Sebastián E Ibáñez Vodnizza1,2, Michael T Nurmohamed1,2, Ingrid M Visman1,2, J Christiaan van Denderen1,2, Willem F Lems1,2, Francisca Jaime1,2, Irene E van der Horst-Bruinsma3,4. 1. From the Amsterdam Rheumatology and Immunology Center, Reade and VU University Medical Center, Amsterdam, the Netherlands; Rheumatology Department, Clínica Alemana de Santiago and Hospital Padre Hurtado, Santiago, Chile. 2. S.E. Ibáñez Vodnizza, MD, Rheumatology Department, Clínica Alemana de Santiago and Hospital Padre Hurtado; M.T. Nurmohamed, MD, Professor, Amsterdam Rheumatology and Immunology Center, Reade and VU University Medical Center; I.M. Visman, Amsterdam Rheumatology and Immunology Center, Reade; J.C. van Denderen, MD, PhD, Amsterdam Rheumatology and Immunology Center; W.F. Lems, MD, Professor, Amsterdam Rheumatology and Immunology Center, Reade and VU University Medical Center; F. Jaime, MD, Faculty of Medicine, Pontificia Universidad Católica de Chile; I.E. van der Horst-Bruinsma, MD, PhD, Amsterdam Rheumatology and Immunology Center, VU University Medical Center. 3. From the Amsterdam Rheumatology and Immunology Center, Reade and VU University Medical Center, Amsterdam, the Netherlands; Rheumatology Department, Clínica Alemana de Santiago and Hospital Padre Hurtado, Santiago, Chile. ie.vanderhorst@vumc.nl. 4. S.E. Ibáñez Vodnizza, MD, Rheumatology Department, Clínica Alemana de Santiago and Hospital Padre Hurtado; M.T. Nurmohamed, MD, Professor, Amsterdam Rheumatology and Immunology Center, Reade and VU University Medical Center; I.M. Visman, Amsterdam Rheumatology and Immunology Center, Reade; J.C. van Denderen, MD, PhD, Amsterdam Rheumatology and Immunology Center; W.F. Lems, MD, Professor, Amsterdam Rheumatology and Immunology Center, Reade and VU University Medical Center; F. Jaime, MD, Faculty of Medicine, Pontificia Universidad Católica de Chile; I.E. van der Horst-Bruinsma, MD, PhD, Amsterdam Rheumatology and Immunology Center, VU University Medical Center. ie.vanderhorst@vumc.nl.
Abstract
OBJECTIVE: Our main objective was to assess the relationship between body composition (BC) and response to tumor necrosis factor-α (TNF-α) blocker treatment in patients with ankylosing spondylitis (AS). Our secondary objective was to evaluate the change of BC after treatment, accounting for sex and age. METHODS: All included patients fulfilled the modified New York criteria for AS and were naive to TNF-α blocker. They were followed for at least 6 months after the start of etanercept or adalimumab. The Ankylosing Spondylitis Disease Activity Score containing C-reactive protein (ASDAS-CRP) and the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) were reported. BC was assessed by whole body dual-energy X-ray absorptiometry. Body fat percentage (BF%), fat mass index (FMI), and fat free mass index (FFMI) were reported as absolute values and as percentiles. RESULTS: Forty-one patients were included (61% men). The median followup was 14.3 months (interquartile range 8.4-19.4). After multivariate regression analysis, more fat at baseline (BF%, FMI, or FMI percentile) was significantly related with a lower chance of achieving a clinically important improvement of the ASDAS-CRP or BASDAI after treatment. The body composition did not change significantly after treatment, but there was a trend toward muscle recovery in men (FFMI change from 34.0th to 37.4th percentile). CONCLUSION: Higher body fat content at baseline was independently associated with a worse response to treatment with TNF-α blockers, measured by ASDAS-CRP and BASDAI change, and might contribute to the lower response rates in female patients. Also, there is a trend toward muscle mass recovery in male patients after treatment.
OBJECTIVE: Our main objective was to assess the relationship between body composition (BC) and response to tumor necrosis factor-α (TNF-α) blocker treatment in patients with ankylosing spondylitis (AS). Our secondary objective was to evaluate the change of BC after treatment, accounting for sex and age. METHODS: All included patients fulfilled the modified New York criteria for AS and were naive to TNF-α blocker. They were followed for at least 6 months after the start of etanercept or adalimumab. The Ankylosing Spondylitis Disease Activity Score containing C-reactive protein (ASDAS-CRP) and the Bath Ankylosing Spondylitis Disease Activity Index (BASDAI) were reported. BC was assessed by whole body dual-energy X-ray absorptiometry. Body fat percentage (BF%), fat mass index (FMI), and fat free mass index (FFMI) were reported as absolute values and as percentiles. RESULTS: Forty-one patients were included (61% men). The median followup was 14.3 months (interquartile range 8.4-19.4). After multivariate regression analysis, more fat at baseline (BF%, FMI, or FMI percentile) was significantly related with a lower chance of achieving a clinically important improvement of the ASDAS-CRP or BASDAI after treatment. The body composition did not change significantly after treatment, but there was a trend toward muscle recovery in men (FFMI change from 34.0th to 37.4th percentile). CONCLUSION: Higher body fat content at baseline was independently associated with a worse response to treatment with TNF-α blockers, measured by ASDAS-CRP and BASDAI change, and might contribute to the lower response rates in female patients. Also, there is a trend toward muscle mass recovery in male patients after treatment.
Entities:
Keywords:
ANKYLOSING SPONDYLITIS; BODY COMPOSITION; FAT MASS; MUSCLE; SEX
Authors: H Nakase; S Motoya; T Matsumoto; K Watanabe; T Hisamatsu; N Yoshimura; T Ishida; S Kato; T Nakagawa; M Esaki; M Nagahori; T Matsui; Y Naito; T Kanai; Y Suzuki; M Nojima; M Watanabe; T Hibi Journal: Aliment Pharmacol Ther Date: 2017-09-08 Impact factor: 8.171