Severe hypercalcaemia in a child secondary to use of alternative therapies

Boyd, Catriona; Moodambail, Abdul

doi:10.1136/bcr-2016-215849

Cited by 6 publications

(5 citation statements)

References 8 publications

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“…Neurological manifestations like hypotonia, hyporeflexia, and encephalopathy as present in our case are less commonly reported. 2 , 3 , 4 , 5 , 6 , 7 , 8 , 9 , 10 Vitamin D intoxication may be incidentally detected due to hypercalcemia. 11 , 12 …”

Section: Discussionmentioning

confidence: 99%

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Vitamin D Intoxication Presenting as Subacute Encephalopathy—A Case Report

Naik

Jagzape

Sunil

2021

Child Neurology Open

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Vitamin D intoxication is uncommon in children and is more commonly suspected in the setting of ingestion of high doses of vitamin D. Its manifestations can be non specific and varied ranging from mild like constipation and vomiting to life threatening like arrhythmias and encephalopathy. Here we present a 14 month female who presented with loss of milestones, floppiness, and poor interaction with mother. She was detected to have hypercalcemia and was subsequently diagnosed with vitamin D intoxication. She was successfully treated with hydration, furosemide, prednisolone and frequent monitoring of electrolytes, electrocardiography and volume status. Subsequently as her serum calcium levels normalized with therapy, she became alert, conscious and started achieving developmental milestones.

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Section: Discussionmentioning

confidence: 99%

“…Neurological manifestations like hypotonia, hyporeflexia, and encephalopathy as present in our case are less commonly reported. 2,3,4,5,6,7,8,9,10 Vitamin D intoxication may be incidentally detected due to hypercalcemia. 11,12 Primary hyperparathyroidism presents with similar features, but has high PTH and low phosphorus levels.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D Intoxication Presenting as Subacute Encephalopathy—A Case Report

Naik

Jagzape

Sunil

2021

Child Neurology Open

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“…The risk of hypocalcemia during the first 2–4 weeks after injection could be compensated in our patients by oral calcium substitution. Recently a rebound hypercalcemia after Denosumab effect ceased has become a reason of concern [22–24]. We monitored calcium excretion and detected a reduction of hypercalcemia in those patients which were sufficiently treated with longer intervals between Denosumab injections.…”

Section: Discussionmentioning

confidence: 99%

Individualized treatment with denosumab in children with osteogenesis imperfecta – follow up of a trial cohort

Hoyer‐Kuhn

Rehberg

Netzer

et al. 2019

Orphanet J Rare Dis

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Background Osteogenesis imperfecta (OI) is a rare disease leading to hereditary bone fragility. Nearly 90% of cases are caused by mutations in the collagen genes COL1A1/A2 (classical OI) leading to multiple fractures, scoliosis, short stature and nonskeletal findings as blue sclera, hypermobility of joints, bone pain and delayed motor function development. Bisphosphonates are used in most moderate and severely affected patients assuming that an increase of bone mineral density might reduce fractures and bone pain in patients with OI. Denosumab as a RANK ligand antibody inhibiting osteoclast maturation has been approved for osteoporosis treatment in adults. First data from small clinical trials promised a high efficacy of Denosumab in children with OI. Aim of this analysis was a retrospective evaluation of an individualized biomarker-associated treatment regime with Denosumab in 10 children with classical OI which were followed for 1 year after their participation in a pilot trial with Denosumab. Therefore urinary deoxypyridinoline levels were evaluated frequently as an osteoclastic activity marker and depending on that levels Denosumab injections were scheduled individually. Methods Ten patients (age range: 6.16–12.13 years; all participated in the former OI-AK phase 2 trial (NCT01799798)) were included in the follow-up period. Denosumab was administered subcutaneously depending on the individual urinary excretion course of deoxypyridinoline (DPD/Crea) as osteoclastic activity marker with 1 mg/kg body weight. DPD/Crea levels were evaluated before denosumab administration and afterwards. If patients present after an initial decrease after injection with a re-increase up to the DPD/crea level before Denosumab injection next dosage was planned. Changes of areal bone mineral density (aBMD) using dual energy x-ray absorptiometry of the lumbar spine after 12 month was evaluated. Safety was assessed by bone metabolism markers and side effect reporting. Results During follow-up mean relative change of lumbar aBMD was − 6.4%. Lumbar spine aBMD z-Scores decreased from − 1.01 ± 2.61 (mean ± SD) to − 1.91 ± 2.12 (p = 0.015). Mobility changed not significantly (GMFM-88 -6.49 ± 8.85% (p = 0.08). No severe side effects occurred. Dose intervals could be extended in the mean from 12 weeks previously to 20.3 weeks. Conclusions On average, it was possible to prolong the intervals between drug administrations and to reduce the total dose about by 25% without a decrease of mobility or change of vertebral shape despite a reduction of lumbar aBMD during 1 year of biomarker-directed Denosumab treatment. Further trials are necessary to balance side effects and highest efficacy in children.

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“…2 Other important mechanisms include accidental overdosing or abusing of Vitamin D analogs. 3-5 In this regard, however, the development of acute anemia has not been reported yet in any of the published studies.…”

Section: Introductionmentioning

confidence: 96%

A Rare Case of Acute Kidney Injury and Anemia Induced by Hypercalcemia

Bormann

Suksompong

Bormann

2019

Clinics and Practice

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Hypercalcemia may result in acute kidney injury (AKI) and arterial hypertension. Anemia as a consequence of this constellation is nowhere described. A female patient underwent total thyroidectomy in 2007, since then being under continuous daily medication with 100 μg thyroxin, 1.6 g calcium and 1.0 μg alfacalcidol. In 2017, after accidentally overdosing alfacalcidol fourfold for several weeks leading to massive hypercalcemia (plasma calcium level 16.7 mg/dL), the otherwise healthy patient developed symptoms of AKI, such as serum creatinine 2.48 mg/dL, plus severe hypertension and acute anemia (hemoglobin concentration 10.2 g/dL). After cessation of calcium and alfacalcidol medication for 9 days, hypercalcemia and AKI symptoms and anemia recovered within 14 and after 62 days, respectively. The patient is currently free of complaints and has been sufficiently treated with half of the yearslong pre-event calcium/alfacalcidol dose. In conclusion, hypercalcemia with consecutive AKI after vitamin D overdose can occur asymptomatically. The treatment does not compulsorily include washout by hyperhydration and diuretics. AKI may lead to anemia, possibly caused by the deterioration of the release of erythropoietin.

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Severe hypercalcaemia in a child secondary to use of alternative therapies

Cited by 6 publications

References 8 publications

Vitamin D Intoxication Presenting as Subacute Encephalopathy—A Case Report

Vitamin D Intoxication Presenting as Subacute Encephalopathy—A Case Report

Individualized treatment with denosumab in children with osteogenesis imperfecta – follow up of a trial cohort

A Rare Case of Acute Kidney Injury and Anemia Induced by Hypercalcemia

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