Anne-Birgitte Garm Blavnsfeldt1, Annette de Thurah2, Malissa Dawn Thomsen3, Simon Tarp4, Bente Langdahl5, Ellen-Margrethe Hauge2. 1. Department of Rheumatology, Aarhus University Hospital, Nørrebrogade 44, byg 3, 8000 Aarhus C, Denmark; Department of Clinical Medicine, Aarhus University, Incuba/Skejby, bygning 2, Palle Juul-Jensens Boulevard 82, 8200 Aarhus N, Denmark. Electronic address: annebnie@rm.dk. 2. Department of Rheumatology, Aarhus University Hospital, Nørrebrogade 44, byg 3, 8000 Aarhus C, Denmark; Department of Clinical Medicine, Aarhus University, Incuba/Skejby, bygning 2, Palle Juul-Jensens Boulevard 82, 8200 Aarhus N, Denmark. 3. Regional Hospital Silkeborg, Falkevej 1-3, 8600 Silkeborg, Denmark. 4. The Parker Institute, Bispebjerg & Frederiksberg Hospital, Nordre Fasanvej 57 Vej 8, Indgang 19, 2000, Frederiksberg, Denmark. 5. Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Tage Hansens Gade 2, 8000 Aarhus C, Denmark; Department of Clinical Medicine, Aarhus University, Incuba/Skejby, bygning 2, Palle Juul-Jensens Boulevard 82, 8200 Aarhus N, Denmark.
Abstract
PURPOSE: The role of glucocorticoids in the treatment of rheumatoid arthritis (RA) is widely debated. Impairment of bone formation may be counter-balanced by reduced systemic inflammation. This review aims to assess the effect of prednisolone/prednisone on bone mineral density (BMD) in patients with RA analyzed in randomized, controlled trials. METHODS: We performed a systematic literature search and identified randomized, double-blinded placebo-controlled studies including patients with RA and using prednisolone or prednisone as the intervention. We selected studies that measured BMD by DXA at baseline and at least once thereafter. Two authors independently performed reference review, data extraction and risk of bias assessment. Primary outcome was mean change in BMD from baseline to follow-up. Secondary endpoints included radiographic scores, RA disease activity indices and fractures. We rated the quality of evidence using the GRADE approach. Outcomes were standardized for meta-analyses and 95% confidence intervals (95% CI) were calculated. RESULTS: We identified 7 studies and included previously unpublished data. Studies were similar regarding study population and intervention. Standard mean difference (SMD) in change in BMD from 0 to 24 months was -0.02 (95%CI -0.16, 0.12) at the lumbar spine and -0.11 (95% CI -0.25, 0.02) at the hip (both high quality evidence) between patients treated with prednisolone/prednisone or not. Data completeness was low in some studies, concomitant treatment of RA differed between studies and differences in use of anti-osteoporotic medication may have influenced the results. However, sensitivity analyses excluding studies in which participants used either the most or the least potent concomitant RA treatment or used anti-osteoporotic therapies did not alter the estimates. CONCLUSIONS: In patients with early and active RA, we found no difference in change in BMD between patients treated with prednisone/prednisolone versus placebo, suggesting that at least through 24 months, the suppression of inflammation by glucocorticoids may counterbalance their adverse effects on bone remodeling.
PURPOSE: The role of glucocorticoids in the treatment of rheumatoid arthritis (RA) is widely debated. Impairment of bone formation may be counter-balanced by reduced systemic inflammation. This review aims to assess the effect of prednisolone/prednisone on bone mineral density (BMD) in patients with RA analyzed in randomized, controlled trials. METHODS: We performed a systematic literature search and identified randomized, double-blinded placebo-controlled studies including patients with RA and using prednisolone or prednisone as the intervention. We selected studies that measured BMD by DXA at baseline and at least once thereafter. Two authors independently performed reference review, data extraction and risk of bias assessment. Primary outcome was mean change in BMD from baseline to follow-up. Secondary endpoints included radiographic scores, RA disease activity indices and fractures. We rated the quality of evidence using the GRADE approach. Outcomes were standardized for meta-analyses and 95% confidence intervals (95% CI) were calculated. RESULTS: We identified 7 studies and included previously unpublished data. Studies were similar regarding study population and intervention. Standard mean difference (SMD) in change in BMD from 0 to 24 months was -0.02 (95%CI -0.16, 0.12) at the lumbar spine and -0.11 (95% CI -0.25, 0.02) at the hip (both high quality evidence) between patients treated with prednisolone/prednisone or not. Data completeness was low in some studies, concomitant treatment of RA differed between studies and differences in use of anti-osteoporotic medication may have influenced the results. However, sensitivity analyses excluding studies in which participants used either the most or the least potent concomitant RA treatment or used anti-osteoporotic therapies did not alter the estimates. CONCLUSIONS: In patients with early and active RA, we found no difference in change in BMD between patients treated with prednisone/prednisolone versus placebo, suggesting that at least through 24 months, the suppression of inflammation by glucocorticoids may counterbalance their adverse effects on bone remodeling.
Authors: N Guañabens; J M Olmos; J L Hernández; D Cerdà; C Hidalgo Calleja; J A Martinez López; L Arboleya; F J Aguilar Del Rey; S Martinez Pardo; I Ros Vilamajó; X Suris Armangué; D Grados; C Beltrán Audera; E Suero-Rosario; I Gómez Gracia; A Salmoral Chamizo; I Martín-Esteve; H Florez; A Naranjo; S Castañeda; S Ojeda Bruno; S García Carazo; A García Vadillo; L López Vives; À Martínez-Ferrer; H Borrell Paños; P Aguado Acín; R Castellanos-Moreira; C Tebé; C Gómez-Vaquero Journal: Osteoporos Int Date: 2021-01-18 Impact factor: 4.507