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! acer ultrabook uw2-313dli black.acvr black.pdf.Normal in vivo levels of plasma immunoreactive parathyroid hormone (iPTH) reflect a homeostatic balance between the amount of PTH excreted into the circulation and its degradation by intact and cleaved/activated forms of the tissue-associated proteinase of the parathyroid gland. Too little or too much PTH results in bone disorder, respectively. It has been known for a long time that the bone disorders associated with high bone turnover are followed by a fall of circulating PTH levels to extremely low values, followed by accelerated bone turnover during the repletion phase, and that the subsequent rise of PTH in these conditions is associated with a slow speed of recovery of the original bone disorder. More recently, it has been found that patients with a normal bone metabolism and PTH levels within the normal range appear to be at risk of developing pathological disorders of bone. Thus, it has been found that high levels of PTH are associated with an excessive resorption of bone matrix, followed by an increase of the proportion of broken long bones in the skeleton. This was revealed by studies involving patients with hyperparathyroidism and the changes were associated with a reduced bone density as indicated by X-ray analysis of bone samples. In addition, it was found that PTH binds to bone at several sites, including the bone matrix itself and that the number of binding sites is increased in the two pathological conditions. This implies that, in the normal state, PTH is continuously removed from the circulation and eliminated by the kidney. It was proposed that the normal functioning of the kidney may be compromised in conditions associated with high PTH levels, with the consequence that only a small amount of PTH is eliminated by the kidney and consequently PTH levels in the circulation remains high. The newly reported that some forms of osteoporosis are associated with elevated concentrations of PTH led us to propose the following hypothesis: those patients with elevated levels of PTH become osteopenic as a result of a reduction in the function of the kidney so that the kidney removes PTH from the circulation to a limited extent. A putative mechanism is therefore increased bone resorption and a corresponding osteoporosis. The preceding model was put to the test by the following studies. 1. Serum PTH levels in women with a low BMD were compared with those in the age-matched normal women. The former group had a BMD

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