Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2012) 28 P20

SFEBES2012 Poster Presentations Bone (22 abstracts)

Vitamin D, no longer the forbidden fruit in hypercalcaemia

Sagen Zac-Varghese 1 , Elaine Hui 2 & Karim Meeran 1


1Endocrinology and Diabetes, Imperial College London, London, United Kingdom; 2Endocrinology and Diabetes, West Middlesex Hospital, London, United Kingdom.


A 70 year old Afro-Caribbean gentleman was referred for investigation of hypercalcaemia. He had a past medical history of prostate cancer treated 10 years previously with radical prostatectomy and radiotherapy, type 2 diabetes and hypertension. There was no family history of note. At the time of his operation, his calcium was noted to be high 2.87 mmol /L (nr 2.15–2.6) and his creatinine was 87 but this was not investigated further. At the first clinic visit, his corrected calcium was 3.15 mmol, PTH 41.8 ng/L, Cr 172 µmol/L and eGFR 34 ml/min/1.73m2. His urinary calcium creatinine ratio (UCCR) was measured to exclude familial hypocalciuric hypercalcaemia (FHH) and was low 0.0088 (<0.01). He was subsequently found to be vitamin D deficient 43 nmol/L (nr 70–150). He did not have renal calculi or osteoporosis. In view of his vitamin D deficiency and renal impairment the UCCR was not considered to be reliable. However, without genetic testing, FHH was difficult to exclude. He was started on vitamin D supplements with careful monitoring of his calcium and the UCCR was repeated. His repeat ratio was 0.0197 and it was considered likely that he had primary hyperparathyroidism. He went on to have a neck ultrasound which did not demonstrate any parathyroid adenoma and a nuclear sestimibi scan which demonstrated a left inferior pole parathyroid adenoma. He was started on cinacalcet and referred to the surgeons for a parathyroidectomy. This case demonstrates that vitamin D deficiency can lead to a misleading UCCR. This has been recently highlighted in the study by Jayasena et al., Ann Clin Biochem 2011. This study suggested that vitamin D deficiency was associated with impaired urinary calcium excretion. This case demonstrates that correction of the vitamin D deficiency led to an increase in the UCCR which helped us to exclude FHH.

Declaration of interest: There is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported.

Funding: No specific grant from any funding agency in the public, commercial or not-for-profit sector.

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