Fasting Versus Postprandial Hyperglycemia as a Treatment Target to Lower Elevated Hemoglobin A1C |
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| Institution: | 1. From University Physicians – Primary Care, Augusta, Georgia;2. Mercy Diabetes Center, Janesville, Wisconsin;3. Sanofi US, Inc, Bridgewater, New Jersey;4. Medpace, Cincinnati, Ohio, Carlsbad, California.;5. Isis Pharmaceuticals, Inc, Carlsbad, California.;1. From the Department of Medicine, Rollins School of Public Health, Emory University, Atlanta, Georgia.;2. Department of Biostatistics and Bioinformatics, Rollins School of Public Health, Emory University, Atlanta, Georgia.;1. Section of Endocrinology and Metabolism, Department of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada;2. Winnipeg Regional Health Authority, Health Sciences Centre, Winnipeg, Manitoba, Canada;3. LMC Diabetes & Endocrinology, Brampton, Ontario, Canada;4. Leadership Sinai Centre for Diabetes, Mount Sinai Hospital, Toronto, Ontario, Canada;5. Montreal Institute for Clinical Research, Division of Endocrinology and Department of Nutrition, Université de Montréal, Montreal, Quebec, Canada;6. Division of Endocrinology, University of Alberta; Diabetic Nephropathy Prevention Clinic, Alberta Health Services, Edmonton, Alberta, Canada |
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| Abstract: | Objective: Postprandial hyperglycemia (PPHG) may need addressing when glycemic control cannot be maintained in patients with type 2 diabetes mellitus. We investigated whether glycated hemoglobin A1c (A1c) levels ≥7.0% can indicate postprandial defects warranting prandial therapy after optimized basal insulin therapy.Methods: From 6 clinical trials of insulin glargine treatment, data were pooled from 496 patients with A1c ≥7.0% after 24 weeks. Patient characteristics and clinical outcomes were summarized according to fasting plasma glucose (FPG) target achievement (<130 mg/dL), postprandial blood glucose (PPBG) levels, and PPBG increments (ΔPPBG). Basal and postprandial contributions to hyperglycemia were determined.Results: After 24 weeks of insulin glargine titration, A1c change from baseline was greater in patients with FPG <130 mg/dL versus ≥130 mg/dL (-1.35% versus -1.11%, respectively; P = .0275), but with increased confirmed hypoglycemia rates (blood glucose <70 mg/dL; 4.06 events/patient-year versus 3.31 events/patient-year; P = .0170). However, increased severe hypoglycemia rates were observed in patients with FPG ≥130 mg/dL. At week 24, postprandial contributions to hyperglycemia increased (>60% regardless of PPBG). Patients with high FPG had lower, but substantial, relative postprandial contributions versus patients achieving FPG target. A similar pattern was observed according to whether patients had a ΔPPBG ≥50 mg/dL after any meal.Conclusion: After optimized basal insulin therapy, elevated A1c is the most effective indicator of residual PPHG, regardless of existent FPG or PPBG. When confronted with an uncontrolled A1c after reasonable titration of basal insulin, clinicians should be aware of probable postprandial contributions to hyperglycemia and consider prandial therapy.Abbreviations:A1c = glycated hemoglobin A1cAUC = area under the curveAUCB = area under the curve (basal hyperglycemia)AUCG = total area under the curve (total glucose)AUCN = area under the curve (normal glycemic exposure)AUCP = area under the curve (postprandial hyperglycemia)BHG = basal hyperglycemiaFBG = fasting blood glucoseFPG = fasting plasma glucoseGLP-1 = glucagon-like peptide 1HE = hyperglycemic exposureOADs = oral antidiabetes drugsPPBG = postprandial blood glucoseΔPPBG = change in postprandial blood glucosePPHG = postprandial hyperglycemiaSMBG = self-monitored blood glucoseT2DM = type 2 diabetes mellitus |
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