Abstract
Parathyroid hormone acts directly on bone by stimulating both bone resorption and bone formation with the relative excess in the former when it acts continuously. Thus in primary hyperparathyroidism characterized by chronic PTH excess, bone mineral density (BMD) is decreased with relatively high levels of bone turnover markers. In contrast, PTH deficient hypoparathyroidism such as post-operative hypoparathyroidism, BMD is increased with relatively low bone tunover markers. In pseudohypoparathyroidism, which characterized by PTH resistance in kidney, bone response to PTH is sometimes preserved. In some cases, high bone turnover state is observed, which correlates with serum PTH levels.
Published Version
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