Giulia Leanza1, Ernesto Maddaloni2, Dario Pitocco3, Caterina Conte4, Andrea Palermo5, Anna Rita Maurizi6, Angelo Lauria Pantano7, Concetta Suraci8, Maria Altomare8, Rocky Strollo9, Silvia Manfrini10, Paolo Pozzilli11, Ann V Schwartz12, Nicola Napoli13. 1. Department of Medicine, Unit of Endocrinology and Diabetes, Campus Bio-Medico University of Rome, Italy. Electronic address: g.leanza@unicampus.it. 2. Department of Medicine, Unit of Endocrinology and Diabetes, Campus Bio-Medico University of Rome, Italy. Electronic address: e.maddaloni@unicampus.it. 3. Diabetology, Catholic University, Rome, Italy. Electronic address: Dario.pitocco@unicatt.it. 4. Vita-Salute San Raffaele University, Milan, Italy; Clinical Transplant Unit, Division of Immunology, Transplantation and Infectious Diseases, IRCCS Ospedale San Raffaele, Milan, Italy. 5. Department of Medicine, Unit of Endocrinology and Diabetes, Campus Bio-Medico University of Rome, Italy. Electronic address: a.palermo@unicampus.it. 6. Department of Medicine, Unit of Endocrinology and Diabetes, Campus Bio-Medico University of Rome, Italy. Electronic address: a.maurizi@unicampus.it. 7. Department of Medicine, Unit of Endocrinology and Diabetes, Campus Bio-Medico University of Rome, Italy. Electronic address: a.lauria@unicampus.it. 8. Diabetes Unit, Sandro Pertini Hospital, Rome, Italy. 9. Department of Medicine, Unit of Endocrinology and Diabetes, Campus Bio-Medico University of Rome, Italy. Electronic address: r.strollo@unicampus.it. 10. Department of Medicine, Unit of Endocrinology and Diabetes, Campus Bio-Medico University of Rome, Italy. Electronic address: s.manfrini@unicampus.it. 11. Department of Medicine, Unit of Endocrinology and Diabetes, Campus Bio-Medico University of Rome, Italy. Electronic address: p.pozzilli@unicampus.it. 12. Department of Epidemiology and Biostatistics, University of California, San Francisco, San Francisco, CA, USA. Electronic address: aschwartz@psg.ucsf.edu. 13. Department of Medicine, Unit of Endocrinology and Diabetes, Campus Bio-Medico University of Rome, Italy; Division of Bone and Mineral Diseases, Washington University in St Louis, USA. Electronic address: n.napoli@unicampus.it.
Abstract
OBJECTIVE: To determine clinical diabetes-related risk factors for fragility fractures in type 1 diabetes (T1D). RESEARCH DESIGN AND METHODS: History of bone fragility fractures occurring after T1D diagnosis was assessed by questionnaire in this cross-sectional study in 600 T1D subjects. Glycated hemoglobin A1c (HbA1c) over the previous 5 years was used as an index of long-term glycemic control; complications were adjudicated by physician assessment. Multinomial logistic regression models were used to assess the associations between diabetes-related risk factors and fracture history. RESULTS: One-hundred-eleven patients (18.5%) reported at least one fracture; of these 73.8% had only one and 26.2% had more than one fracture. Average age was 41.9 ± 12.8 years, with even gender distribution; disease duration was 19.9 ± 12.0 years; and BMI was 24.4 ± 3.7 kg/m2. The 5-year average HbA1c was 7.6 ± 1.0% (60 mmol/mol). In adjusted models, reduced risk for 1 fracture was found in those with higher creatinine clearance rate (CCr) (RRR 0.22 [95% CI: 0.06-0.83] for 1 unit increase in lnCCr, p = 0.03) and increased risk in those with neuropathy (RRR 2.57 [1.21-5.46], p = 0.01). Increased risk for ≥2 fractures was found in subjects in the highest tertile of HbA1c (≥7.9%) compared with the lowest tertile (≤7.17%) (RRR 3.50 [1.04-11.7], p = 0.04) and of disease duration (≥26 years versus <14 years) (RRR 7.59 [1.60-35.98], p = 0.01). CONCLUSIONS: Poor glycemic control and long exposure to the disease are independent diabetes-related risk factors for multiple bone fractures in T1D.
OBJECTIVE: To determine clinical diabetes-related risk factors for fragility fractures in type 1 diabetes (T1D). RESEARCH DESIGN AND METHODS: History of bone fragility fractures occurring after T1D diagnosis was assessed by questionnaire in this cross-sectional study in 600 T1D subjects. Glycated hemoglobin A1c (HbA1c) over the previous 5 years was used as an index of long-term glycemic control; complications were adjudicated by physician assessment. Multinomial logistic regression models were used to assess the associations between diabetes-related risk factors and fracture history. RESULTS: One-hundred-eleven patients (18.5%) reported at least one fracture; of these 73.8% had only one and 26.2% had more than one fracture. Average age was 41.9 ± 12.8 years, with even gender distribution; disease duration was 19.9 ± 12.0 years; and BMI was 24.4 ± 3.7 kg/m2. The 5-year average HbA1c was 7.6 ± 1.0% (60 mmol/mol). In adjusted models, reduced risk for 1 fracture was found in those with higher creatinine clearance rate (CCr) (RRR 0.22 [95% CI: 0.06-0.83] for 1 unit increase in lnCCr, p = 0.03) and increased risk in those with neuropathy (RRR 2.57 [1.21-5.46], p = 0.01). Increased risk for ≥2 fractures was found in subjects in the highest tertile of HbA1c (≥7.9%) compared with the lowest tertile (≤7.17%) (RRR 3.50 [1.04-11.7], p = 0.04) and of disease duration (≥26 years versus <14 years) (RRR 7.59 [1.60-35.98], p = 0.01). CONCLUSIONS: Poor glycemic control and long exposure to the disease are independent diabetes-related risk factors for multiple bone fractures in T1D.
Authors: V Van Hulten; Nicklas Rasmussen; J H M Driessen; A M Burden; A Kvist; J P van den Bergh Journal: Curr Osteoporos Rep Date: 2021-12-21 Impact factor: 5.096