The Environmental Determinants of Diabetes in the Young (TEDDY) Study: 2018 Update
Current Diabetes Reports, ISSN: 1539-0829, Vol: 18, Issue: 12, Page: 136
2018
- 77Citations
- 171Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations77
- Citation Indexes77
- CrossRef77
- Captures171
- Readers171
- 171
Review Description
Purpose of Review: The environmental triggers of islet autoimmunity leading to type 1 diabetes (T1D) need to be elucidated to inform primary prevention. The Environmental Determinants of Diabetes in the Young (TEDDY) Study follows from birth 8676 children with T1D risk HLA-DR-DQ genotypes in the USA, Finland, Germany, and Sweden. Most study participants (89%) have no first-degree relative with T1D. The primary outcomes include the appearance of one or more persistent islet autoantibodies (islet autoimmunity, IA) and clinical T1D. Recent Findings: As of February 28, 2018, 769 children had developed IA and 310 have progressed to T1D. Secondary outcomes include celiac disease and autoimmune thyroid disease. While the follow-up continues, TEDDY has already evaluated a number of candidate environmental triggers, including infections, probiotics, micronutrient, and microbiome. Summary: TEDDY results suggest that there are multiple pathways leading to the destruction of pancreatic beta-cells. Ongoing measurements of further specific exposures, gene variants, and gene-environment interactions and detailed “omics” studies will provide novel information on the pathogenesis of T1D.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85055450125&origin=inward; http://dx.doi.org/10.1007/s11892-018-1113-2; http://www.ncbi.nlm.nih.gov/pubmed/30353256; http://link.springer.com/10.1007/s11892-018-1113-2; https://dx.doi.org/10.1007/s11892-018-1113-2; https://link.springer.com/article/10.1007/s11892-018-1113-2
Springer Science and Business Media LLC
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