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Euthyroid hypothyrotropinemia in children of short stature
T Sato1, H Hashimoto, K Miyagawa
1Department of Pediatrics, School of Medicine, Kanazawa University.
Insights
This study describes two children with short stature, exhibiting low thyroid-stimulating hormone (TSH) levels despite normal thyroid function. Their pituitary glands showed resistance to thyrotropin-releasing hormone (TRH), suggesting a unique pituitary-thyroid state potentially linked to intrauterine growth retardation (IUGR).
Area of Science:
- Pediatric Endocrinology
- Neuroendocrinology
- Growth Disorders
Background:
- Investigating rare endocrine disorders in children with short stature.
- Understanding the complex regulation of thyroid-stimulating hormone (TSH) secretion.
- Exploring the role of intrauterine growth retardation (IUGR) in endocrine development.
Observation:
- Two children presented with short stature, normal growth post-infancy, and normal growth hormone secretion.
- Absence of TSH response to TRH stimulation was noted, despite normal serum thyroid hormone levels.
- Exaggerated prolactin response to TRH and preserved TSH response to high-dose TRH stimulation were observed.
Findings:
- The children demonstrated hypothyrotropinemia with preserved euthyroidism, indicating a unique pituitary-thyroid state.
- Thyrotrophs appeared resistant to TRH stimulation, with a high pituitary setpoint for TSH release.
- Stanozolol treatment in one case accelerated growth and decreased T4, without altering TSH response to TRH.
Implications:
- This pituitary-thyroid state, characterized by TRH resistance, may be influenced by a history of IUGR.
- Further research is needed to elucidate the exact mechanisms maintaining euthyroidism in such cases.
- Findings contribute to understanding the intricate feedback mechanisms between the pituitary and thyroid glands in growth and development.
Abstract:
Unique association of hypothyrotropinemia with euthyroidism was described in 2 children of short stature. Both had a history of intrauterine growth retardation (IUGR), but showed an appropriate growth rate after infancy (5 cm/y). Growth hormone secretion after provocation tests was normal, whereas TSH response to TRH was absent. With a highly sensitive TSH radioimmunoassay (RIA) and a specific RIA for TSH-alpha-subunit, both responded to a high dose of TRH stimulation. Serum thyroid hormones were within the normal range, while prolactin response to TRH was exaggerated. Exogenous thyroxine (T4) supplement in case 1 did not improve his growth rate, indicating absence of hypothyroidism. Case 2 was treated with stanozolol, which accelerated his growth velocity to 8 cm/y. During the treatment, serum T4 gradually decreased to 50% of the initial level, but blunted TSH response to TRH remained unchanged. These results indicate that their thyrotrophs are resistant to TRH stimulation and the pituitary setpoint of TSH release is unusually high. The exact mechanism involved in maintaining euthyroidism despite hypothyrotropinemia remains to be elucidated, but a common history of IUGR appears to play a role in producing this pituitary-thyroid state.