Of bone and genes: vitamin D receptor polymorphism and primary hyperparathyroidism

in European Journal of Endocrinology
Restricted access

Serum levels of calcium and phosphate, two essential ions for the maintenance of bone metabolism, are mainly controlled by parathyroid hormone (PTH), calcitonin and vitamin D upon activation of their respective receptors in kidneys, gut and bone. Synthesis and secretion of the peptide hormone PTH is inversely correlated with the serum level of ionized calcium: sensing of appropriately high serum ionized calcium levels by parathyroid cells suppresses PTH release and results in calcium deposition into bone. In contrast, hypocalcaemia leads to a counter-regulatory PTH surge that enhances the absorption of calcium by kidneys and gut, thus promoting mobilization of calcium from bone (1). In addition, vitamin D directly inhibits transcription of PTH. In the setting of primary hyperparathyroidism this tightly regulated feedback loop gets out of control. As a result of an altered set point, excessive secretion of PTH occurs despite the presence of hypercalcaemia. Consequently, the above-mentioned calcium-sparing mechanisms

 

     European Society of Endocrinology

Related Articles

Article Information

Metrics

All Time Past Year Past 30 Days
Abstract Views 55 55 1
Full Text Views 61 61 0
PDF Downloads 27 27 0

Altmetrics

PubMed

Google Scholar