Maria A C van der Weijden1, J Christiaan van Denderen2, Willem F Lems2, Michael T Nurmohamed2, Ben A C Dijkmans2, Irene E van der Horst-Bruinsma2. 1. From the Department of Rheumatology, VU University Medical Center; Department of Rheumatology, Jan van Breemen Research Institute/Reade, Amsterdam, the Netherlands.M.A. van der Weijden, MD, MSc, PhD, Department of Rheumatology, VU University Medical Center, and Department of Rheumatology, Jan van Breemen Research Institute/Reade; J.C. van Denderen, MD, PhD, Department of Rheumatology, Jan van Breemen Research Institute/Reade; W.F. Lems, MD, Professor, Department of Rheumatology, VU University Medical Center, and Department of Rheumatology, Jan van Breemen Research Institute/Reade; M.T. Nurmohamed, MD, Professor, Department of Rheumatology, VU University Medical Center, and Department of Rheumatology, Jan van Breemen Research Institute/Reade; B.A. Dijkmans, MD, Professor, Department of Rheumatology, VU University Medical Center; I.E. van der Horst-Bruinsma, MD, PhD, Department of Rheumatology, VU University Medical Center, and Department of Rheumatology, Jan van Breemen Research Institute/Reade. mac.vanderweijden@vumc.nl. 2. From the Department of Rheumatology, VU University Medical Center; Department of Rheumatology, Jan van Breemen Research Institute/Reade, Amsterdam, the Netherlands.M.A. van der Weijden, MD, MSc, PhD, Department of Rheumatology, VU University Medical Center, and Department of Rheumatology, Jan van Breemen Research Institute/Reade; J.C. van Denderen, MD, PhD, Department of Rheumatology, Jan van Breemen Research Institute/Reade; W.F. Lems, MD, Professor, Department of Rheumatology, VU University Medical Center, and Department of Rheumatology, Jan van Breemen Research Institute/Reade; M.T. Nurmohamed, MD, Professor, Department of Rheumatology, VU University Medical Center, and Department of Rheumatology, Jan van Breemen Research Institute/Reade; B.A. Dijkmans, MD, Professor, Department of Rheumatology, VU University Medical Center; I.E. van der Horst-Bruinsma, MD, PhD, Department of Rheumatology, VU University Medical Center, and Department of Rheumatology, Jan van Breemen Research Institute/Reade.
Abstract
OBJECTIVE: Ankylosing spondylitis (AS) is characterized by chronic inflammation leading to ankylosis, but also to low bone mineral density (BMD) and vertebral fractures (VFx). Treatment with tumor necrosis factor-α blockers decreases inflammation and has shown to be effective in increasing BMD. We studied the effects of etanercept (ETN) on BMD and VFx in patients with AS after 2 years of treatment. Further, we studied changes in bone turnover markers and radiological damage. METHODS: Patients with active AS, treated with ETN for 2 years, were included. BMD lumbar spine and hip were measured at baseline and after 2 years, as well as radiological damage (modified Stoke Ankylosing Spondylitis Spinal Score with the addition of the thoracic spine), VFx (Genant method), and change in bone turnover markers. RESULTS: Forty-nine patients with AS were included. After 2 years of ETN, hip BMD increased by 2.2% (p = 0.014) and lumbar spine BMD by 7.0% (p < 0.001). The Bath Ankylosing Spondylitis Disease Activity Index decreased significantly (p < 0.001), as well as C-reactive protein and erythrocyte sedimentation rate (p < 0.001). Despite ETN therapy, the number of patients with VFx more than doubled (from 6 to 15 patients, p = 0.003). Also, the radiological damage increased significantly over time (from 12.1 to 18.5, p < 0.001); however, no significant change in bone turnover markers was found. CONCLUSION: This prospective longitudinal observational cohort study showed that after 2 years of ETN, BMD of the hip and spine increased significantly, but the number of patients with VFx and the severity of VFx increased as well. Besides that, radiological progression, including the thoracic spine, increased significantly. Thus, the favorable bone-preserving effect is accompanied by unfavorable outcomes on VFx and radiological damage.
OBJECTIVE:Ankylosing spondylitis (AS) is characterized by chronic inflammation leading to ankylosis, but also to low bone mineral density (BMD) and vertebral fractures (VFx). Treatment with tumor necrosis factor-α blockers decreases inflammation and has shown to be effective in increasing BMD. We studied the effects of etanercept (ETN) on BMD and VFx in patients with AS after 2 years of treatment. Further, we studied changes in bone turnover markers and radiological damage. METHODS:Patients with active AS, treated with ETN for 2 years, were included. BMD lumbar spine and hip were measured at baseline and after 2 years, as well as radiological damage (modified Stoke Ankylosing Spondylitis Spinal Score with the addition of the thoracic spine), VFx (Genant method), and change in bone turnover markers. RESULTS: Forty-nine patients with AS were included. After 2 years of ETN, hip BMD increased by 2.2% (p = 0.014) and lumbar spine BMD by 7.0% (p < 0.001). The Bath Ankylosing Spondylitis Disease Activity Index decreased significantly (p < 0.001), as well as C-reactive protein and erythrocyte sedimentation rate (p < 0.001). Despite ETN therapy, the number of patients with VFx more than doubled (from 6 to 15 patients, p = 0.003). Also, the radiological damage increased significantly over time (from 12.1 to 18.5, p < 0.001); however, no significant change in bone turnover markers was found. CONCLUSION: This prospective longitudinal observational cohort study showed that after 2 years of ETN, BMD of the hip and spine increased significantly, but the number of patients with VFx and the severity of VFx increased as well. Besides that, radiological progression, including the thoracic spine, increased significantly. Thus, the favorable bone-preserving effect is accompanied by unfavorable outcomes on VFx and radiological damage.
Entities:
Keywords:
ANKYLOSING SPONDYLITIS; BONE MINERAL DENSITY; BONE TURNOVER MARKERS; RADIOLOGICAL DAMAGE; VERTEBRAL FRACTURES
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