Denosumab-induced hypocalcaemia in metastatic gastric cancer

2020 ◽  
pp. bmjspcare-2020-002548
Author(s):  
Craig Gouldthorpe ◽  
Richard Quinton ◽  
Donna Wakefield

Hypocalcaemia in malignancy is infrequently reported and the underlying cause is often multifactorial. Denosumab, an antiresorptive medication, can be used to treat a number of cancer-related complications including hypercalcaemia, metastatic bone pain and to reduce fracture-events. We present a case of a hospice inpatient with profound and recurring hypocalcaemia following a single denosumab infusion which required repeated hospitalisation, for intravenous calcium, alongside a prolonged course of vitamin D and electrolyte replacement. The case highlights the risk of hypocalcaemia with denosumab use, together with the need to identify and treat vitamin D deficiency in both the prevention and management of such a complication.

2005 ◽  
Vol 25 (4) ◽  
pp. 362-366 ◽  
Author(s):  
Nirav Shah ◽  
Judith Bernardini ◽  
Beth Piraino

Background Peritoneal dialysis (PD) patients are at risk for 25(OH) vitamin D deficiency due to effluent loss in addition to traditional risk factors. Objectives To measure 25(OH) vitamin D deficiency in prevalent PD patients, to evaluate a replacement dose, and to determine the effects of correction. Methods 25(OH) vitamin D levels were drawn on prevalent PD patients. Patients deficient in 25(OH) vitamin D were given ergocalciferol, 50 000 IU orally once per week for 4 weeks. Patients scored muscle weakness, bone pain, and fatigue on a scale of 0 (none) to 5 (severe). Serum calcium, phosphate, parathyroid hormone (PTH), and 25(OH) vitamin D, and 1,25(OH)2 vitamin D levels were obtained before and after treatment. Results 25(OH) vitamin D levels were measured in 29 PD patients. Deficiency (<15 ng/mL) was found in 28/29 (97%); 25/29 (86%) had undetectable levels (<7 ng/mL). One course of ergocalciferol corrected the deficiency in all but 1 patient, who required a second course. Scores for muscle weakness and bone pain fell from pre- to posttreatment ( p < 0.001). 1,25(OH)2 vitamin D levels rose post ergocalciferol (from 20 to 26 pg/mL, n = 20, p = 0.09). Serum calcium, phosphate, and PTH levels did not change with ergocalciferol. Conclusions Most PD patients had marked 25(OH) vitamin D deficiency, which was readily and safely corrected with one course of 50000 IU ergocalciferol, having no effect on serum calcium, phosphorus, or PTH, but complaints of muscle weakness and bone pain decreased. A prospective, placebo-controlled double-blinded study is needed to determine whether replacement of 25(OH) vitamin D is beneficial in PD patients.


2016 ◽  
Vol 2016 ◽  
pp. 1-4
Author(s):  
Victoria Mendoza-Zubieta ◽  
Mauricio Carvallo-Venegas ◽  
Jorge Alberto Vargas-Castilla ◽  
Nicolás Ducoing-Sisto ◽  
Alfredo Alejandro Páramo-Lovera ◽  
...  

Persistent primary hyperparathyroidism (PHPT) refers to the sustained hypercalcemia state detected within the first six months following parathyroidectomy. When it coexists with severe vitamin D deficiency, the effects on bone can be devastating. We report the case of a 56-year-old woman who was sent to this center because of persistent hyperparathyroidism. Her disease had over 3 years of evolution with nephrolithiasis and hip fracture. Parathyroidectomy was performed in her local unit; however, she continued with hypercalcemia, bone pain, and pathological fractures. On admission, the patient was bedridden with multiple deformations by fractures in thoracic and pelvic members. Blood pressure was 100/80, heart rate was 86 per minute, and body mass index was 19 kg/m2. Calcium was 14 mg/dL, parathormone 1648 pg/mL, phosphorus 2.3 mg/dL, creatinine 2.4 mg/dL, urea 59 mg/dL, alkaline phosphatase 1580 U/L, and vitamin D 4 ng/mL. She received parenteral treatment of hypercalcemia and replenishment of vitamin D. The second surgical exploration was radioguided by gamma probe. A retroesophageal adenoma of 4 cm was resected.Conclusion. Persistent hyperparathyroidism with severe vitamin D deficiency can cause catastrophic skeletal bone softening and fractures.


