DOI 10.1515/jpem-2013-0322 J Pediatr Endocr Met 2014; 27(3-4): 379–382
Patient report Oksana Lazarevaa, Aristotle Panayiotopoulosa, Irina Kazachkova and Elka Jacobson-Dickman*
A teenage boy with hypocalcemia after radioablation for Graves’ disease 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. Keywords: Graves’ disease; hungry bone syndrome; hypocalcemia. Oksana Lazareva and Aristotle Panayiotopoulos are co-first authors. *Corresponding author: Elka Jacobson-Dickman, MD, Division of Pediatric Endocrinology, Department of Pediatrics, State University of New York Downstate Medical Center, 450 Clarkson Avenue, Box 49, Brooklyn, NY 11203, USA, E-mail: [email protected] Oksana Lazareva: Division of Pediatric Endocrinology, Inova Fairfax Hospital for Children, Department of Pediatrics, Fairfax, VA, USA Aristotle Panayiotopoulos and Irina Kazachkova: Division of Pediatric Endocrinology, Infants and Children’s Hospital of Brooklyn at Maimonides, Department of Pediatrics, Brooklyn, NY, USA a
Introduction Hypocalcemia is a recognized complication of surgical, medical, and radioactive iodine (131I) therapy (RAI) for Graves’ disease, seemingly due to subsequent functional
or relative hypoparathyroidism (1–3). Excessive thyroid hormone stimulates osteoblast-mediated bone turnover in favor of bone resorption (4); patients with untreated hyperthyroidism often have consequent bone mineral density (BMD) loss known as ‘thyroid osteodystrophy’ (5). Acute reversal of bone resorption can lead to hungry bone syndrome (HBS), a state of rapid calcium deposition into newly synthesized osteoid, resulting in potentially lifethreatening hypocalcemia. HBS is most frequently recognized as an outcome of rapid correction of vitamin D deficiency. Our case demonstrates hypocalcemia post-RAI in the presence of elevated parathyroid hormone (PTH), suggesting HBS due to the sudden correction of hyperthyroidism. This report highlights the risk of HBS and severe hypocalcemia following treatment for Graves’ disease in pediatric patients, particularly in the setting of coexisting vitamin D deficiency.
Case presentation A 16-year-old boy with Graves’ disease presented to his pediatric endocrinologist 11 weeks post-RAI with bilateral hand tetany. At age 15 years 10 months, he had been diagnosed with hyperthyroidism due to Graves’ disease (Thyroid Stimulating Hormone [TSH],
Patient report Oksana Lazarevaa, Aristotle Panayiotopoulosa, Irina Kazachkova and Elka Jacobson-Dickman*
A teenage boy with hypocalcemia after radioablation for Graves’ disease 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. Keywords: Graves’ disease; hungry bone syndrome; hypocalcemia. Oksana Lazareva and Aristotle Panayiotopoulos are co-first authors. *Corresponding author: Elka Jacobson-Dickman, MD, Division of Pediatric Endocrinology, Department of Pediatrics, State University of New York Downstate Medical Center, 450 Clarkson Avenue, Box 49, Brooklyn, NY 11203, USA, E-mail: [email protected] Oksana Lazareva: Division of Pediatric Endocrinology, Inova Fairfax Hospital for Children, Department of Pediatrics, Fairfax, VA, USA Aristotle Panayiotopoulos and Irina Kazachkova: Division of Pediatric Endocrinology, Infants and Children’s Hospital of Brooklyn at Maimonides, Department of Pediatrics, Brooklyn, NY, USA a
Introduction Hypocalcemia is a recognized complication of surgical, medical, and radioactive iodine (131I) therapy (RAI) for Graves’ disease, seemingly due to subsequent functional
or relative hypoparathyroidism (1–3). Excessive thyroid hormone stimulates osteoblast-mediated bone turnover in favor of bone resorption (4); patients with untreated hyperthyroidism often have consequent bone mineral density (BMD) loss known as ‘thyroid osteodystrophy’ (5). Acute reversal of bone resorption can lead to hungry bone syndrome (HBS), a state of rapid calcium deposition into newly synthesized osteoid, resulting in potentially lifethreatening hypocalcemia. HBS is most frequently recognized as an outcome of rapid correction of vitamin D deficiency. Our case demonstrates hypocalcemia post-RAI in the presence of elevated parathyroid hormone (PTH), suggesting HBS due to the sudden correction of hyperthyroidism. This report highlights the risk of HBS and severe hypocalcemia following treatment for Graves’ disease in pediatric patients, particularly in the setting of coexisting vitamin D deficiency.
Case presentation A 16-year-old boy with Graves’ disease presented to his pediatric endocrinologist 11 weeks post-RAI with bilateral hand tetany. At age 15 years 10 months, he had been diagnosed with hyperthyroidism due to Graves’ disease (Thyroid Stimulating Hormone [TSH],
