Endocrine Abstracts

Introduction: Vitamin D deficiency/insufficiency in patients with primary hyperparathyroidism may be associated with more severe and progressive disease. In such patients there is higher levels of parathormone and markers of bone turnover, large parathyroid adenomas and more frequent fractures than vitamin D replete patients.

Aims and objectives: To determine whether vitamin D repletion of patients with PHPT and co-existing vitamin D insufficiency or deficiency has any adverse effects on their biochemical parameters.

Methods: A retrospective analysis of data for one year (2012) from the hospital database for patients who had biochemical evidence of raised PTH and had a vitamin D levels checked at presentation (n=111). Patients with satisfactory levels of 25(OH) D levels at onset (n=37), those with insufficient data at beginning or follow up and those who were not replaced with vitamin D (n=35) and those who had normocalcemia with raised PTH (n=23) due to secondary hyperparathyroidism were excluded. 16 patients were included for the study (with hypercalcemia >2.62 mmol/l and raised PTH levels) and were considered to have insufficient levels of vitamin D if their 25(OH) D were between 10–20 μg/l (n=9) and deficient in vitamin D if the 25(OH) D levels were < 10 μg/l (n=7). Patients were treated with either different dosage of colecalciferol (Fultium-D3) (800IU, 1600IU, and 3200IU) alone or a combination of calcium carbonate and colecalciferol (500 mg/400IU).

Results: The mean age of the combined study group was 68.25 ± 11.48 years and the average follow up period was 9.81 ± 6.49 months. After replacement with colecalciferol, 25 (OH) D levels improved significantly (11.63 ± 4.31 vs 28.67 ± 11.91 μg/l, P<0.0001) together with a fall in adjusted calcium (2.75 ± 0.12 to 2.65 ± 0.15 mmol/l, P=0.02). However, PTH levels remained unchanged (18.57 ± 8.12 to 17.96 ± 12.47, P=0.43).

Conclusion: In contrast to what would be perceived, our data reveal that vitamin D repletion in patients with PHPT appears to modestly reduce calcium concentrations. The mechanism for this is unclear but as with the increase in 25 (OH) D attenuation of secondary hyperparathyroidism may assist. The study also reveals that vitamin D3 can be safely used to replace deficiency/insufficiency in patients with hypercalcemic PHPT.