SAT-746 - Multifactorial Refractory Hypocalcemia after Total Thyroidectomy for Graves' Disease: Hungry Bone Syndrome Unmasked by Celiac Disease

Post-thyroidectomy hypocalcemia is a common complication, typically attributed to transient or permanent hypoparathyroidism. In patients with severe thyrotoxicosis, other mechanisms such as hungry bone syndrome (HBS) and electrolyte disturbances may predominate, leading to refractory hypocalcemia and recurrent readmissions if unrecognized.

A 31-year-old woman with Graves’ disease was referred for endocrine evaluation due to persistent hyperthyroidism despite methimazole therapy, with emergency visits for palpitations and chest pain. Laboratory evaluation showed suppressed TSH with markedly elevated free T4 and total T3. Thyroid ultrasound demonstrated a diffusely enlarged, hypervascular gland, and thyroid-stimulating immunoglobulin was positive. She reported ocular symptoms consistent with thyroid eye disease.

Preoperatively, she had no history of calcium or parathyroid disease, normal renal function, and normal serum calcium (8.5 mg/dL), though vitamin D deficiency (25-OH vitamin D 22 ng/mL) was present. Prior records revealed hypomagnesemia (1.7 mg/dL) with QTc prolongation, suggesting baseline magnesium vulnerability.

She underwent total thyroidectomy with documented identification and preservation of the parathyroid glands. Postoperatively, she developed severe hypocalcemia beginning on postoperative day zero, with calcium nadir of 5.7 mg/dL and ionized calcium to 0.75 mmol/L, persistent hypomagnesemia, high-normal phosphorus, and initially low-normal PTH (22–23 pg/mL). Her course was complicated by significant QTc prolongation exceeding 520 ms requiring ICU admission and intravenous calcium and magnesium replacement.

Despite therapy, she experienced recurrent symptomatic hypocalcemia requiring multiple readmissions. PTH levels subsequently normalized, arguing against permanent hypoparathyroidism. Alkaline phosphatase was markedly elevated (three times the upper limit of normal), indicating high bone turnover. In the setting of severe hyperthyroidism and recovering PTH, findings supported HBS due to reversal of thyrotoxic osteodystrophy. Further evaluation revealed markedly elevated tissue transglutaminase IgA (>600 U/mL; normal < 10), confirming celiac disease and suggesting malabsorption as a contributing factor.

Hungry bone syndrome is an underrecognized cause of post-thyroidectomy hypocalcemia. This case highlights the importance of identifying preoperative risk factors, including severe thyrotoxicosis, high bone turnover, nutritional deficiencies, and coexisting autoimmune disease; as this may reduce morbidity, prevent recurrent admissions, and guide anticipatory management.

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