Riboflavin metabolism in the hypothyroid newborn

• Published in: The American journal of clinical nutrition Vol. 47; no. 3; pp. 481 - 483
• Main Authors: Cimino, JA, Noto, RA, Fusco, CL, Cooperman, JM
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Elsevier Inc 01-03-1988; American Society for Clinical Nutrition
• Subjects: Biological and medical sciences; Congenital Hypothyroidism; Endocrinopathies; Erythrocytes - enzymology; Flavin-Adenine Dinucleotide - metabolism; Glutathione Reductase - blood; Humans; Hypothyroidism - metabolism; Infant, Newborn; Malignant tumors; Medical sciences; Riboflavin - metabolism; Thyroid. Thyroid axis (diseases); Thyroxine - physiology; Human; Endocrinopathy; Newborn; Etiopathogenesis; Thyroid diseases; Vitamin; Riboflavin; Hypothyroidism; Metabolism
• ISSN: 0002-9165; 1938-3207
• DOI: 10.1093/ajcn/47.3.481

In the hypothyroid rat the flavin adenine dinucleotide (FAD) content of the liver is similar to that observed in rats maintained on a riboflavin-deficient diet. Thyroxine regulates the enzyme flavin kinase. Human adults with hypothyroidism have levels of erythrocyte glutathione reductase (EGR), an FAD-containing enzyme, in the range indicative of riboflavin deficiency, which can be corrected with thyroxine therapy. In the present study six newborns with severe congenital hypothyroidism because of athyrosis, ectopic thyroidism, or congenital hypothyroidism with Down's syndrome had normal levels of EGR, and treatment with thyroxine had no effect on these levels.