| [ Summary ] |
With recent advances in the treatment of secondary hyperparathyroidism, over secretion of PTH can now be controlled. However, blood PTH levels 2 to 6 times higher than normal are considered necessary to maintain normal bone turnover in patients with renal failure. Furthermore, excessive inhibition of PTH secretion suppresses bone turnover, and may result in the onset of low bone turnover. Various causes of skeletal resistance to PTH have been reported, including decreases in PTH receptors in osteoblasts, accumulation of 7-84 PTH fragments, and accumulation of osteoprotegerin (OPG), which is an inhibitor of osteoclastogenesis. This skeletal resistance to PTH is not only a high-turnover bone condition accompanying secondary hyperparathyroidism, but may also play a crucial role in the onset of low turnover bone disease. |