BSPED2025 Oral Communications Endocrine Oral Communications 4 (8 abstracts)
1Stockport Hospital Trust, Greater Manchester, United Kingdom; 2Bolton Hospital Trust, Greater Manchester, United Kingdom; 3Great North Childrens Hospital, Newcastle, United Kingdom; 4Birmingham Childrens Hospital, Birmingham, United Kingdom; 5Alderhey Childrens Hospital, Liverpool, United Kingdom; 6Royal Hospital for Children, Glasgow, United Kingdom; 7Crosshouse Hospital, Kilmarnock, Ayrshire and Arran, United Kingdom; 8Leicester Royal Infirmary, Leicester, United Kingdom; 9Royal Manchester Childrens Hospital, Manchester, United Kingdom; 10Manchester Academic Health Science Centre, Manchester, United Kingdom
Introduction: Vitamin D supplementation has become increasingly widespread in the UK, increasing the risk of vitamin D toxicity, particularly among infants. While vitamin D is essential for calcium regulation and bone development, excessive intake can result in hypercalcaemia. Although vitamin D toxicity remains rare, an acute national surge prompted a review of cases. Relaxed regulatory standards for over-the-counter food supplements, a lack of clear treatment guidelines, and growing use of high-dose vitamin D for both supplementation and therapeutic purposes may lie behind this.
Methods: We present a case series of 12 children who developed vitamin D toxicity and were admitted to secondary and tertiary care centers across the UK between December 2024 - March 2025. In all cases, toxicity was attributed to formulation errors in prescribed vitamin D preparations.
Results: Age of presentation ranged from 2 months - 12 years, with 33% of patients ≤ 1 year. The most common presenting symptoms were vomiting (50%), lethargy (42%), altered bowel habits (33%), and poor feeding with weight loss (33%). The mean (SD) adjusted calcium on admission was 3.51 mmol/l (±0.48). Mean (SD) serum 25(OH)D levels were 1281 nmol/l (±462), although inter-assay variability across laboratories may limit the reliability of this measurement. All patients had suppressed parathyroid hormone (PTH) levels, confirming vitamin Dinduced hypercalcaemia. Treatment was promptly initiated in all cases. Eleven of twelve patients (92%) received intravenous hyper-hydration. Seven (55%) received pamidronate infusions, with three requiring repeat doses. One patient received furosemide due to deteriorating renal function, and another was treated with tapering prednisolone. Seven (58%) patients required strict adherence to a low calcium diet. Two patients (18%) developed nephrocalcinosis, and four (33%) experienced acute kidney injury (AKI). All patients were receiving Vitamin D treatment prior to admission, with 92% prescribed a defective batch of Vitamin D3, which was subsequently withdrawn by the manufacturer.
Conclusion: This case series highlights Vitamin D toxicity as a serious but preventable cause of hypercalcaemia in children. Stricter regulation of food supplement formulations and the development of national treatment guidelines are urgently needed to minimise the risk of iatrogenic harm in this vulnerable population.