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Thyroid hormone and carrier protein interrelationships in children recovering from kwashiorkor
Insights
Severe protein energy malnutrition (PEM) in infants significantly reduces thyroid hormones and binding proteins. Recovery involves progressive increases in these levels and transient thyroid-stimulating hormone (TSH) secretion.
Area of Science:
- Endocrinology
- Nutritional Science
- Pediatrics
Background:
- Protein energy malnutrition (PEM) is a critical condition affecting infant health.
- Nutritional nonthyroidal illness presents complex hormonal changes.
- Thyroid hormone status is vital for infant growth and development.
Purpose of the Study:
- To investigate thyroid hormone and binding protein dynamics in infants with severe PEM.
- To assess the recovery patterns of thyroid function during nutritional rehabilitation.
- To evaluate the interrelationships between thyroid hormones, binding proteins, and TSH during recovery.
Main Methods:
- Studied 15 infants with severe protein energy malnutrition (PEM).
- Assessed serum concentrations of total thyroxine (TT4), triiodothyronine (T3), and thyroxine-binding proteins (TBG) before and during refeeding.
- Evaluated T4:TBG molar ratio and various free thyroxine (FT4) estimates (FTI, analogue FT4, dialysis FT4).
- Monitored serum thyroid-stimulating hormone (TSH) levels.
Main Results:
- Extremely reduced serum TT4, T3, and TBG concentrations observed in untreated PEM.
- Progressive increases in TT4, T3, and TBG during 3 weeks of refeeding.
- T4:TBG molar ratio increased significantly during recovery (0.180 to 0.344).
- Varied changes in FT4 estimates depending on the assay method used.
- Transient increase in serum TSH levels during the recovery phase.
Conclusions:
- Untreated PEM involves reduced T4 and T3 binding to TBG, with recovery taking 2-3 weeks.
- Methodological differences exist in assessing free T4 levels in PEM.
- Increased TSH secretion is a key component of recovery from severe PEM.
Abstract:
We have studied 15 infants with severe protein energy malnutrition (PEM) as a model of nutritional nonthyroidal illness. Changes in circulating thyroid hormones, binding proteins, and their interrelationships were assessed before and during recovery. Serum concentrations of total thyroxine and triiodothyronine and of thyroxine-binding proteins were extremely reduced, and increased progressively during 3 wk of refeeding. The T4:TBG molar ratio was initially 0.180 +/- 0.020, and increased progressively, parallel to the increases in TT4, to 0.344 +/- 0.038 after 21 days (p less than 0.025). The changes in free T4 estimates varied according to the methods used--FTI and analogue FT4 increased, dialysis FT4 fraction decreased. Serum TSH levels increased transiently during recovery. It is concluded 1) there is reduced binding of T4 and T3 to TBG in untreated PEM which takes 2-3 wk to recover; 2) there are methodological differences in evaluating free T4 levels in PEM; 3) increased TSH secretion appears to be an integral part of the recovery from PEM.