| アブストラクト | UNLABELLED: In this retrospective cohort study using the Clinical Practice Research Datalink (CPRD), patients with sarcoidosis have an increased risk of clinical vertebral fractures and when on recent treatment with oral glucocorticoids, also an increased risk of any fractures and osteoporotic fractures. INTRODUCTION: Sarcoidosis is a chronic inflammatory disease, in which fragility fractures have been reported despite normal BMD. The aim of this study was to assess whether patients with sarcoidosis have an increased risk of clinical fractures compared to the general population. METHODS: A retrospective cohort study was conducted using the CPRD. All patients with a CPRD code for sarcoidosis between January 1987 and September 2012 were included. Cox proportional hazards models were used to derive adjusted relative risks (RRs) of fractures in all sarcoidosis patients compared to matched controls, and within the sarcoidosis group according to use and dose of systemic glucocorticoids. RESULTS: Five thousand seven hundred twenty-two sarcoidosis patients (mean age 48.0 years, 51 % females, mean follow-up 6.7 years) were identified. Compared to 28,704 matched controls, the risk of any fracture was not different in patients with sarcoidosis. However, the risk of clinical vertebral fractures was significantly increased (adj RR 1.77; 95 % CI 1.06-2.96) and the risk of non-vertebral fractures was decreased although marginally significant (adj RR 0.87; 95 % CI 0.77-0.99). Compared to sarcoidosis patients not taking glucocorticoids, recent use of systemic glucocorticoids was associated with an increased risk of any fracture (adj RR 1.50; 95 % CI 1.20-1.89) and of an osteoporotic fracture (adj RR 1.47; 95 % CI 1.07-2.02). CONCLUSIONS: Patients with sarcoidosis have an increased risk of clinical vertebral fractures, and when using glucocorticoid therapy, an increased risk of any fractures and osteoporotic fractures. In contrast, the risk of non-vertebral fractures maybe decreased. Further investigation is needed to understand the underlying mechanisms of these contrasting effects on fracture risk. |
|---|
| 投稿者 | Bours, S; de Vries, F; van den Bergh, J P W; Lalmohamed, A; van Staa, T P; Leufkens, H G M; Geusens, P P P; Drent, M; Harvey, N C |
|---|
| 組織名 | Department of Internal Medicine, Subdivision of Rheumatology, Maastricht;University Medical Centre, Maastricht, The Netherlands.;Division of Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute of;Pharmaceutical Sciences, Utrecht, The Netherlands. f.devries@uu.nl.;MRC Lifecourse Epidemiology Unit, University of Southampton, Southampton General;Hospital, Southampton, UK. f.devries@uu.nl.;Department of Clinical Pharmacy and Toxicology, Maastricht University Medical;Centre, Maastricht, The Netherlands. f.devries@uu.nl.;CAPHRI School for Public Health and Primary Care, Maastricht University,;Maastricht, The Netherlands. f.devries@uu.nl.;Division of Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute for;Pharmaceutical Sciences, Utrecht University, Utrecht, The Netherlands.;f.devries@uu.nl.;Department of Internal Medicine, Viecuri MC Venlo, Venlo, The Netherlands.;NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht;University, Maastricht, The Netherlands.;Biomedical Research Institute, Hasselt University, Hasselt, Belgium.;Pharmaceutical Sciences, Utrecht, The Netherlands.;Department of Clinical Pharmacy, University Medical Center Utrecht, Utrecht, The;Netherlands.;Farr Institute, University of Manchester, Manchester, UK.;ILD Center of Excellence, St. Antonius Hospital, Nieuwegein, The Netherlands.;Department of Pharmacology and Toxicology, FHML, University Maastricht,;Maastricht, The Netherlands.;Hospital, Southampton, UK. |
|---|
