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   <subfield code="a">Bone Fracture Risk is Not Associated with the Use of Glucagon-Like Peptide-1 Receptor Agonists: A Population-Based Cohort Analysis</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Johanna Driessen, Ronald Henry, Hein van Onzenoort, Arief Lalmohamed, Andrea Burden, Daniel Prieto-Alhambra, Cees Neef, Hubert Leufkens, Frank de Vries]</subfield>
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   <subfield code="a">Glucagon-like Peptide-1 receptor agonists (GLP1-ra) are a relatively new class of anti-hyperglycemic drugs which may positively affect bone metabolism and thereby decrease (osteoporotic) bone fracture risk. Data on the effect of GLP1-ra on fracture risk are scarce and limited to clinical trial data only. The aim of this study was to investigate, in a population-based cohort, the association between the use of GLP1-ra and bone fracture risk. We conducted a population-based cohort study, with the use of data from the Clinical Practice Research Datalink (CPRD) database (2007-2012). The study population (N=216,816) consisted of all individuals with type 2 diabetes patients with at least one prescription for a non-insulin anti-diabetic drug and were over 18years of age. Cox proportional hazards models were used to estimate the hazard ratio of fracture in GLP1-ra users versus never-GLP1-ra users. Time-dependent adjustments were made for age, sex, lifestyle, comorbidity and the use of other drugs. There was no decreased risk of fracture with current use of GLP1-ra compared to never-GLP1-ra use (adjusted HR 0.99, 95% CI 0.82-1.19). Osteoporotic fracture risk was also not decreased by current GLP1-ra use (adjusted HR 0.97; 95% CI 0.72-1.32). In addition, stratification according to cumulative dose did not show a decreased bone fracture risk with increasing cumulative GLP1-ra dose. We showed in a population-based cohort study that GLP1-ra use is not associated with a decreased bone fracture risk compared to users of other anti-hyperglycemic drugs. Future research is needed to elucidate the potential working mechanisms of GLP1-ra on bone.</subfield>
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   <subfield code="a">The Author(s), 2015</subfield>
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   <subfield code="u">Division of Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute of Pharmaceutical Sciences, Utrecht University, Utrecht, The Netherlands</subfield>
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   <subfield code="a">Henry</subfield>
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   <subfield code="a">van Onzenoort</subfield>
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   <subfield code="u">Department of Clinical Pharmacy and Toxicology, Maastricht University Medical Centre+, Maastricht, The Netherlands</subfield>
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   <subfield code="t">Calcified Tissue International</subfield>
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   <subfield code="a">Metadata rights reserved</subfield>
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