Parathyroid hormone (PTH) is produced and secreted by the parathyroid glands and has primary effects on kidney and bone. During the pathological growth of one or more parathyroid glands, the plasma level of PTH increases and causes primary hyperparathyroidism (PHPT). This disease is normally characterised by hyperparathyroid hypercalcaemia. In PHPT a continuously elevated PTH stimulates the kidney and bone causing a condition with high bone turnover, elevated plasma calcium and increased fracture risk. If bone resorption is not followed by a balanced formation of new bone, irreversible bone loss may occur in these patients. Medical treatment can help to minimise the loss of bone but the cure of PHPT is by parathyroidectomy. After operation, bone mineral density increases during the return to normal bone metabolism. Supplementation with calcium and vitamin D after operation may improve the normalisation to normal bone metabolism with a secondary reduction in fracture risk.
KeywordsPrimary hyperparathyroidism, bone mineral density, parathyroidectomy, vitamin D, PTH, calcium, bone remodelling, fracture absorption from the intestine. In the bone, PTH controls Ca 2+ release to the extracellular fluid 4 with both a rapid release from a calcium pool as a buffer mechanism and the more slow mechanism with stimulation of increased bone turnover. 4 The effect is an increase in plasma Ca 2+ . Also plasma phosphate is regulated by PTH but in the opposite direction.Hence, an increased plasma PTH leads to increased renal phosphate excretion 5 with decreased plasma phosphate levels.PTH is a major regulator of bone remodelling, the process by which the skeleton is being renewed constantly throughout life (see Figure 1).The primer of bone remodelling is bone resorption by osteoclasts, which after a reversal phase changes to bone formation by osteoblasts. 6 This process of bone remodelling is critical to maintain healthy bone. The regulation of the remodelling process goes primarily through the osteoblasts, which expresses receptors for both PTH and 1,25(OH) 2 D.
7It is believed that PTH mainly has an indirect stimulation on osteoclasts by binding to neighbouring osteoblasts. 8 Elevated PTH levels induce an increased release of receptor activator of nuclear factor-aa ligand (RANKL), which binds to its receptor (RANK) on osteoclast precursor cells leading to activation and formation of osteoclasts. 9 In younger and otherwise healthy individuals, increased activation of osteoclasts is normally followed by a balanced formation of new bone under the process of bone remodelling 10 (see Figure 2). However, this increased resorption of bone is seen in both trabecular and cortical bone in PHPT and causes a temporary, but reversible, bone loss if the remodelling cavities are refilled with new bone.The PTH-induced increase in bone turnover is probably the main reason for reduced bone mineral density (BMD) in PHPT. However, if the remodelling process is not balanced, the increased bone resorption will lead to a catabolic state with a...