A teenage boy with hypocalcemia after radioablation for Graves’ disease
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Oksana Lazareva
Abstract
Excessive thyroid hormone production, as seen in Graves’ disease, stimulates osteoblast-mediated bone turnover in favor of bone resorption. Acute reversal of bone resorption can lead to hungry bone syndrome (HBS), a state of rapid calcium deposition into newly synthesized osteoid resulting in hypocalcemia. Hypocalcemia due to subsequent functional or relative hypoparathyroidism is a recognized complication of therapy for Graves’ disease. HBS is most recognized as an outcome of rapid correction of vitamin D deficiency or of acute hypoparathyroidism in cases of parathyroid gland function disruption after surgical removal of the thyroid. We report the case of an adolescent boy with Graves’ disease who presented with hypocalcemia after radioactive iodine (131I) therapy due to HBS. Our report highlights the risk of HBS and severe hypocalcemia following treatment for Graves’ disease in pediatric patients and also underscores the importance of pretreatment assessment and intervention for coexistent vitamin D deficiency.
Acknowledgments
The authors acknowledge Dr. Harald Jüppner for his generous guidance in the preparation of this manuscript.
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©2014 by Walter de Gruyter Berlin Boston
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