Glucocorticoid-induced osteoporosis: An indication for anabolic therapy

Abstract

Introduction: Glucocorticoid (GC) use is associated with disturbed calcium homeostasis and an increased risk of osteoporosis, muscle weakness, and fractures; these changes occur dose-dependently from the initiation of GCs [1]. Bone remodeling includes disturbed suppression of bone formation, stimulation of bone resorption, and osteocyte death [2,3]. The increase of bone resorption has often been related to increased parathyroid hormone (PTH) secretion secondary to decreased calcium absorption from the gut, but a review of the literature could not confi rm this [4], except for changes in spontaneous pulsatile secretion of PTH [5]. Increased bone resorption during GC treatment is related to an increase in the ratio of the receptor activator of the nuclear factorκB ligand over osteoprotegerin (RANKL/OPG) [2]. Catabolic effects of GCs on muscle result in muscle weakness [6,7], which contributes to an increased risk of falls. In case-fi nding algorithms such as FRAX (the World Health Organization risk assessment tool), any pre vious use of GCs is considered to be a clinical risk factor for fractures, but the dose of GCs and fall risk are not included [8]. Other algorithms, such as the fracture incidence in GC users (FIGS), include the dose of GCs and fall risk [9]. Using FIGS, a history of falls contributed as much to fracture risk as a high dose of GCs. Clearly, the etiology of GC-induced osteoporosis (GIOP) is multifactorial and related to skeletal and non-skeletal factors. The current standard of care for the prevention and treatment of GIOP is to provide suffi cient calcium and vitamin D [10]. In addition, in high-risk patients, bisphosphonate therapy has been shown to increase bone mineral density (BMD), decrease bone remodeling, and decrease the risk of fractures in post-hoc analyses [10]. From a pathophysiologic standpoint, one would expect that anabolic bone-directed therapy would have a positive impact on GIOP. In a study of postmenopausal women with GIOP, treatment with synthetic teriparatide and estrogen signifi cantly increased BMD at the lumbar spine, as compared with estrogen alone [11].