Johanna H M Driessen1, Hein A W van Onzenoort2, Ronald M A Henry3, Arief Lalmohamed4, Joop P van den Bergh5, Cees Neef6, Hubert G M Leufkens7, Frank de Vries8. 1. Division of Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute of Pharmaceutical Sciences, Utrecht, The Netherlands; Care and Public Health Research Institute (CAPHRI), Maastricht, The Netherlands; Department of Clinical Pharmacy and Toxicology, Maastricht University Medical Centre+, Maastricht, The Netherlands. 2. Department of Clinical Pharmacy and Toxicology, Maastricht University Medical Centre+, Maastricht, The Netherlands; Department of Pharmacy, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands. 3. Department of Medicine, Maastricht University Medical Centre+, The Netherlands; Cardiovascular Research Institute Maastricht, Maastricht University Medical Centre+, The Netherlands. 4. Division of Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute of Pharmaceutical Sciences, Utrecht, The Netherlands; Department of Clinical Pharmacy, University Medical Centre Utrecht, Utrecht, The Netherlands. 5. Department of Internal Medicine, Viecuri Medical Centre, Venlo, The Netherlands; Department of Internal Medicine, Maastricht University Medical Centre+, Maastricht, The Netherlands; Biomedical Research Institute, University Hasselt, Hasselt, Belgium. 6. Care and Public Health Research Institute (CAPHRI), Maastricht, The Netherlands; Department of Clinical Pharmacy and Toxicology, Maastricht University Medical Centre+, Maastricht, The Netherlands. 7. Division of Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute of Pharmaceutical Sciences, Utrecht, The Netherlands. 8. Division of Pharmacoepidemiology and Clinical Pharmacology, Utrecht Institute of Pharmaceutical Sciences, Utrecht, The Netherlands; Care and Public Health Research Institute (CAPHRI), Maastricht, The Netherlands; Department of Clinical Pharmacy and Toxicology, Maastricht University Medical Centre+, Maastricht, The Netherlands; MRC Epidemiology Lifecourse Unit, Southampton General Hospital, Southampton UK. Electronic address: f.devries@uu.nl.
Abstract
INTRODUCTION: Although patients with type 2 diabetes mellitus have an increased bone mineral density as compared to healthy patients, their risk of fracture is elevated. Incretins, new anti-diabetic drugs, may have a protective effect on bone mineral density. However, data on the effect of incretins on fracture risk are limited. Therefore the aim of this study was to investigate the association between the use of DPP4-I and the risk of fracture. METHODS: A retrospective population based cohort study, using data from the Clinical Practice Research Datalink (CPRD) database (2007-2012), was conducted. Patients (N=216,816) with at least one prescription for a non-insulin anti-diabetic drug (NIAD), aged 18+ during data collection, were matched to one control patient. Cox proportional hazards models were used to estimate the hazard ratio of any fracture in DPP4 inhibitor (DPP4-I) users versus controls and versus other NIAD patients. Time-dependent adjustments were made for age, sex, life style, comorbidity and drug use. RESULTS: The actual duration of DPP4-I use was 1.3years. There was no different risk of fracture comparing current DPP4-I users to controls (adjusted hazard ratio (adj. HR) 0.89, 95% confidence interval (CI) 0.71-1.13). There was also no increased risk comparing current DPP4-I users to other NIAD users, adj. HR 1.03 (95% CI 0.92-1.15). CONCLUSIONS: DPP4-I use was not associated with fracture risk compared to controls and to other NIAD users. However, the duration of DPP4-I use in our database might have been too short to show an association with fracture risk.
INTRODUCTION: Although patients with type 2 diabetes mellitus have an increased bone mineral density as compared to healthy patients, their risk of fracture is elevated. Incretins, new anti-diabetic drugs, may have a protective effect on bone mineral density. However, data on the effect of incretins on fracture risk are limited. Therefore the aim of this study was to investigate the association between the use of DPP4-I and the risk of fracture. METHODS: A retrospective population based cohort study, using data from the Clinical Practice Research Datalink (CPRD) database (2007-2012), was conducted. Patients (N=216,816) with at least one prescription for a non-insulin anti-diabetic drug (NIAD), aged 18+ during data collection, were matched to one control patient. Cox proportional hazards models were used to estimate the hazard ratio of any fracture in DPP4 inhibitor (DPP4-I) users versus controls and versus other NIAD patients. Time-dependent adjustments were made for age, sex, life style, comorbidity and drug use. RESULTS: The actual duration of DPP4-I use was 1.3years. There was no different risk of fracture comparing current DPP4-I users to controls (adjusted hazard ratio (adj. HR) 0.89, 95% confidence interval (CI) 0.71-1.13). There was also no increased risk comparing current DPP4-I users to other NIAD users, adj. HR 1.03 (95% CI 0.92-1.15). CONCLUSIONS:DPP4-I use was not associated with fracture risk compared to controls and to other NIAD users. However, the duration of DPP4-I use in our database might have been too short to show an association with fracture risk.
Authors: Richard H Lee; Richard Sloane; Carl Pieper; Kenneth W Lyles; Robert A Adler; Courtney Van Houtven; Joanne LaFleur; Cathleen Colón-Emeric Journal: J Bone Miner Res Date: 2019-10-09 Impact factor: 6.741
Authors: Johanna H M Driessen; Frank de Vries; Hein van Onzenoort; Nicholas C Harvey; Cees Neef; Joop P W van den Bergh; Peter Vestergaard; Ronald M A Henry Journal: Br J Clin Pharmacol Date: 2016-12-07 Impact factor: 4.335