High fracture risk patients with glucocorticoid-induced osteoporosis should get an anabolic treatment first
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POSITION PAPER
High fracture risk patients with glucocorticoid-induced osteoporosis should get an anabolic treatment first E. Lespessailles 1,2
&
R. Chapurlat 3
Received: 12 June 2020 / Accepted: 23 July 2020 # International Osteoporosis Foundation and National Osteoporosis Foundation 2020
Abstract Long-term glucocorticoid (GC) therapy induces glucocorticoid-induced osteoporosis (GIOP) and its associated fractures. Most specialty organizations recommend bisphosphonates as first-line therapies based only on bone mineral density efficacy data. Effective treatment of GIOP based on head-to-head trials with fracture endpoint has not yet been established. The pathophysiologic mechanisms of GIOP that lead to the detrimental effects on bone are not yet fully elucidated. Although GCs in an early and transitory period promote osteoclastic activity, in the current paper, we outline why GIOP is in fact a disease of the bone formation and then provide the rationale for the use of bone-forming agents as first-line therapy for patients with high fracture risk in GIOP. Keywords Glucocorticoid . Fracture . Bisphosphonate . Denosumab . Teriparatide . Bone mineral density
Introduction
GIOP is a disease of the bone formation
The treatment of many inflammatory conditions is still based on glucocorticoids (GCs), even if their use may be supplanted by biologics in the near future. Almost 1% of the adult population in the UK [1] and the USA [2] was treated long term with GCs. This long-term use, however, is associated with well-documented complications such as bone loss and fracture, up to 40% of individuals treated long term with GCs experiencing fractures [3]. Dose-dependent GC effects on fragility fracture have been shown with the rate of 5 to 9 per 1000 person years at low GC doses, increasing 2- to 2.5-fold at doses > 15 mg/day [4]. Despite this burden, only one out of five patients taking long-term GCs is prescribed for osteoporosis medications [5].
The mechanisms through which GCs decrease bone strength are complex and differ from those implicated in postmenopausal osteoporosis, i.e., a profound inhibition of bone formation [6]. The fracture risk has been shown to be higher in patients with glucocorticoid-induced osteoporosis (GIOP) than in patients with postmenopausal osteoporosis for the same level of bone mineral density (BMD) measured by dual X-ray absorptiometry (DXA) [7]. But bone fragility in GIOP is not only explained by the reduction in BMD. Increased fracture risk is seen within the first 3 to 6 months after initiating GCs, the greatest risk being seen for vertebral fracture [3]. GC initiators had higher annual incidence rate of vertebral fracture at 5.1% (95% CrI 2.8–8.2) than chronic GC users at 3.2% (95% CrI 1.8–5) [8]. The risk of fracture increases as much as 75% within the first 3 months suggesting also other defective factors associated with GIOP that may be not captured by DXA [9]. The glucocorticoid actions on bone modify the biology of all three major bone cells (Fig. 1). However the most consistent ske
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