Glucocorticoid-induced osteoporosis: pathophysiological role of GH/IGF-I and PTH/VITAMIN D axes, treatment options and guidelines

Endocrine. 2016 Dec;54(3):603-611. doi: 10.1007/s12020-016-1146-8. Epub 2016 Oct 20.

Abstract

Glucocorticoid-induced osteoporosis is the most frequent form of secondary osteoporosis caused by chronic exposure to glucocorticoid excess. Pathogenesis of glucocorticoid-induced osteoporosis is multifactorial including direct effects of glucocorticoids on bone cells and indirect effects of glucocorticoids on several neuroendocrine and metabolic pathways. Fragility fractures occur early in glucocorticoid-induced osteoporosis and anti-osteoporotic drugs along with calcium and vitamin D should be started soon after exposure to glucocorticoid excess. This paper summarizes some of the main topics discussed during the 9th Glucocorticoid-Induced Osteoporosis Meeting (Rome, April 2016) with a specific focus on the role of growth hormone/insulin-like growth factor-1 and parathyroid hormone/vitamin D axes in the pathogenesis of glucocorticoid-induced osteoporosis and the controversial aspects concerning therapeutic approach to skeletal fragility in this clinical setting.

Keywords: Glucocorticoids; Growth hormone; Guidelines; Osteoporosis; PTH; Vitamin D.

Publication types

  • Congress

MeSH terms

  • Bone Density Conservation Agents / therapeutic use
  • Glucocorticoids / adverse effects*
  • Growth Hormone / metabolism
  • Humans
  • Insulin-Like Growth Factor I / metabolism
  • Osteoporosis / chemically induced*
  • Osteoporosis / drug therapy
  • Osteoporosis / metabolism
  • Parathyroid Hormone / metabolism
  • Vitamin D / metabolism

Substances

  • Bone Density Conservation Agents
  • Glucocorticoids
  • IGF1 protein, human
  • Parathyroid Hormone
  • Vitamin D
  • Insulin-Like Growth Factor I
  • Growth Hormone