Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2025) 110 EP525 | DOI: 10.1530/endoabs.110.EP525

ECEESPE2025 ePoster Presentations Diabetes and Insulin (245 abstracts)

Severe hypercalcemia in a teenager with inaugural diabetic ketoacidosis

Salma El Hilali 1 , Sara Ijdda 1 , Sana Rafi 1 , Ghizlane El Mghari 1 & Nawal El Ansari 1


1University Hospital Center Mohammed VI, Department of Endocrinology and Metabolic Diseases, Marrakesh, Morocco


JOINT2457

Introduction: Ketoacidosis is the presenting condition in a third of cases of type 1 diabetes, mainly affecting children or young subjects. Many associated electrolyte abnormalities have been described, such as dysnatremia and dyskalemia. However, severe hypercalcemia in diabetic ketoacidosis remains rare, with very few publications in the literature. We report the case of a patient with major hypercalcemia discovered during diabetic ketoacidosis (DKA).

Case report: A 16-year-old patient was admitted to the intensive care unit for management of status epilepticus, where an inaugural DKA was diagnosed. After conditioning and first-line treatment, a laboratory work-up revealed major hypercalcemia corrected to 152 mg/l. After rehydration and intravenous insulin therapy, the ketoacidosis was brought under control and the calcemia recontrolled at 83 mg/l (86-103). The rest of the work-up showed mild hypophosphatemia at 22 mg/l (27-45), 25 OH vitamin D deficiency at 14.20 ng/ml and a low parathormon level at 4 ng/l (9-80).

Discussion: Calcium is the most abundant cation in the human body and plays an essential role in nerve transmission, enzyme activity, myocardial function, coagulation and other functions\.. Phosphocalcic metabolism is tightly regulated by 3 main hormones: parathyroid hormone (PTH), vitamin D and calcitonin. The etiologies of hypercalcemia can be divided into 2 major categories: PTH-mediated (primary and tertiary hyperparathyroidism and familial hypocalciuric hypercalcemia) and non-PTH-mediated (neoplasia, drugs, hyperthyroidism, immobilization, etc.). Hypercalcemia in diabetic ketoacidosis may be explained by several mechanisms. Metabolic acidosis induces calcium efflux from the bones through increased osteoclastic bone resorption and reduced osteoblastic bone formation. Acidosis also directly reduces tubular reabsorption of calcium and increases its ionization. Dehydration, secondary to hyperglycemia, osmotic diuresis and insufficient oral intake, also causes hypercalcemia. Rhabdomyolysis, which is sometimes observed in patients with ACD, can lead to hypercalcemia.

Conclusion: Electrolyte disorders are common in diabetic ketoacidosis. However, severe hypercalcemia remains a rare complication, and its treatment essentially consists in correcting acidosis and dehydration with sufficient and appropriate fluid intake.

Volume 110

Joint Congress of the European Society for Paediatric Endocrinology (ESPE) and the European Society of Endocrinology (ESE) 2025: Connecting Endocrinology Across the Life Course

European Society of Endocrinology 
European Society for Paediatric Endocrinology 

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