Kateryna Komarovskiy1, Susan Raghavan. 1. Division of Endocrinology Metabolism and Diabetes, University of Louisville, Louisville, Kentucky, USA.
Abstract
BACKGROUND: Hypocalcemia is a rarely recognized complication of (131)I therapy that has been previously reported in only one child with Graves' disease treated with radioiodine (RAI). Here we report a second child with this occurrence. PATIENT FINDINGS: A 12-year-old African American girl with hyperthyroidism due to Graves' disease and moderate persistent asthma, requiring oral prednisone, was treated with 11.1 mCi of RAI. While normocalcemic initially, the patient developed symptomatic hypocalcemia (6.6 mg/dL), within 3 months postablation. Concomitant findings included hyperphosphatemia, an inappropriately normal parathyroid hormone (PTH) level, vitamin D deficiency, and normal axial bone mineral density. After 2 weeks of treatment with calcium and calcitriol the symptoms of hypocalcemia resolved, and the calcium level returned to normal. PTH levels remained within the reference range throughout. SUMMARY: In this child with Graves' disease, who was normocalcemic on presentation, RAI treatment was followed by compromised function of the parathyroid glands which was sufficient to produce symptomatic hypocalcemia. It is noteworthy and likely pertinent that the patient had a background of vitamin D deficiency and was receiving prednisone for asthma. CONCLUSION: Patients scheduled to receive (131)I should be evaluated for risk factors for hypocalcemia in order to minimize the likelihood of this potentially serious complication.
BACKGROUND:Hypocalcemia is a rarely recognized complication of (131)I therapy that has been previously reported in only one child with Graves' disease treated with radioiodine (RAI). Here we report a second child with this occurrence. PATIENT FINDINGS: A 12-year-old African American girl with hyperthyroidism due to Graves' disease and moderate persistent asthma, requiring oral prednisone, was treated with 11.1 mCi of RAI. While normocalcemic initially, the patient developed symptomatic hypocalcemia (6.6 mg/dL), within 3 months postablation. Concomitant findings included hyperphosphatemia, an inappropriately normal parathyroid hormone (PTH) level, vitamin Ddeficiency, and normal axial bone mineral density. After 2 weeks of treatment with calcium and calcitriol the symptoms of hypocalcemia resolved, and the calcium level returned to normal. PTH levels remained within the reference range throughout. SUMMARY: In this child with Graves' disease, who was normocalcemic on presentation, RAI treatment was followed by compromised function of the parathyroid glands which was sufficient to produce symptomatic hypocalcemia. It is noteworthy and likely pertinent that the patient had a background of vitamin Ddeficiency and was receiving prednisone for asthma. CONCLUSION:Patients scheduled to receive (131)I should be evaluated for risk factors for hypocalcemia in order to minimize the likelihood of this potentially serious complication.