Searchable abstracts of presentations at key conferences in endocrinology
Endocrine Abstracts (2012) 28 P111

SFEBES2012 Poster Presentations Clinical practice/governance and case reports (90 abstracts)

Asymptomatic hypercalcaemia in a hypoparathyroid patient: vitamin D toxicity or calcium alkali syndrome?

Shivani Misra 1 , Radha Ramachandran 1 , Sagen Zac-Varghese 2 , Malvika Gulati 2 , Karim Meeran 2 & Nick Oliver 2


1Clinical Biochemistry / Metabolic Medicine, Imperial Healthcare NHS Trust, London, United Kingdom; 2Diabetes and Endocrinology, Imperial Healthcare NHS Trust, London, United Kingdom.


A 65-year-old lady presented to the emergency department with breathlessness due to an exacerbation of chronic airways disease. Her past medical history included laryngeal carcinoma treated with total-laryngectomy, thyroidectomy and adjuvant radiotherapy in 2003. She remained on stable post-operative replacement doses of 125mcg of levothyroxine and 1mcg 1-Alfacalcidol/1g Sandocal TDS for hypoparathyroidism for several years. Three days prior to her admission, strontium ranelate was started for osteoporosis. On admission an adjusted calcium of 4.91 mmol/L was incidentally noted, however on further questioning no symptoms of hypercalcaemia were reported. Repeat total calcium and ionised calcium measurements confirmed hypercalcaemia and she was managed with rehydration whilst supplements were withheld. Further investigations revealed: creatinine 148 umol/L, phosphate 2.18 mmol/L, PTH <1.1 pmol/L, freeT4 26 pmol/L, freeT3 4.4 pmol/L, TSH<0.05 mU/L, 25-OHVitD3 66 nmol/L and 1,25-OHVitD3 164 pmol/L (40–150 pmol/L). Arterial blood gas demonstrated a metabolic alkalosis(pH7.50). The possibility of strontium interference in the calcium assay was explored, though literature suggests levels considerably higher than calcium are required. Strontium levels (70.2 umol/L) were within the therapeutic range (10–200 umol/L). A differential diagnosis of vitamin D toxicity and calcium alkali syndrome (CAS) was considered. Calcium rapidly normalised and a lower dose of 1-Alfacalcidol was reintroduced. At follow-up she reported intermittent excess calcium intake to alleviate perceived symptoms of hypocalcaemia. Excessive Sandocal may explain the alkalosis, though the elevated 1,25-OHVitD3 also indicates excessive 1-Alfacalcidol ingestion. Hypoparathyroid patients have a fixed calcium and vitamin D homeostasis governed by replacement dosages. In the absence of PTH this is very susceptible to disruption. In this case excessive consumption of calcium supplements may have led to CAS, compounded by excess and unmodifiable levels of 1,25OHVitD3. Recurrent excursions of calcium may reduce sensitivity to hypercalcaemia. CAS has been reported in post-surgical hypoparathyroidism and is increasingly seen in post-menopausal women on calcium for osteoporosis. Clinicians should be alert to the re-emergence of CAS.

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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