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Type 2 Diabetes Glucose Management Goals

Type 2 Diabetes Glucose Management Goals. AACE Comprehensive Diabetes Care: Glucose Goals . Handelsman Y, et al. Endocr Pract . 2011;17(suppl 2):1-53. Well-Recognized Risks for Hypoglycemia in T2DM. Use of insulin secretagogues and insulin therapy in any of the following settings:

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Type 2 Diabetes Glucose Management Goals

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  1. Type 2 Diabetes Glucose Management Goals

  2. AACE Comprehensive Diabetes Care: Glucose Goals Handelsman Y, et al. EndocrPract. 2011;17(suppl 2):1-53.

  3. Well-Recognized Risks for Hypoglycemia in T2DM • Use of insulin secretagogues and insulin therapy in any of the following settings: • Missed or irregular meals • Advanced age • Longer duration of diabetes • Impaired awareness of hypoglycemia • Exercise • Taking greater than the prescribed medication dose • Excessive alcohol intake • Preexisting impairment, or sudden worsening, of renal or hepatic function • Less well-recognized risks: female sex, African-American race, less education (ACCORD) AmielSA, et al. Diabet Med. 2008;25:245-254. ADA. Diabetes Care. 2005;28:1245-1249.

  4. Limitations of Management Goals: Potential Consequences of Hypoglycemia • Neurogenic symptoms • Tremor, palpitations, anxiety, sweating, hunger (weight gain), paresthesias • Neuroglycopenia morbidity • Cognitive impairment, psychomotor abnormalities, abnormal behavior, seizure, coma, mortality (brain death) • Rebound hyperglycemia, brittle diabetes • Barrier to glycemic control and adherence to treatment secondary to fear of hypoglycemia • Greater risk of dementia • Prolonged QT interval with increased risk of dysrhythmias, sudden death • Harm to property or to others (eg, if driving) Cryer PE. J Clin Invest. 2007;117:868-870. Cryer PE. Diabetes Care. 2003;26:1902-1912.

  5. Glucose Control and Mortality:ACCORD Posthoc Analysis Adjusted Log (Hazard Ratio) by Treatment StrategyRelative to Standard at A1C of 6% Risk increase with each 1% increasein A1C Mortality Risk Intensive P Value 66% <0.0001 1 Log (Hazard Ratio) 0 14% 0.17 Mortality Benefit Standard -1 6 7 8 9 Average A1C (%) Riddle MC, et al. Diabetes Care. 2010;33:983-990.

  6. Algorithm for Individualizing Glycemic Targets Most intensive Less intensive Least intensive 6.0% 7.0% 8.0% Psychosocioeconomic considerations Less motivated, nonadherent, limited insight, poor self-care capacities, and weak support systems Highly motivated, adherent, knowledgeable, excellent self-care capacities, and comprehensive support systems Hypoglycemia risk Low Moderate High Patient age, years 40 45 50 55 60 65 70 75 Disease duration, years 5 10 15 20 Other comorbid conditions None Few or mild Multiple or severe Established vascular complications None Cardiovascular disease Early microvascular Advanced microvascular Ismail-Beigi F, Moghissi E, et al. Ann Intern Med. 2011;154:554-559.

  7. ADA-Recommended Approach to Management of Hyperglycemia More Stringent Less Stringent Patient attitude and expected treatment efforts Highly motivated, adherent,excellent self-care capacities Less motivated, nonadherent, poor self-care capacities Risks potentially associated with hypoglycemia, other adverse events Low High Disease duration Newly diagnosed Long-standing Life expectancy Long Short Important comorbidities Absent Few/mild Severe Established vascular complications Absent Few/mild Severe Resources, support system Readily available Limited Inzucchi SE, et al. Diabetes Care. 2012;35:1364-1379.

  8. Hyperglycemia and Microvascular Complications

  9. Hyperglycemia-Induced Tissue Damage: General Features • Cumulative long-term changes in stable macromolecules • Genetic determinants of individual susceptibility • Hyperglycemia • Repeated acute changes in cellular metabolism • Independent accelerating factors • (eg, hypertension, dyslipidemia) • Diabetic tissue damage Brownlee M. Diabetes. 2005;54:1615-1625.

