition, Se supplementation significantly decreased LDL-cholesterol (-0·23 (sd 0·29) v. -0·04 (sd 0·28) mmol/l, P=0·03) and total-:HDL-cholesterol ratio (-0·47 (sd 0·31) v. -0·06 (sd 0·42), P<0·001), and significantly increased HDL-cholesterol levels (+0·18 (sd 0·19) v. +0·02 (sd 0·13) mmol/l, P=0·001) compared with the placebo. In addition, taking Se supplements was associated with a significant reduction in high-sensitivity C-reactive protein (hs-CRP) (-1880·8 (sd 3437·5) v. +415·3 (sd 2116·5) ng/ml, P=0·01), and a significant elevation in plasma total antioxidant capacity (TAC) (+30·9 (sd 118·0) v. -187·9 (sd 412·7) mmol/l, P=0·004) and total glutathione levels (+33·7 (sd 130·4) v. -39·2 (sd 132·8) µmol/l, P=0·003) compared with the placebo. When we applied Bonferroni correction for multiple outcome testing, QUICKI (P=0·11), LDL-cholesterol (P=0·51), hs-CRP (P=0·17), TAC (P=0·06) and GSH (P=0·05) became non-significant, and other metabolic profiles did not alter. Overall, our study supported that Se supplementation for 12 weeks to patients with CHF had beneficial effects on insulin metabolism and few markers of cardio-metabolic risk.