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We searched The Cochrane Library, MEDLINE, EMBASE and Web of Science for randomized controlled trials.Study selection, data extraction, assessment of risk of bias and analyses were carried out by two independent review authors.Natural selenium-rich sources include Brazil nuts, organ meat, muscle meat, cereals, shellfish and fish .
Its prevalence is influenced by ethnicity, environmental factors, such as iodine and selenium status, age and gender [1,2].
Selenium 100 μg or 200 μg (sodium selenite or selenomethionine) only or combined with titrated LTWe searched for RCTs in The Cochrane Library, MEDLINE, EMBASE and Web of Science and in reference lists of articles (from inception until 2 October 2012). The degree of heterogeneity between the studies was assessed using the I).
We also examined several online trial registries for on-going trials and attempted to contact trial investigators to provide missing data or to clarify study details. Six studies were excluded after careful evaluation of the full text of the publication [10,14,15,16,17,18]. nonrandomized) clinical trials, of which four [10,16,17,18] were confirmed to be quasi-randomized after communication with the trialists (i.e.
We performed a systematic review to assess the effects of selenium supplementation for Hashimoto's thyroiditis, and this report is a summary of the Cochrane systematic review . Our three primary outcomes were: (1) change from baseline in HRQo L assessed using any validated quality-of-life instrument; (2) change from baseline in symptoms, such as mood, fatigue and muscle weakness, assessed using any validated instrument, and (3) proportion of participants reporting an adverse event throughout the study period. Dichotomous outcomes data were presented as risk ratios (RRs) and if significant were converted to the number needed to treat (NNT) for an additional beneficial outcome.
We conducted a systematic review of randomized controlled trials (RCTs) assessing the effects of selenium supplementation in adults with Hashimoto's thyroiditis. Secondary outcomes were: (a) change from baseline in serum levels of anti-thyroid peroxidase antibodies; (b) change from baseline in LTThree review authors (E. All outcomes data were reported with their associated 95% CIs and were analyzed using a random-effects model and the Mantel-Haenzel test for dichotomous outcomes data and invariance analysis for continuous outcomes data, unless stated otherwise.
The active form of thyroid hormone, tri-iodothyronine (T3), is produced by de-iodination of the prohormone T4 by type I and type II iodothyronine de-iodinasesin, a two-substrate ‘ping-pong’ mechanism of reaction, along with degradation of H to water by GPx.