  10. Microvascular Complications of Diabetes Nephropathy Retinopathy Neuropathy

  11. 20 Retinopathy 18 16 Nephropathy 14 Neuropathy 12 Microalbuminuria 10 8 6 4 2 0 Microvascular Complications Increase With Increasing A1C Diabetes Control and Complications Trial Relative Risk 6 7 8 9 10 11 12 A1C (%) Skyler JS. EndocrinolMetabClin North Am. 1996;25:243-254.

  12. Reducing A1C Reduces Microvascular Risk United Kingdom Prospective Diabetes Study 10 P<0.0001 Microvascular ComplicationsHazard Ratio 1 37% Decreaseper 1% reduction in A1C 0.5 0 5 6 7 8 9 10 Updated Mean A1C Stratton IM, et al. BMJ. 2000;321:405-412.

  13. Reducing A1C Reduces Nephropathy Riskin T2DM *Intensive vs standard glucose control. 1. UK Prospective Diabetes Study (UKPDS) Group. Lancet. 1998;352:837-853.2. ADVANCE Collaborative Group. N Engl J Med. 2008;358:2560-2572.3. Ismail-Beigi F, et al. Lancet. 2010;376:419-430.

  14. Prevalence of CKD in Diagnosed Diabetes Diabetic Kidney Disease Is the Leading Cause of Kidney Failure in the United States *Pathologic abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies. ESRD, end-stage renal disease; GFR, glomerular filtration rate (mL/min/1.73 m2); NKF, National Kidney Foundation. CDC. National diabetes fact sheet, 2011. http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf. PlantingaLC, et al. Clin J Am SocNephrol. 2010;5:673-682.

  15. Development ofDiabetic Nephropathy Genetically susceptible individuals • Renal failure • Hyperglycemia • Hypertension • Angiotensin II • Hyperfiltration • Enlarged kidneys • Breakdown of glomerular filtration barrier • Micro-albuminuria • Protein reabsorption and accumulation in renal epithelial cells • Capillary occlusion • Decreasing GFR • Macro-albuminuria • Release of vasoactive and inflammatory cytokines • Tubule and podocyte damage • Tubular atrophy and fibrosis, podocyte destruction RadbillB, et al. Mayo Clin Proc. 2008;83:1373-1381. Remuzzi G, Bertani T. N Engl J Med. 1998;339:1448-1456.

  16. x 2.8 x 2.0 x 2.1 x 1.7 x 2.5 x 2.3 CV Risk Increases With Comorbid Diabetes and CKD AMI, acute myocardial infarction; ASVD, atherosclerotic vascular disease; CHF, congestive heart failure; CVA/TIA, cerebrovascular accident/transient ischemic attack; PVD, peripheral vascular disease. *ASVD was defined as the first occurrence of AMI, CVA/TIA, or PVD. Foley RN, et al. J Am SocNephrol. 2005;16:489-495.

  17. Appropriate Staging and Management of DKD DKD, diabetic kidney disease. *Includesactions from preceding stages. †Pathologic abnormalities or markers of damage, including abnormalities in blood or urine tests or imaging studies. National Kidney Foundation. Am J Kidney Dis. 2002;39(suppl 1):S1-S266.

  18. KDIGO CKD Classification by Relative Risk Levey AS, et al. Kidney Int. 2011;80:17-28.

  19. DKD Risk Factor Management Handelsman Y, et al. EndocrPract. 2011;17(suppl 2):1-53. National Kidney Foundation. Am J Kidney Dis. 2007;49(suppl 2):S1-S179.

  20. Use of Noninsulin Antidiabetic Therapies in Patients With Kidney Disease Inzucchi SE, et al. Diabetes Care. 2012;35:1364-1379. HandelsmanY, et al. EndocrPract. 2011;17(suppl 2):1-53. National Kidney Foundation. Am J Kidney Dis. 2007;49(suppl 2):S1-S179.

  21. Dietary Guidelines for DKD Handelsman Y, et al. EndocrPract. 2011;17(suppl 2):1-53. National Kidney Foundation. Am J Kidney Dis. 2007;49(suppl 2):S1-S179.

