Of the many diseases that have significant alterations in P homeostasis, only two are reviewed in any depth here. The first is persistently elevated PTH in response to a low Ca:P dietary intake pattern, whereas the second is renal secondary hyperparathyroidism resulting from chronic renal failure. Previously, the former was often referred to - perhaps erroneously in the case of humans (in contrast to animals) - as nutritional secondary hyperparathyroidism. In the context of human disease, the term “hyperparathyroidism” is inappropri-
Figure IV. B.5 3. Schematic diagram of phosphorus balance of an adult male. (Adapted from various sources.)
Ate because the PTH levels that result from a low Ca:P ratio typically remain within the normal range of blood concentration, although usually at the high end of the range. As mentioned, a persistently elevated PTH, even if it remains within the normal range, contributes to increased bone turnover that can result in a reduction of bone mass and density (Calvo et al. 1990). If this condition continues for a year or longer, it could contribute to fragility fractures because of the thinning of trabecular plates at bone sites, such as the vertebrae, wrist, and proximal femur. On the basis of obtaining a benefit from a PTH value at the lower end of the range, individuals with a low Ca:P ratio would be advised to increase their calcium intake from foods first and from supplements second. An adequate calcium intake is known to reduce serum PTH concentration (Krall and Dawson-Hughes 1994).
Figure fVB.5.4 diagrams the mechanism through which a low dietary Ca:P ratio contributes to the development of a persistently elevated PTH concentration. Figure W. B.5.5 illustrates the potential changes in bone mass and mineralization of the skeleton in individuals who typically consume diets with low Ca:P ratios compared to those who have normal intake ratios. The persistently elevated PTH is responsible for the limited bone mineralization and the loss of bone mass (Anderson 1996).
World History
