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SAT0480 Effects of A Previous Treatment With18 Months of Teriparatide on the Cortical Bone Mineral Density Response to Three Years of Bisphosphonate Treatment in Severe Osteoporosis
  1. M. Chemel-Mary
  1. Rheumatology, CHU Nantes, Nantes Cedex 1, France

Abstract

Background The actual challenge in the management of the severe osteoporosis is to find the best therapeutic strategy to increase bone mineral density (BMD) at the cortical sites, where gains with any osteoporotic treatment used as monotherapy are much lower than those obtained at the lumbar spine. The use of an anabolic agent before an antiresoptive drug could be a way to optimize the effect of the latter treatment. Indeed, the use of Bisphosphonate after Teriparatide may promote mineralization of a new formed and slightly mineralized bone, due to the osteoblastic stimulation, and leads to a better effect in the cortical BMD.

Objectives The goal of our study was to assess if the gain in BMD at the total hip after 3 years of Bisphosphonate could be improved by a pre-treatment with 18 months of Teriparatide.

Methods This was a monocentric retrospective study conducted at the University Hospital of Nantes. We included patients with severe osteoporosis (BMD with Tscore<-2.5 and at least one prevalent fracture), who received Bisphosphonate for 3 years either before (BP1) or after (BP2) 18 months of Teriparatide. All patients had an evaluation of their BMD at the lumbar spine and total hip by Dual-Energy X-ray Absorptiometry (Lunar Prodigy Advance) before and after the treatment with Bisphosphonate. Change in BMD was calculated as the difference in raw density and express in g/cm2 . We recorded all new fractures and secondary effects. The 2 groups were compared using a non-parametric test (Wilcoxon).

Results We included 92 patients: 47 in the group BP1 and 45 in the group BP 2.

The clinical characteristics of the two populations are summaries in Table 1.

The two populations differ by their BMD at baseline of each Bisphosphonate sequence (p<0.05 at lumbar spine and total hip). This could be explained by the strong effect at lumbar spine of the Teriparatide sequence that preceded BP2.The proportions of each Bisphosphonate are also different: more Zoledronate in BP2, due to the fact that this treatment wasn't available at the period when the BP1 patients were treated (before a Teriparatide sequence).

The BMD gain during the Bisphosphonate sequence at the total hip was significantly higher in BP2 than in BP1:+ 0,026g/cm2 (+3.98%) versus -0,004g/cm2 (-0.67%) (p<0,0001). At the lumbar spine, BP2 leads also to a higher but not significant densitometric gain compared to BP1:+ 0.029g/cm2 (+3.31%) versus +0.013g/cm2 (+1.85%),(p=0.0769). The number of new fractures was 4 in BP2 versus 7 in BP2. No major adverse effect occurred.

Conclusions In this “real life population” with severe osteoporosis, a previous treatment with 18 months of Teriparatide was associated with an improvement of the cortical bone mineral density response to 3 years of Bisphosphonate. Our results suggest that the anabolic treatment should be the first used in a therapeutic sequence.

Disclosure of Interest None declared

DOI 10.1136/annrheumdis-2014-eular.5518

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