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Riboflavin metabolism in the hypothyroid newborn.

J A Cimino1, R A Noto, C L Fusco

  • 1Department of Community and Preventive Medicine, New York Medical College, Valhalla 10595.

The American Journal of Clinical Nutrition
|March 1, 1988
PubMed
Summary

Thyroid hormone (thyroxine) influences riboflavin metabolism in adult humans but not in newborns with congenital hypothyroidism. Congenital hypothyroidism in infants does not affect erythrocyte glutathione reductase (EGR) levels, unlike in adults.

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Area of Science:

  • Biochemistry
  • Endocrinology
  • Nutritional Science

Background:

  • Flavin adenine dinucleotide (FAD) is essential for cellular function, and its levels can be affected by thyroid hormone status.
  • In hypothyroid adult rats, liver FAD content is similar to riboflavin deficiency, and thyroxine regulates flavin kinase.
  • Adult humans with hypothyroidism exhibit erythrocyte glutathione reductase (EGR) levels indicative of riboflavin deficiency, which normalize with thyroxine therapy.

Purpose of the Study:

  • To investigate the relationship between congenital hypothyroidism and riboflavin status in newborns.
  • To determine if thyroxine therapy affects EGR levels in infants with congenital hypothyroidism.

Main Methods:

  • Assessed EGR levels in six newborns with severe congenital hypothyroidism (due to athyrosis, ectopic thyroidism, or Down's syndrome).

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  • Administered thyroxine therapy to the infants.
  • Monitored EGR levels before and after thyroxine treatment.

    • Main Results:

    • Newborns with severe congenital hypothyroidism had normal EGR levels.
    • Thyroxine treatment did not alter EGR levels in these infants.

    Conclusions:

    • Congenital hypothyroidism in newborns does not impair riboflavin status as indicated by EGR levels.
    • Thyroxine's role in regulating riboflavin metabolism, observed in adults, is not evident in infants with congenital hypothyroidism.