Bone ◽  
2011 ◽  
Vol 48 ◽  
pp. S238
Author(s):  
I. Bergström ◽  
J. Persson ◽  
A. Blanck ◽  
M. Palmér

2000 ◽  
Vol 163 (1) ◽  
pp. 187-190 ◽  
Author(s):  
PETER J. VAN VELDHUIZEN ◽  
SARAH A. TAYLOR ◽  
STEPHEN WILLIAMSON ◽  
BETTY M. DREES

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A200-A200
Author(s):  
Carlos C Becerril Romero ◽  
Rebecca Schneider Aguirre ◽  
Erik Allen Imel ◽  
Linda A DiMeglio ◽  
Anisha Gohil

Abstract Background: Diabetic ketoacidosis and significant hyperglycemia are associated with known electrolyte derangements in sodium, potassium, and phosphorus. Hypocalcemia and hypoparathyroidism occurring in uncontrolled diabetes are rare. We present a case of new-onset diabetes with severe hypocalcemia. Case: A 15-year-old obese Caucasian male with ADHD and autism presented to the Emergency room due to hyperglycemia found on laboratory evaluation for hypertension. Serum glucose was 563 mg/dL, serum bicarbonate 24 meq/L (21 - 31 meq/L), and HgbA1C 11.4% (4.0 - 5.6%). He was admitted to initiate insulin and for diabetes education. On admission, hypocalcemia was noted: serum calcium 6.6 mg/dL (8.5 - 10.5 mg/dL), alkaline phosphatase 352 units/L (48 - 277 units/L), and albumin 4.6 g/dL (3.5 - 5.0 g/dL). Repeat testing revealed serum calcium 5.1 mg/dL, phosphorus 4.3 mg/dL (2.5 - 4.5 mg/dL), and magnesium 1.7 mg/dL (1.6 - 2.9 mg/dL). He endorsed a 2 month history of tetany, paresthesia, and muscle weakness. Due to food aversions, his dietary intake of calcium and vitamin D was minimal. He had limited sun exposure. Subsequent PTH was 40 pg/mL (10 - 65 pg/mL) with concurrent serum calcium of 6.5 mg/dL. QTc was prolonged [529 msec (&lt;440 msec)], prompting transfer to the intensive care unit for telemetry, intravenous calcium gluconate, and regular calcium monitoring. Treatment was commenced with cholecalciferol 2000 international units daily and oral calcium carbonate (50 mg elemental calcium/kg/day) in divided doses for presumed Vitamin D deficiency. After several intravenous calcium gluconate doses over 24 hours, the patient’s QTc and ionized calcium normalized. At discharge, calcium was 8.5 mg/dL. He was discharged on the above regimen of calcium and cholecalciferol, and basal and bolus insulin. After discharge, laboratory results returned indicating negative diabetes autoantibodies (GAD 65, Insulin, IA-2) and 25-OH Vitamin D &lt;10 ng/mL (30 - 100ng/mL). Two days after discharge, calcium was 7.3 mg/dL. Two weeks later, labs were: 25-OH Vitamin D 11.3 ng/mL, PTH 10.4 pg/mL, and calcium 9.6 mg/dL. Conclusion: This teen presented with new-onset type 2 diabetes and symptomatic hypocalcemia, an atypical feature of new-onset diabetes. This patient’s hypocalcemia was likely due to both vitamin D deficiency and hypoparathyroidism. He had a low vitamin D level and poor calcium intake with elevated alkaline phosphatase; however, his high normal serum phosphorus and inappropriately normal PTH (instead of elevated in the setting of severe hypocalcemia) indicated a component of hypoparathyroidism. Calcium normalized with detectable 25-OH Vitamin D levels but PTH remained low. Our case highlights the importance of recognizing both that electrolyte abnormalities at diabetes onset may not be directly attributable to diabetes/hyperglycemia and that vitamin D deficiency and hypoparathyroidism may co-exist.


2012 ◽  
Vol 2012 ◽  
pp. 1-3 ◽  
Author(s):  
Robert C. Oh ◽  
Jeremy D. Johnson

Vitamin D is integral for bone health, and severe deficiency can cause rickets in children and osteomalacia in adults. Although osteomalacia can cause severe generalized bone pain, there are only a few case reports of chest pain associated with vitamin D deficiency. We describe 2 patients with chest pain that were initially worked up for cardiac etiologies but were eventually diagnosed with costochondritis and vitamin D deficiency. Vitamin D deficiency is known to cause hypertrophic costochondral junctions in children (“rachitic rosaries”) and sternal pain with adults diagnosed with osteomalacia. We propose that vitamin D deficiency may be related to the chest pain associated with costochondritis. In patients diagnosed with costochondritis, physicians should consider testing and treating for vitamin D deficiency.


2011 ◽  
Vol 6 (1-2) ◽  
pp. 209-213 ◽  
Author(s):  
Noortje M. Rabelink ◽  
Hans M. Westgeest ◽  
Nathalie Bravenboer ◽  
Maarten A. J. M. Jacobs ◽  
Paul Lips

2018 ◽  
Vol 21 (4) ◽  
pp. 788-795 ◽  
Author(s):  
Mansour Babaei ◽  
Mehdi Esmaeili Jadidi ◽  
Behzad Heidari ◽  
Hemmat Gholinia

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