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J Clin Endocrinol Metab. 2016 Feb;101(2):723-9. doi: 10.1210/jc.2015-3504. Epub 2015 Dec 22.

Serum 25-Hydroxyvitamin D Concentrations in Children Progressing to Autoimmunity and Clinical Type 1 Diabetes.

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Medicity (M.M., M.Ko., V.S.), Department of Pediatrics (M.M., J.M., M.Ko., J.T.), Immunogenetics Laboratory (J.I.), University of Turku and Turku University Hospital, and Research Center of Applied and Preventive Cardiovascular Medicine (O.S.), and Department of Physiology (J.T.), Institute of Biomedicine, University of Turku, FI-20520 Turku, Finland; Department of Pediatrics (R.V.), Research Unit for Pediatrics, Dermatology, Clinical Genetics, Obstetrics and Gynecology, Medical Research Center Oulu, University of Oulu, FI 90014 Oulu, Finland; Department of Children and Adolescents (R.V.), Oulu University Hospital, FI 90029 Oulu, Finland; Department of Virology (H.H.), School of Medicine, University of Tampere, and Department of Pediatrics (M.Kn.), Tampere University Hospital, FI-33520 Tampere, Finland; Fimlab Laboratories (H.H.), Pirkanmaa Hospital District, FI-33014 Tampere, Finland; Children's Hospital (M.Kn.), University of Helsinki and Helsinki University Hospital, Research Programs Unit (M.Kn.), Diabetes and Obesity, University of Helsinki, and Folkhälsan Research Center (M.Kn.), FI-00290 Helsinki, Finland.



The role of vitamin D in the development of type 1 diabetes (T1D) remains controversial.


The objective of the investigation was to study whether there are detectable differences in serum 25-hydroxyvitamin D (25[OH]D) concentrations between children who later progressed to T1D (cases) and matched children who remained nondiabetic and negative for islet autoantibodies (controls) when followed up from birth until disease onset.


A total of 3702 prospective serum samples from 252 children were measured for 25(OH)D from the age of 3 months onward using an enzyme immunoassay. Differences between the groups were compared by the mixed-model analysis of variance.


T1D prediction and prevention study clinics in Turku, Oulu, and Tampere University Hospitals, Finland, participated in the study.


By the end of 2012, all 126 case children were diagnosed with T1D. The control children (n = 126) were matched for age, sex, study site, and human leukocyte antigen-HLA-DQ-conferred risk for T1D.


Median circulating 25(OH)D concentration (nanomoles per liter) was measured.


The patterns of variation in circulating 25(OH)D concentrations were similar between cases and controls and did not correlate with the age at seroconversion to autoantibody positivity (P = .79) or disease onset (P = .13). The median concentration of all collected samples did not differ between case and control children (66.6 nmol/L [range 14.0-262.8] vs 67.4 nmol/L [range 19.9-213.0]) P = .56).


This study shows that serum 25(OH)D concentrations are not associated with the development of T1D in Finland.

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