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

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