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Bone mass in children with congenital hypothyroidism treated with thyroxine since birth
S W Kooh1, L Brnjac, R M Ehrlich
1Department of Pediatrics and Physics, University of Toronto, Ontario, Canada.
Insights
Congenital hypothyroidism (CH) treatment with high-dose thyroxine in childhood does not negatively impact bone mass. Bone mineral density in treated CH patients remains within normal ranges, comparable to sibling controls.
Area of Science:
- Pediatric Endocrinology
- Bone Metabolism
- Thyroid Disorders
Background:
- Congenital hypothyroidism (CH) requires early and often high-dose thyroxine replacement therapy.
- Potential long-term effects of high-dose thyroxine on bone health in children are not fully understood.
Purpose of the Study:
- To investigate whether large doses of thyroxine treatment early in life adversely affect bone mass in children with CH.
Main Methods:
- Bone mass was measured using dual-energy X-ray absorptiometry (DXA) in 20 CH patients treated since birth.
- Bone mineral density (BMD) and height-adjusted bone mineral content (BMC) were compared to nine sibling controls.
Main Results:
- CH patients exhibited normal bone mineral density, comparable to both population and sibling controls.
- Height-adjusted bone mineral content in patients was equivalent to expected values in siblings.
- Thyroid function and calcium homeostasis markers were normal at the time of assessment.
Conclusions:
- High-dose thyroxine therapy for congenital hypothyroidism does not appear to cause osteopenia in childhood.
- Early and continuous thyroxine treatment is safe for bone development in CH patients.
Abstract:
To determine whether the large doses of thyroxine treatment early in life adversely affect bone mass, we measured bone mass of 20 congenital hypothyroid (CH) patients (8.4 +/- 2.2 years) who were diagnosed and treated since birth. Starting thyroxine dose and current dose were 8.5 +/- 1.9 micrograms/kg/day and 3.1 + 1.2 micrograms/kg/day respectively. Thyroid function and serum biochemical tests for calcium homeostasis were normal at the time of study. Bone mass was measured by dual energy X-ray absorptiometry. Nine siblings served as controls. The patients' bone mineral density was within the normal range of population controls, and was not different from the sibling controls. The patients also had height-adjusted bone mineral content equal to the expected height-adjusted values in the siblings. Our studies indicate that the large doses of thyroxine therapy for CH do not cause osteopenia in childhood.