Diabetologie und Stoffwechsel 2007; 2 - A45
DOI: 10.1055/s-2007-984791

Does alfacalcidol prevent pancreatic beta cells from further destruction in children at the onset of diabetes mellitus type 1?

L Szewczyk 1, Y Azab 1, A Bury 1, R Piekarski 1
  • 1Medical Academy of Lublin, Department of Pediatric Endocrinology and Neurology, Poland

In recent years studies focused on prevention of type 1 diabetes mellitus (DM) and possibility of beta-cell protection at the clinical diagnosis of DM. Some recent studies have demonstrated beneficial role of vit. D3 analogue in human beta-cell activity maintenance at the early stages of DM.

Material and methods: The study was performed in 63 children and adolescents (32 female and 31 male) aged 4–16 years who received insulin and vit D3 analogue (alfacalcidol –1alpha-OH-vitamin D3) in daily dose 0.25µg. 37 peers (17 female and 20 male) with type 1 DM who received only insulin therapy without vit. D3 administration were the control group. After one year therapy we compared the level of HbA1c, body mass, daily insulin dose in both groups.

Results: There are no differences in mean body mass and in metabolic control of diabetes reported by mean HbA1c level at the onset of the DM and after one year observation of these patients among studied groups. However, daily insulin dose in group of patients who received vit. D3 therapy after one year observation were at the similar level compared to the early stage of DM (0.36u/kg –0.37u/kg). On the contrary, insulin requirement in the group of patients without vit. D3 treatment significantly increased after one year observation (from 0.37u/kg to 0.63u/kg).

Conclusions: In group of children treated alfacalcidol insulin requirement after one year therapy with vit. D3 analogue sustained at the level found at the early stage of DM. Children without vit. D3 administration had twofold increrase of insulin requirement after one year observation from clinical diagnosis. Our observations suggest, that alfacalcidol could play a role in prevention of further beta-cells destruction.