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Age-related patterns of thyroid-stimulating hormone response to thyrotropin-releasing hormone stimulation in Down
Insights
Children with Down syndrome show higher thyroid-stimulating hormone levels, indicating potential thyroid dysfunction. This exaggerated response normalizes by age three, suggesting developmental delays in the hypothalamic-pituitary-thyroid axis.
Area of Science:
- Endocrinology
- Pediatrics
- Genetics
Background:
- Down syndrome is associated with an increased risk of thyroid dysfunction.
- The hypothalamic-pituitary-thyroid axis regulation in individuals with Down syndrome requires further investigation.
Purpose of the Study:
- To evaluate thyroid function in infants and children with Down syndrome.
- To assess the response to thyrotropin-releasing hormone (TRH) stimulation in this population.
Main Methods:
- Thyroid function was assessed in 47 infants and children with Down syndrome (ages 1 month to 7 years) using the TRH test.
- Basal levels of thyroxine (T4), triiodothyronine (T3), and thyroid-stimulating hormone (TSH) were measured.
- TSH response to TRH stimulation was analyzed, with a subset undergoing longitudinal follow-up.
Main Results:
- Mean basal T4 and T3 levels were within normal ranges; all thyroid antibody titers were negative.
- Mean basal TSH levels were significantly higher in subjects with Down syndrome compared to age-matched controls.
- Peak TSH response to TRH stimulation was significantly greater in children with Down syndrome.
Conclusions:
- Individuals with Down syndrome exhibit an exaggerated TSH response to TRH, suggesting altered thyroid regulation.
- This exaggerated response appears to normalize by age three, potentially indicating delayed maturation of the hypothalamic-pituitary-thyroid axis.
- Thyroid dysfunction during infancy or delayed axis maturation are proposed mechanisms for these findings.
Abstract:
Thyroid function in subjects with Down syndrome was studied using the thyrotropin-releasing hormone test. Forty-seven infants and children with Down syndrome were investigated. Ages ranged from 1 month to 7 years; there were 26 boys and 21 girls. Fourteen of the subjects with Down syndrome who had an exaggerated thyroid-stimulating hormone response to thyrotropin-releasing hormone stimulation had two or more annual follow-up tests. The remaining 33 subjects who only underwent one thyrotropin-releasing hormone test were compared with 22 age-matched controls (11 boys and 11 girls). Mean basal thyroxine 4 and triiodothyronine 3 values were in the normal ranges. All thyroid antibody titers were negative. Mean basal thyroid-stimulating hormone levels of subjects with Down syndrome were significantly higher than those of controls for all ages, even though there was a decline in thyroid-stimulating hormone levels in both groups. Peak thyroid-stimulating hormone response levels were significantly greater in the subjects with Down syndrome than in the controls. Longitudinal study of the 14 children with Down syndrome with an exaggerated thyroid-stimulating hormone response showed that the response remained exaggerated until the third year of life, when it declined to normal levels. Thyroid dysfunction during the growth spurt of infancy or delayed maturation of the hypothalamic pituitary thyroid axis are proposed mechanisms.