Louis Potier1,2,3, Ronan Roussel4,2,3, Michel Marre4,2,3,5, Petter Bjornstad5, David Z Cherney6, Ray El Boustany4,3, Frédéric Fumeron2,3, Nicolas Venteclef3, Jean-François Gautier2,3,7, Samy Hadjadj8, Kamel Mohammedi9,10,11, Gilberto Velho3. 1. Department of Diabetology, Endocrinology and Nutrition, DHU FIRE, Bichat Hospital, Assistance Publique - Hôpitaux de Paris, Paris, France louis.potier@gmail.com. 2. Université de Paris, Paris, France. 3. INSERM, UMRS 1138, Cordeliers Research Center, Paris, France. 4. Department of Diabetology, Endocrinology and Nutrition, DHU FIRE, Bichat Hospital, Assistance Publique - Hôpitaux de Paris, Paris, France. 5. Section of Endocrinology, Department of Pediatrics, and Division of Nephrology, Department of Medicine, University of Colorado School of Medicine, Aurora, CO. 6. Division of Nephrology, Department of Medicine, Toronto General Hospital, University of Toronto, Toronto, Ontario, Canada. 7. Department of Diabetes, Clinical Investigation Centre (CIC-9504), Lariboisière Hospital, Assistance Publique - Hôpitaux de Paris, Paris, France. 8. L'Institut du thorax, INSERM, CNRS, Université de Nantes, Centre Hospitalier Universitaire de Nantes, Nantes, France. 9. Department of Diabetology, Endocrinology and Nutrition, Hôpital Haut-Lévêque, Bordeaux, France. 10. Bordeaux University, Bordeaux, France. 11. INSERM U1219 "Bordeaux Population Health," Bordeaux, France.
Abstract
OBJECTIVE: Diabetes is the leading cause of nontraumatic lower-extremity amputations (LEAs). Identification of patients with foot ulcers at risk for amputation remains clinically challenging. Plasma copeptin, a surrogate marker of vasopressin, is associated with the risk of cardiovascular and renal complications in diabetes. RESEARCH DESIGN AND METHODS: We assessed the association between baseline plasma copeptin and risk of LEA during follow-up in four cohorts of people with type 1 (GENESIS, n = 503, and GENEDIAB, n = 207) or type 2 diabetes (DIABHYCAR, n = 3,101, and SURDIAGENE, n = 1,452) with a median duration of follow-up between 5 and 10 years. Copeptin concentration was measured in baseline plasma samples by an immunoluminometric assay. RESULTS: In the pooled cohorts with type 1 diabetes (n = 710), the cumulative incidence of LEA during follow-up by increasing tertiles (tertile 1 [TER1], TER2, and TER3) of baseline plasma copeptin was 3.9% (TER1), 3.3% (TER2), and 10.0% (TER3) (P = 0.002). Cox regression analyses confirmed the association of copeptin with LEA: hazard ratio (HR) for 1 SD increment of log[copeptin] was 1.89 (95% CI 1.28-2.82), P = 0.002. In the pooled cohorts of type 2 diabetes (n = 4,553), the cumulative incidence of LEA was 1.1% (TER1), 2.9% (TER2), and 3.6% (TER3) (P < 0.0001). In Cox regression analyses, baseline plasma copeptin was significantly associated with LEA: HR for 1 SD increment of log[copeptin] was 1.42 (1.15-1.74), P = 0.001. Similar results were observed in the cohort with type 2 diabetes for lower-limb revascularization (HR 1.20 [95% CI 1.03-1.39], P = 0.02). CONCLUSIONS: Baseline plasma copeptin is associated with cumulative incidence of LEA in cohorts of people with both type 1 and type 2 diabetes and may help to identify patients at risk for LEA.
OBJECTIVE:Diabetes is the leading cause of nontraumatic lower-extremity amputations (LEAs). Identification of patients with foot ulcers at risk for amputation remains clinically challenging. Plasma copeptin, a surrogate marker of vasopressin, is associated with the risk of cardiovascular and renal complications in diabetes. RESEARCH DESIGN AND METHODS: We assessed the association between baseline plasma copeptin and risk of LEA during follow-up in four cohorts of people with type 1 (GENESIS, n = 503, and GENEDIAB, n = 207) or type 2 diabetes (DIABHYCAR, n = 3,101, and SURDIAGENE, n = 1,452) with a median duration of follow-up between 5 and 10 years. Copeptin concentration was measured in baseline plasma samples by an immunoluminometric assay. RESULTS: In the pooled cohorts with type 1 diabetes (n = 710), the cumulative incidence of LEA during follow-up by increasing tertiles (tertile 1 [TER1], TER2, and TER3) of baseline plasma copeptin was 3.9% (TER1), 3.3% (TER2), and 10.0% (TER3) (P = 0.002). Cox regression analyses confirmed the association of copeptin with LEA: hazard ratio (HR) for 1 SD increment of log[copeptin] was 1.89 (95% CI 1.28-2.82), P = 0.002. In the pooled cohorts of type 2 diabetes (n = 4,553), the cumulative incidence of LEA was 1.1% (TER1), 2.9% (TER2), and 3.6% (TER3) (P < 0.0001). In Cox regression analyses, baseline plasma copeptin was significantly associated with LEA: HR for 1 SD increment of log[copeptin] was 1.42 (1.15-1.74), P = 0.001. Similar results were observed in the cohort with type 2 diabetes for lower-limb revascularization (HR 1.20 [95% CI 1.03-1.39], P = 0.02). CONCLUSIONS: Baseline plasma copeptin is associated with cumulative incidence of LEA in cohorts of people with both type 1 and type 2 diabetes and may help to identify patients at risk for LEA.
Authors: Samy Hadjadj; Franck Péan; Yves Gallois; Philippe Passa; Robert Aubert; Laurent Weekers; Vincent Rigalleau; Bernard Bauduceau; Amine Bekherraz; Ronan Roussel; Bernard Dussol; Michel Rodier; Richard Marechaud; Pierre J Lefebvre; Michel Marre Journal: Diabetes Care Date: 2004-11 Impact factor: 19.112
Authors: Bruce Neal; Vlado Perkovic; Kenneth W Mahaffey; Dick de Zeeuw; Greg Fulcher; Ngozi Erondu; Wayne Shaw; Gordon Law; Mehul Desai; David R Matthews Journal: N Engl J Med Date: 2017-06-12 Impact factor: 91.245
Authors: Dana Bar-Shalom; Mikael K Poulsen; Lars M Rasmussen; Axel C P Diederichsen; Niels P R Sand; Jan E Henriksen; Mads Nybo Journal: Diab Vasc Dis Res Date: 2014-08-05 Impact factor: 3.291