Endocrine Abstracts

JOINT862

Introduction: Graves’ disease (GD) is the leading cause of hyperthyroidism in children and the most common etiology of thyrotoxicosis. Clinical manifestations resulting from excessive thyroid hormone production affect multiple systems. Among these, disturbances of mineral homeostasis, particularly calcium, phosphorus, and magnesium, are often overlooked. Increased osteoclast numbers and activity driven by excess thyroid hormones contribute to these changes. Hypercalcemia occurs in approximately 20% of patients with hyperthyroidism and is usually mild and asymptomatic. Severe hypercalcemia is rare but requires immediate intervention to prevent serious complications, including nephrocalcinosis, cardiac dysfunction, and skeletal abnormalities.

Case: An 8 years and 11 months old girl was admitted to our hospital due to persistent nausea and vomiting for the past month. Seven months prior to admission, she visited the hospital due to 2 episodes of unprovoked seizure and started to take the antiseizure medication. After 1 month of medication, she was hospitalized for drug reaction with eosinophilia and systemic symptoms (DRESS) syndrom and was treated with intravenous (IV) corticosteroids. During the tapering period of steroid treatment, she developed new-onset facial palsy that progressed to bilateral lower extremity weakness, leading to re-admission and a diagnosis of acute inflammatory demyelinating polyneuropathy (AIDP). During admission, she was treated with IV immunoglobulin (IVIG) and IV corticosteroids, which was gradually tapered over 2 weeks. One month prior to admission, after discontinuation of corticosteroids, nausea and vomiting occurred. Both symptoms temporarily improved after IV hydration, but recurred and persisted for more than a month. Thyroid function tests revealed elevated T3 and free T4 levels with suppressed TSH. Thyroid autoantibody testing, thyroid ultrasonography, and scintigraphy showed results consistent with GD. Complete blood count, serum electrolytes, and liver function test results were all within normal limits. However, abnormalities of mineral metabolism, including hypercalcemia, hypophosphatemia, hypomagnesemia, and decreased serum alkaline phosphatase levels, have been identified. Intravenous hydration with diuretics and steroid therapy, and antithyroid medications led to rapid improvement in clinical symptoms and normalization of mineral and thyroid hormone levels. During the 7-month follow-up period, the patient continued to take antithyroid medications and remained in good condition.

Conclusion: This is a case of severe hypercalcemia manifested in a new-onset pediatric GD. This case demonstrates that severe hypercalcemia, although rare, has clinical significance in pediatric GD and highlights the importance of performing thyroid function tests in addition to calcium monitoring in patients with persistent nausea and vomiting.