Abstract
It has recently been suggested that parathyroid hormone (PTH), administered chronically in low doses so as to induce a positive calcium balance, may be effective in the treatment of osteoporosis (11). This hypothesis was based in part on the relative sensitivity of the multiple effects of the parathyroids on calcium metabolism (12) and in part on the known anabolic effects of PTH in low doses on young rat bone (17, 5, 21). In the adult dog, which provides a better model than the rat of adult human calcium metabolism, Parsons and Reit demonstrated that chronic low-dose infusions of bovine PTH (0.025 to 0.1 µg/kg/h) resulted in increased calcium absorption without a concomitant rise in urinary calcium, in spite of moderate hypercalcaemia at the higher dose levels. These results provided the justification for a preliminary trial of low doses of a synthetic amino-terminal fragment of human PTH (hPTH 1–34 (8, 20)) in the treatment of primary osteoporosis.
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