Faculty of Medicine, Universiti Teknologi MARA, Sungai Buloh, Malaysia.
J Med Case Rep. 2023 Mar 2;17(1):73. doi: 10.1186/s13256-023-03764-w.
Denosumab is known to cause abnormalities in calcium homeostasis. Most of such cases have been described in patients with underlying chronic kidney disease or severe vitamin D deficiency. Previous bariatric surgery could also contribute to hypocalcemia and deterioration in bone health.
We present a case of a 61-year-old Malay female with worsening bilateral limb weakness, paresthesia, and severe carpopedal spasm a week after receiving subcutaneous denosumab for osteoporosis. She had a history of gastric bypass surgery 20 years ago. Post gastric bypass surgery, she was advised and initiated on lifelong calcium, vitamin D, and iron supplementations that she unfortunately stopped taking 5 years after surgery. Her last serum blood tests, prior to initiation on denosumab, were conducted in a different center, and she was told that she had a low calcium level; hence, she was advised to restart her vitamin and mineral supplements. Laboratory workup revealed severe hypocalcemia (adjusted serum calcium of 1.33 mmol/L) and mild hypophosphatemia (0.65 mmol/L), with normal magnesium and renal function. Electrocardiogram showed a prolonged QTc interval. She required four bolus courses of intravenous calcium gluconate, and three courses of continuous infusions due to retractable severe hypocalcemia (total of 29 vials of 10 mL of 10% calcium gluconate intravenously). In view of her low vitamin D level of 33 nmol/L, she was initiated on a loading dose of cholecalciferol of 50,000 IU per week for 8 weeks. However, despite a loading dose of cholecalciferol, multiple bolus courses, and infusions of calcium gluconate, her serum calcium hovered around only 1.8 mmol/L. After 8 days of continuous intravenous infusions of calcium gluconate, high doses of calcitriol 1.5 μg twice daily, and 1 g calcium carbonate three times daily, her serum calcium stabilized at approximately 2.0 mmol/L. She remained on these high doses for over 2 months, before they were gradually titrated down to ensure sustainability of a safe calcium level.
This case report highlights the importance of screening for risk factors for iatrogenic hypocalcemia and ensuring normal levels before initiating denosumab. The patient history of bariatric surgery could have worsened the hypocalcemia, resulting in a more severe presentation and protracted response to oral calcium and vitamin D supplementation.
地舒单抗已知可引起钙稳态异常。此类病例大多数发生在存在基础慢性肾脏病或严重维生素 D 缺乏的患者中。先前的减重手术也可能导致低钙血症和骨骼健康恶化。
我们报告了一例 61 岁马来女性病例,在骨质疏松症接受皮下注射地舒单抗一周后,出现双侧肢体无力、感觉异常和严重掌弓痉挛恶化。她 20 年前曾行胃旁路手术。手术后,她被建议并开始终身补充钙、维生素 D 和铁,但在手术后 5 年后不幸停止了服用。她在开始使用地舒单抗之前的最后一次血清血液检查是在另一家中心进行的,她被告知血钙水平较低,因此被建议重新开始服用维生素和矿物质补充剂。实验室检查显示严重低钙血症(校正血清钙 1.33mmol/L)和轻度低磷血症(0.65mmol/L),镁和肾功能正常。心电图显示 QTc 间期延长。由于严重低钙血症可回缩(总共静脉内给予 10%葡萄糖酸钙 29 支,每支 10mL),她需要进行四次静脉钙葡萄糖酸盐推注和三次连续输注。鉴于她的维生素 D 水平为 33nmol/L,她开始每周服用 50,000IU 的胆钙化醇负荷剂量,持续 8 周。然而,尽管使用了胆钙化醇负荷剂量、多次推注和葡萄糖酸钙输注,她的血清钙仍徘徊在 1.8mmol/L 左右。在连续静脉输注葡萄糖酸钙 8 天后,她开始每天两次服用 1.5μg 骨化三醇和每天三次服用 1g 碳酸钙,她的血清钙稳定在 2.0mmol/L 左右。她仍在服用这些高剂量药物超过 2 个月,然后逐渐减少剂量,以确保安全的钙水平可持续性。
本病例报告强调了在开始使用地舒单抗之前筛查医源性低钙血症的危险因素和确保正常水平的重要性。减重手术史可能使低钙血症恶化,导致更严重的表现和对口服钙和维生素 D 补充的反应延长。