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Hypercalcemia in infants with congenital hypothyroidism and its relation to vitamin D and thyroid hormones
Insights
Mild hypercalcemia in infants with congenital hypothyroidism may stem from residual thyroid function before treatment. During thyroxine therapy, it is linked to vitamin D supplementation, not altered vitamin D metabolism.
Area of Science:
- Pediatric Endocrinology
- Neonatal Metabolism
- Thyroid Disorders
Background:
- Congenital hypothyroidism (CH) is a condition requiring timely treatment.
- Infants with CH may experience metabolic disturbances.
- The relationship between CH, thyroid function, and calcium/vitamin D metabolism needs clarification.
Purpose of the Study:
- To investigate calcium, phosphorus, and vitamin D metabolite levels in infants with CH.
- To differentiate causes of hypercalcemia before and during thyroxine therapy.
Main Methods:
- Assessed serum calcium, phosphorus, and vitamin D metabolites in 25 infants with CH.
- Measurements were taken before treatment and during the first 6 months of thyroxine therapy.
Main Results:
- Five infants showed mild hypercalcemia before treatment; four during early therapy.
- Pre-treatment hypercalcemia was associated with residual thyroid secretion, not vitamin D status.
- Hypercalcemia during therapy correlated with vitamin D supplementation, independent of measured vitamin D metabolites.
Conclusions:
- Residual thyroid secretion may cause hypercalcemia in untreated CH infants.
- Vitamin D supplementation, not altered metabolism, appears linked to hypercalcemia during CH treatment.
- Further research into CH-associated mineral and vitamin D interactions is warranted.
Abstract:
The circulating concentrations of calcium, phosphorus, and vitamin D metabolites were measured in 25 infants (fifteen to 30 days of age) with congenital hypothyroidism before treatment or during the first 6 months of thyroxine therapy. Five of the children before treatment and four during the early 3 months of treatment had mild hypercalcemia (10.8 to 12.4 mg/dl). Hypercalcemia before treatment did not appear to be related to the vitamin D status of the infant nor to an alteration in vitamin D metabolism, but to the presence of a residual thyroid secretion. In contrast, hypercalcemia during thyroxine therapy was related to vitamin D supplementation, even though the serum calcium concentration could not be correlated with the circulating concentration of any of the vitamin D metabolites assayed and obvious changes in vitamin D metabolism could not be demonstrated.