SUN-768 Treatment of Sarcoidosis Precipitated Severe Hypocalcemia, Unmasking Post Surgical Hypoparathyroidism

Abstract Disclosure: M. Malik: None. S. Minhas: None. N. Bielawski: None. M. Deshmukh: None. Introduction:Patients undergoing total thyroidectomy have a risk of developing transient or permanent hypoparathyroidism requiring monitoring of calcium levels and possible lifelong treatment. Hypocalcemia can be unmasked when these patients undergo steroid treatment for other conditions, such as sarcoidosis. Case:A 66-year-old female with a medical history of follicular-variant papillary thyroid carcinoma post total thyroidectomy and radioactive iodine ablation in 2013, postsurgical hypothyroidism and hypoparathyroidism, sarcoidosis presented to emergency department with perioral numbness, twitching and muscle cramps of two weeks’ duration. Evaluation revealed presence of Chvostek’s sign and corrected serum calcium level of 5.5 mg/dL verified on repeat measurement. ionized Ca 0.67 mg/dl (4.8-5.6 mg/dl), phosphorus 6.2 mg/dl, parathyroid hormone of 2.6, 25-hydroxy vitamin D of 21, and 1,25 dihydroxyvitamin D of 8.8 (24.8-81.5 pg/ml) Postsurgical hypoparathyroidism-related hypocalcemia had initially been managed with calcitriol until 2018, when she was noted to have hypercalcemia and diagnosed with sarcoidosis. At that time, calcitriol was discontinued. She was started on prednisone 30 mg once daily 25 days prior to presentation for treatment of sarcoidosis when her calcium level was noted to increase to 11.0 mg/dl. She received intravenous calcium infusion with resolution of symptoms and improvement of calcium to 9.3 mg/dL. Prednisone was held and patient discharged on calcitriol, vitamin D, and calcium supplementation. Discussion: Glucocorticoids are a mainstay in the treatment of sarcoidosis due to effects on calcium homeostasis. In patients with sarcoidosis, pulmonary alveolar macrophages synthesize 1,25-dihydroxyvitamin D from 25-hydroxy vitamin D in the absence of interferon gamma or lipopolysaccharide activation, resulting in hypercalcemia. Treatment with glucocorticoids can decrease intestinal absorption of calcium by decreasing the expression of calcium receptors in the duodenum and by opposing the effects of vitamin D. At prednisone doses of 20 mg to 40 mg daily, lowering of serum calcium level can be seen within two to five days of treatment. In patients with primary hypoparathyroidism, impaired response of parathyroid hormone to this net negative calcium balance can result in severe hypocalcemia.In this case, the presence of sarcoidosis had masked the hypocalcemia resulting from postsurgical hypoparathyroidism. Initiation of prednisone for treatment of sarcoidosis precipitated severe symptomatic hypocalcemia requiring hospitalization. Intravenous calcium and glucocorticoid discontinuation can treat this complication in the hospital. Calcitriol, calcium and vitamin D supplementation should be considered for patients with co-existing sarcoidosis undergoing glucocorticoid treatment with close monitoring of serum calcium levels Presentation: Sunday, July 13, 2025