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Bone mineralization and calciotropic hormones in children with hyperthyroidism. Effects of methimazole therapy
G Saggese1, S Bertelloni, G I Baroncelli
1Istituto di Clinica Pediatrica, Università di Pisa, Italy.
Insights
Thyrotoxicosis in children disrupts bone mineralization and calcium balance, but methimazole therapy reverses these effects. Treatment normalizes vitamin D metabolism, restoring bone health and calcium homeostasis.
Area of Science:
- Pediatric Endocrinology
- Bone Metabolism
- Mineral Homeostasis
Background:
- Hyperthyroidism in children significantly impacts bone mineralization and calcium homeostasis.
- Assessing the effects of thyrotoxicosis and its treatment on mineral metabolism is crucial for pediatric endocrine care.
Observation:
- Two young girls with hyperthyroidism exhibited severe osteoporosis, decreased 1,25(OH)2D, and altered calcium/phosphate levels.
- Thyroid function tests, osteocalcin, and bone mineral content (BMC) were significantly affected by the condition.
Findings:
- Methimazole therapy led to euthyroidism, normalizing 1,25(OH)2D and intact PTH levels.
- Calcium and phosphate levels decreased, while osteocalcin returned to normal within a year.
- Bone mineral content (BMC) and BMC/Body Weight (BMC/BW) showed gradual recovery, reaching normal ranges within two years.
Implications:
- Hyperthyroidism causes reversible disturbances in vitamin D metabolism and mineral homeostasis.
- Treatment normalizes mineral metabolism and promotes recovery of bone mineralization in pediatric patients.
- Osteocalcin levels serve as a valuable indicator for monitoring bone metabolism during hyperthyroidism treatment.
Abstract:
We studied bone mineralization and calcium homeostasis in two children with hyperthyroidism before and during 3 yr of methimazole therapy in order to evaluate the effects of thyrotoxicosis and its therapy on mineral metabolism. Case 1, female, 4.1 year old with hyperthyroidism from 6 months. Biochemical data: increased thyroid function, phosphate and osteocalcin, decreased 1,25(OH)2D levels. X-ray: severe osteoporosis; bone mineral content (BMC) -23.0%, BMC/BW -25.1%. Case 2, female, 7.4 year old with hyperthyroidism from 9 months. Biochemical data: thyroid function, ionized calcium and osteocalcin were increased, 1,25(OH)2D and intact PTH were decreased. X-ray: severe osteoporosis: BMC -32.8%, BMC/BW -36.0. After the patients were euthyroid, they showed an increase of 1,25(OH)2D and intact PTH into normal values and a fall in calcium and phosphate. Osteocalcin levels returned in normal range one yr after first evaluation. Bone mineral analysis showed no variation of BMC and BMC/BW in the first 6 months of therapy and an increase in the following 6 months. In the following two years BMC and BMC/BW rose to normal range. Our study provides further evidence that in hyperthyroidism an altered mineral homeostasis is present with a reversible disturbance in vitamin D metabolism. We found that the return to euthyroidism was associated with a normalization of mineral homeostasis and with a recovery of bone mineralization. Osteocalcin assay may be an useful index to monitor bone metabolism in hyperthyroidism.
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