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Modulation of the neuroendocrine system and immune functions by zinc supplementation in children with Down's syndrome

F Licastro1, E Mocchegiani, M Masi

  • 1Department of Experimental Pathology, University of Bologna, Italy.

Journal of Trace Elements and Electrolytes in Health and Disease
|December 1, 1993
PubMed

Insights

Children with Down syndrome (DS) often have thyroid dysfunction linked to zinc deficiency. Supplementing with zinc sulfate (ZnSO4) restored zinc, thymulin, and thyroid hormone levels in DS children, suggesting zinc

Area of Science:

  • Endocrinology
  • Genetics
  • Nutritional Science

Background:

  • Children with Down syndrome (DS) exhibit a higher prevalence of thyroid dysfunction, particularly autoimmune hypothyroidism.
  • Thyroid hormone levels (TSH, T4, T3, rT3) and zinc status are frequently altered in individuals with DS.

Purpose of the Study:

  • To investigate the relationship between zinc deficiency and thyroid dysfunction in children with Down syndrome.
  • To evaluate the impact of zinc supplementation on thyroid hormone levels and thymulin in DS.

Main Methods:

  • Measurement of plasma TSH, T4, T3, rT3, zinc, and thymulin in 51 children with DS and 15 controls.
  • Administration of zinc sulfate (ZnSO4) supplementation to children with DS.
  • Follow-up assessment of biochemical markers after zinc therapy and after its cessation.

Main Results:

  • Children with DS showed elevated TSH and decreased rT3 levels compared to controls, with normal T3 and T4.
  • Plasma zinc and thymulin levels were significantly lower in children with DS.
  • Zinc supplementation normalized plasma zinc, thymulin, TSH, and rT3 levels.
  • One year after zinc cessation, zinc levels decreased and TSH slightly increased.

Conclusions:

  • Zinc deficiency is implicated in the pathogenesis of thyroid dysfunction observed in Down syndrome.
  • Dietary zinc supplementation can effectively restore thyroid function and thymulin levels in children with DS.
  • Zinc plays a critical role in maintaining thyroid homeostasis, and its deficiency may contribute to autoimmune hypothyroidism in this population.

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