Oral Presentation ESA-SRB Conference 2015

Introduction​ Vitamin D deficiency is defined as a serum 25-hydroxy-vitamin D (25(OH)D) <30 nmol/L, a value presumed to signal the likelihood of osteomalacia or secondary hyperparathyroidism [1]. Vitamin D insufficiency is held to be present with values <75nmol/L for reasons that are less clear [2]. If correct, ~4% of individuals are ‘deficient’ and ~75% are ‘insufficient’ and in need of therapy [3]. We aimed to determine whether there is (i) a serum 25(OH)D that signals secondary hyperparathyroidism, and so, by inference, an increased risk for bone disease, and (ii) another level above which serum parathyroid hormone (PTH) has reached a nadir and ceases to diminish.

Method​ Concentrations of 25(OH)D, PTH, calcium and creatinine measured in the serum of 10349 women and 3582 men were collected by Melbourne Pathology. We excluded persons <20 years, patients with hyper- or hypocalcaemia, chronic kidney disease and a 25(OH)D >180nmol/L.

Results​ Serum PTH correlated negatively with serum 25(OH)D with no evidence of a threshold 25(OH)D distinguishing persons with and without an elevated PTH; PTH was within the ‘normal’ range in over half (714/1416) of subjects with 25(OH)D ≤ 30 nmol/L. Nor was there a nadir or plateau; the higher the 25(OH)D, the lower the PTH (Fig 1). For both sexes, PTH was higher in ≥55 than <45 year olds (p<0.001) after adjusting for 25(OH)D, serum calcium and eGFR.

Conclusion​ PTH is a continuous trait. There is no serum 25(OH)D threshold that sensitively discriminates persons with and without secondary hyperparathyroidism. Further work is underway examining the association between these measurements and bone microarchitectural deterioration. Given the limited evidence of bone disease based on histomorphometry or antifracture efficacy using vitamin D supplements in community dwellers [4,5], these data challenge the existence of an ‘insufficiency’ state.