Poster Presentation The Annual Scientific Meeting of the Endocrine Society of Australia and the Society for Reproductive Biology 2014

Primary hyperparathyroidism and the relationship between 25-vitamin D, 1,25 vitamin D and parathyroid hormone: A prospective case series (#249)

Thomas I Hadwen 1 , Melissa S Clarke 2 , Ashim K Sinha 2 , Anna G McLean 2
  1. Princess Alexandra Hospital, Brisbane, QLD, Australia
  2. Cairns Base Hospital, Cairns, QLD, Australia


Primary hyperparathyroidism is a common endocrinological disease with an evolving clinical presentation1.  Vitamin D deficiency is more common in PHPT than the general population, partly related to the elevated PTH converting 25-hydroxyvitaminD into 1,25-dihydroxyvitaminD2.  Observational studies have shown that a low 25-hydroxyvitaminD is associated with reduced BMD, post-op hypocalcaemia and elevated PTH3.  In a small RCT 25-hydroxyvitaminD replacement decreased PTH and increased lumbar BMD without increasing adverse events3.  The role of 1,25-dihydroxyvitaminD was not investigated.


To analyse the data of patients with PHPT looking for correlations between PTH, calcium, 25-hydroxyvitaminD, 1,25-dihydroxyvitaminD and 25-hydroxyvitaminD replacement.


We performed a prospective case series of all patients referred to the Cairns Hospital endocrine outpatients clinic with hypercalcaemia.


49 patients with hypercalcaemia were identified. 40 were diagnosed with PHPT.  Average corrected calcium in the PHPT group, expressed as mmo/L above normal, was 0.2.  The average PTH, expressed as a multiple above normal, was 1.73.   The average 25-hydroxyvitaminD was 61nmol/L (50-150),the average 1,25-dihydroxyvitaminD  was elevated at 173pmol/L (40-150). There was a statistically significant difference in PTH level between vitamin D replete and deficient groups, 1.51 and 2.45 times normal respectively (p=0.003) without a difference in corrected calcium.  The correlation factor of PTH and 25-hydroxyvitaminD was -0.56.  The correlation factor of PTH and 1,25-dihydroxyvitaminD was 0.43.  There was a negative correlation between 25-hydroxyvitaminD and 1,25-dihydroxyvitaminD (r=-0.64).  Replacing vitamin D did not alter hypercalcaemia.


In our study low 25-hydroxyvitaminD is associated with increased PTH but not hypercalcaemia and 25-hydroxyvitaminD replacement didn’t worsen hypercalcaemia.  Interestingly 25 and 1,25-hydroxyvitaminD are inversely related.  There is conflicting evidence about this relationship in the literature4.  The proposed mechanism for 25-hydroxyvitaminD replacement suppressing PTH is by increasing the level of 1,25-hydroxyvitaminD. Our finding of elevated 1,25-hydroxyvitaminD in the vitamin D deficient does not support this.

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  2. Tassone F, Gianotti L, Baffoni C, Visconti G, Pellegrino M, Cassibba S, Croce C, Magro G, Cesario F, Attanasio R, Borretta G. Vitamin D status in primary hyperparathyroidism: a Southern European perspective. Clinical Endocrinology. 2013. 79: 784–790
  3. Rolighed L, Rejnmark L, Sikjaer T, Heickendorff L, Vestergaard P, Mosekilde L, Christiansen P. Vitamin D Treatment in Primary Hyperparathyroidism: a Randomized Placebo Controlled Trial. Journal of Clinical Endocrinology and Metabolism. 2014. 99:1072-1080
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