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Updated: Aug 14, 2026
An Ex vivo Culture System to Study Thyroid Development
Published on: June 6, 2014
Changes in thyroid hormone levels during growth hormone therapy in initially euthyroid patients: lack of need for
D T Wyatt1, N Gesundheit, B Sherman
1Department of Pediatrics, Medical College of Wisconsin, Milwaukee 53226, USA. dtwyatt@mcw.edu
Insights
Growth hormone (GH) therapy in children with GH deficiency rarely causes central hypothyroidism. Acute thyroid profile changes occur initially but typically resolve without clinical symptoms or need for thyroid hormone supplementation.
Area of Science:
- Pediatric Endocrinology
- Endocrinology
- Metabolism
Background:
- Central hypothyroidism incidence during growth hormone (GH) therapy varies.
- Euthyroid children with GH deficiency require monitoring during GH therapy.
Purpose of the Study:
- To monitor acute effects on the hypothalamic-pituitary-thyroid axis during the first year of GH therapy in euthyroid children.
- To assess the development of clinically significant hypothyroidism in these patients.
Main Methods:
- 15 euthyroid children with GH deficiency underwent thyroid profile testing (TSH, T4, free T4, T3, rT3) at baseline and various intervals up to 12-15 months.
- Thyrotropin-releasing hormone (TRH) stimulation tests were performed at baseline and at 1, 3, and 9 months.
- Clinical signs of hypothyroidism and cholesterol levels were monitored.
Main Results:
- Within 1 month, significant decreases in T4, free T4 index, and rT3, and increases in T3 and the T3/T4 ratio were observed.
- These thyroid profile changes peaked at 1 month and gradually returned to baseline between 3-12 months.
- No clinical hypothyroidism, altered baseline or TRH-stimulated TSH levels, or elevated cholesterol were noted.
Conclusions:
- Clinically significant hypothyroidism is uncommon in most initially euthyroid children receiving GH therapy.
- Thyroxine (T4) supplementation is rarely necessary for these patients.
- Acute, transient thyroid axis alterations occur but do not typically lead to overt hypothyroidism.
Abstract:
The occurrence of central hypothyroidism in previously euthyroid children during GH therapy has been reported with widely varying incidence. We monitored the acute effects on the hypothalamic-pituitary-thyroid axis in 15 euthyroid children with classic GH deficiency during the first year of GH therapy. All were initially euthyroid, as assessed by normal baseline TSH, T4, free T4, and T3 levels and negative antithyroid antibodies. A thyroid profile (T4, free T4 index, T3, rT3, and TSH) was performed at baseline and 1, 3, 6, 9, and 12-15 months after GH therapy began; a TRH stimulation test was performed at baseline and after 1, 3, and 9 months of therapy. By 1 month, there were significant decreases in T4, free T4 index, and rT3, and significant increases in T3 and the T3/T4 ratio. The changes from baseline values were greatest at 1 month, were almost universal for all thyroid values, and showed a gradual return to baseline from 3-12 months. There were no clinical signs of hypothyroidism and no change in baseline or TRH-stimulated TSH levels or in cholesterol levels, and all patients grew at velocities expected for the treatment schedule. There is little evidence for the development of clinically significant hypothyroidism in the great majority of initially euthyroid patients after GH therapy is begun. T4 supplementation is seldom needed in such patients.
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