4.2 Article

Low levels of 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3 in patients with newly diagnosed type 1 diabetes

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HORMONE AND METABOLIC RESEARCH
卷 37, 期 11, 页码 680-683

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GEORG THIEME VERLAG KG
DOI: 10.1055/s-2005-870578

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vitamin D-3; type 1 diabetes; immune response

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Background and aims: An epidemiological retrospective study and a recent prospective study from Finland have both concluded that vitamin D-3 supplementation at birth protects individuals from type I diabetes later in life. Moreover, it is thought that vitamin D-3 supplementation, in particular its activated form, 1,25-dihydroxyvitamin D-3 [1,25-(OH)(2)D-3] may act as an immunomodulator, facilitating the shift from a Th1 to a Th2 immune response. The aim of this surveillance study was to measure levels of both 25-hydroxyvitamin D-3 (25OHD(3)) and 1,25- dihydroxyvitamin D-3 in patients with newly diagnosed type 1 diabetes as compared to normal subjects. Methods: We measured plasma levels of 25-hydroxyvitamin D-3(25OHD(3)) and 1,25-dihydroxyvitamin D-3 by radioimmunoassay in 88 consecutive patients with newly diagnosed type I diabetes (mean age 14.6 years; diagnosis within the last week), and in 57 healthy age and sex-matched subjects (mean age 16.5 years) born and residing in the Lazio region of continental Italy. Results: Mean levels of both 25OHD(3) and 1,25-(OH)(2)D-3 were significantly lower in patients compared to controls (p < 0.01 and p < 0.03, respectively). There was no correlation between 1,25-(OH)(2)D-3 plasma level and metabolic control status at disease diagnosis, age, gender, or most importantly, seasonality of disease diagnosis. This new observation endorses the findings of the Finnish study, even though Italy is a geographic area with more hours of sunlight than Finland. Conclusions: These findings Suggest that vitamin D-3 may be an important pathogenic factor in type I diabetes independent of geographical latitude, and that its supplementation should be considered not only at birth, but also at diagnosis of type I diabetes with the aim of favouring a Th2 immune response and protecting residual beta cells from further destruction.

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