Effects of PTH and PTH Hypersecretion on Bone: a Clinical Perspective
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EPIDEMIOLOGY AND PATHOPHYSIOLOGY (G EL-HAJJ FULEIHAN AND D SHOBACK, SECTION EDITORS)
Effects of PTH and PTH Hypersecretion on Bone: a Clinical Perspective Lars Rejnmark 1,2 & Henriette Ejlsmark-Svensson 1
# Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Purpose of Review Hyperparathyroidism may be due to an autonomous hypersecretion of parathyroid hormone (PTH) or occurs in response to a number of physiological stimuli. A number of recent findings have provided new insights into the importance of the calcium-parathyroid-vitamin D axis to bone in normal physiology and pathological conditions. Recent Findings PTH is known to affect bone microarchitecture with different effects on cortical and trabecular bone compartments. In trabecular bone, PTH may exert anabolic effects, whereas PTH promotes bone resorption in cortical bone. Vertebral fractures are prevalent in primary hyperparathyroidism (PHPT), and patients seem to fracture at higher values of bone mineral density (BMD) than patients with osteoporosis. This may be explained by changes in bone microarchitecture, which cannot be detected by measuring BMD. Even in mild PHPT, bone seems to benefit from parathyroidectomy. In secondary hyperparathyroidism, bone seems much more susceptible to fracture with insufficient levels of vitamin D compared with a replete vitamin status. If elevated PTH levels cannot be explained by conditions known to cause secondary hyperparathyroidism, the condition is termed normocalcemic PHPT, which also has been associated with an increased risk of fractures. Summary Hyperparathyroidism is harmful to bone, which is why it is of importance to normalize PTH levels either by parathyroidectomy in PHPT or by counteracting conditions known to increase PTH in secondary hyperparathyroidism. Keywords Hyperparathyroidism . Bone . Fractures . Parathyroid hormone . Vitamin D
Introduction Parathyroid hormone (PTH) is synthesized and secreted only by the parathyroid glands. The secretion is regulated by serum ionized calcium (Cai) through the calcium-sensing receptor (CaSR), which is expressed on the plasma membrane of chief cells in the parathyroid glands [1]. If serum calcium (and therefore Cai) levels are high, secretion of PTH is inhibited, whereas PTH secretion is increased in response to hypocalcemia. This effect takes place within minutes to ensure that This article is part of the Topical Collection on Epidemiology and Pathophysiology * Lars Rejnmark [email protected] 1
Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, DK-8200 Aarhus, Denmark
2
Department of Clinical Medicine, Aarhus University, Aarhus, Denmark
serum calcium level remains within a tight physiologic range. A set point for calcium-regulated PTH release can be defined, by which PTH secretion is half of the maximal secretion capacity [2]. The main effect of PTH is the regulation of calcium homeostasis in order to maintain normocalcemia by acting on several organ systems (Fig. 1). In th
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