Hypercalcemia upon denosumab withdrawal in primary hyperparathyroidism: a case report and literature review
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CASE REPORT
Hypercalcemia upon denosumab withdrawal in primary hyperparathyroidism: a case report and literature review C. Camponovo 1 & B. Aubry-Rozier 2 & O. Lamy 2
&
E. Gonzalez Rodriguez 2
Received: 22 June 2020 / Accepted: 6 October 2020 # The Author(s) 2020
Abstract Denosumab discontinuation is associated with a rapid increase in bone resorption and a decrease in bone mineral density. Spontaneous vertebral fractures may occur as a side effect of the rebound of bone resorption. Cases of rebound-linked hypercalcemia have also been described, moderate in women with osteoporosis and breast cancer and severe in children receiving oncological doses of denosumab. We report the case of an adult woman with primary hyperparathyroidism and moderate hypercalcemia, treated with denosumab for osteoporosis, who developed severe hypercalcemia and spontaneous vertebral fractures (SVFs) after denosumab discontinuation. An 86-year-old woman with densitometric osteoporosis was treated for 3 years with 60 mg of subcutaneous denosumab every 6 months. She was known to have primary hyperparathyroidism, with a serum albumin-corrected calcium of 2.82 mmol/l (NV 2.15–2.5) at the end of denosumab effect. Nine months after the last denosumab injection, she was hospitalized due to worsening overall health. Clinical evaluation revealed severe hypercalcemia (calcium 3.35 mmol/l). Very high values of bone turnover markers (BTMs) suggested a rebound effect due to denosumab discontinuation. An X-ray showed multiple new SVFs. After injection of denosumab 60 mg, serum calcium rapidly decreased and BTMs were dramatically reduced. A surgical approach by minimally invasive parathyroidectomy allowed for definite resolution of hyperparathyroidism and hypercalcemia. This case suggests that hypercalcemia can be a side consequence of denosumab discontinuation, which can become severe when other causes of hypercalcemia, such as primary hyperparathyroidism, are present. Keywords Bone turnover markers . Case report . Denosumab discontinuation . Hypercalcemia . Hyperparathyroidism . Osteoporosis
Introduction Denosumab, a fully human monoclonal antibody that blocks the receptor activator of nuclear factor k-B ligand (RANKL), is a potent anti-resorptive osteoporosis treatment. Due to its reversible mode of action, bone turnover markers (BTMs) increase rapidly after its discontinuation, accompanied by a quick loss of bone mineral density (BMD) [1]. Spontaneous vertebral fractures (SVFs) have been described in this
* E. Gonzalez Rodriguez [email protected] 1
2
situation and a causative link to the rebound of bone resorption has been suggested [2]. Cases of rebound-linked hypercalcemia have also been described after denosumab discontinuation, from completely asymptomatic [3, 4] to severe clinical consequences [5–13]. Only two cases have been described in patients with moderate symptoms treated with denosumab for osteoporosis [4, 14]; all other patients had received denosumab at high (oncological) and/or frequent (minimum every 3 months) d
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