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• W2109361390 abstract "Aside from the skeletal health affection, vitamin D deficiency has been implicated as a potential environmental factor triggering for some autoimmune disorders. Vitamin D might play a role in the regulation of the production of auto-antibodies. Immunomodulatory effects of vitamin D may act not only through modulation of T-helper cell function, but also through induction of CD4+CD25high regulatory T-cells. We are the first to investigate the relationship between serum levels of 25-hydroxy vitamin D and anti-myelin-associated glycoprotein (anti-MAG) auto-antibodies in autistic children. Serum levels of 25-hydroxy vitamin D and anti-MAG auto-antibodies were measured in 50 autistic children, aged between 5 and 12 years, and 30 healthy-matched children. Serum 25-hydroxy vitamin D levels 10–30 ng/mL and < 10 ng/mL were defined as vitamin D insufficiency and deficiency, respectively. Autistic children had significantly lower serum levels of 25-hydroxy vitamin D than healthy children (P < 0.001) with 40% and 48% being vitamin D deficient and insufficient, respectively. Serum 25-hydroxy vitamin D had significant negative correlations with Childhood Autism Rating Scale (P < 0.001). Increased levels of serum anti-MAG auto-antibodies were found in 70% of autistic patients. Serum 25-hydroxy vitamin D levels had significant negative correlations with serum levels of anti-MAG auto-antibodies (P < 0.001). Vitamin D deficiency was found in some autistic children and this deficiency may contribute to the induction of the production of serum anti-MAG auto-antibodies in these children. However, future studies looking at a potential role of vitamin D in the pathophysiology and treatment of autism are warranted." @default.
• W2109361390 created "2016-06-24" @default.
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• W2109361390 date "2012-08-17" @default.
• W2109361390 modified "2023-10-12" @default.
• W2109361390 title "Reduced serum concentrations of 25-hydroxy vitamin D in children with autism: Relation to autoimmunity" @default.
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• W2109361390 doi "https://doi.org/10.1186/1742-2094-9-201" @default.
• W2109361390 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3476426" @default.
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• W2109361390 hasPublicationYear "2012" @default.
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