SFEBES2025 Poster Presentations Bone and Calcium (25 abstracts)
Vimut-Theptarin Hospital, Bangkok, Thailand
Background: Calcium-Alkali Syndrome (CAS) characterized by the triad of hypercalcemia, renal impairment, and metabolic alkalosis often occurred in patients receiving calcium and vitamin D supplementation for bone health. Here, we present a case of acute CAS following postsurgical hypocalcemia.
Clinical case: A 52-year-old female presented with a 3-day history of vomiting and abdominal discomfort. Her recent medical history included postsurgical hypoparathyroidism following thyroidectomy due to huge thyroid goiter in the previous week. Pathology of thyroid gland revealed oncocytic adenoma of thyroid. She was prescribed 5,400 mg of elemental calcium carbonate and 1.5 µg of calcitriol per day at the time of discharge after switching from intravenous calcium gluconate. Her latest plasma calcium was 8.3 mg/dL with low plasma intact parathyroid hormone (iPTH) level at 4.2 pg/ml. She denied intake of diuretics, other supplements, antacids, or NSAIDs. Initial investigations showed severe hypercalcemia, metabolic alkalosis, slightly impaired renal function but normal plasma potassium and phosphate levels (plasma calcium 18.6 mg/dL). Plasma iPTH was still low at 3.5 pg/mL and plasma 25-OH vitamin D level was 61 ng/ml. Calcium and vitamin D supplements were suspended and hypercalcemia resolved within 3 days after aggressive intravenous fluids and subcutaneous calcitonin injection. However, hypocalcemia with ongoing hypoparathyroidism developed and intravenous calcium gluconate was required. The plasma calcium levels normalized, and the renal function improved to the baseline. At 1 month later, she was asymptomatic with a normal plasma calcium and recovery of parathyroid function. Finally, she was diagnosed with acute CAS as a consequence of oral calcium carbonate and transient hypoparathyroidism following total thyroidectomy.
Conclusions: Individuals with postsurgical hypoparathyroidism requiring calcium and active vitamin D supplementation could develop CAS at any stage of hypoparathyroidism. Close monitoring of calcium levels are required, especially when high doses of active vitamin D are administered.