  22. Reducing A1C Reduces Retinopathy Progression in T2DM *Intensive vs standard glucose control. UK Prospective Diabetes Study (UKPDS) Group. Lancet. 1998;352:837-853.Ismail-BeigiF, et al. Lancet. 2010;376:419-430.Chew EY, et al. N Engl J Med. 2010;363:233-244.

  23. Prevalence of Diabetic Retinopathy Diabetic Retinopathy Is the Leading Cause of Adult Blindness in the United States NHANES 2005-2008 Adults Age ≥40 Years (N=1006) *Severe NPDR, PDR, or clinically significant macular edema. NPDR, nonproliferative diabetic retinopathy; PDR, proliferative diabetic retinopathy; T2DM, type 2 diabetes mellitus. CDC. National diabetes fact sheet, 2011. http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf. Zhang X, et al. JAMA. 2010;304:649-656.

  24. Diabetic Retinopathy Management • Goal: detect clinically significant retinopathy before vision is threatened • Annual dilated eye examination by experienced ophthalmologist, starting at diagnosis for all T2DM patients Handelsman Y, et al. EndocrPract. 2011;17(suppl 2):1-53.

  25. Reducing A1C Reduces Neuropathy Risk in T2DM *Intensive vs standard glucose control. Ismail-BeigiF, et al. Lancet. 2010;376:419-430.

  26. Prevalence of Diabetic Neuropathy Diabetic Peripheral Neuropathy Is the LeadingCause of Nontraumatic Amputations in the United States • Neuropathy is a heterogenous disorder • 70% to 100% of T2DM patients may have at least mild damage to • Proximal nerves • Distal nerves • Somatic nerves • Autonomic nerves • Neuropathy may be • Acuteand self-limiting • Chronic and indolent NHANES 1999-2004 Adults With Diabetes, Age ≥40 Years3 (N=559) CDC. National diabetes fact sheet, 2011. http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf. Gregg EW, et al. Diabetes Res ClinPract. 2007;77:485-488. Handelsman Y, et al. EndocrPract. 2011;17(suppl 2):1-53.

  27. Diabetic Neuropathies: Key Characteristics and Management Recommendations • Optimize glucose, lipid, and blood pressure control for all T2DM patients HandelsmanY, et al. EndocrPract. 2011;17(suppl 2):1-53.

  28. Diabetic Neuropathies: Key Characteristics and Management Recommendations • Optimize glucose, lipid, and blood pressure control for all T2DM patients HandelsmanY, et al. EndocrPract. 2011;17(suppl 2):1-53.

  29. Diabetic Neuropathies: Key Characteristics and Management Recommendations • Optimize glucose, lipid, and blood pressure control for all T2DM patients HandelsmanY, et al. EndocrPract. 2011;17(suppl 2):1-53.

  30. Diabetic Neuropathies: Key Characteristics and Management Recommendations • Optimize glucose, lipid, and blood pressure control for all T2DM patients HandelsmanY, et al. EndocrPract. 2011;17(suppl 2):1-53.

  31. Diabetic Neuropathies: Key Characteristics and Management Recommendations • Optimize glucose, lipid, and blood pressure control for all T2DM patients HandelsmanY, et al. EndocrPract. 2011;17(suppl 2):1-53.

  32. Hyperglycemia and Macrovascular Complications

  33. Diabetes Is a Cardiovascular Disease Risk Equivalent 7-Year Incidence of MI (%) P<0.001 P<0.001 No prior MI Prior MI No prior MI Prior MI Nondiabetic (n=1373) Diabetic (n=1059) MI, myocardial infarction. Grundy SM, et al. Circulation. 2004;110:227-239.HaffnerSM, et al. N Engl J Med. 1998;339:229-234.

  34. Lower A1C Is Associated With Lower Risk of Myocardial Infarction United Kingdom Prospective Diabetes Study 10 P<0.0001 Myocardial InfarctionHazard Ratio 1 14% Decreaseper 1% reduction in A1C 0.5 0 5 6 7 8 9 10 Updated Mean A1C Stratton IM et al. BMJ. 2000;321:405-412.

  35. Intensive Glycemic Control Reduces Long-term Macrovascular Risk in Younger Patients With Shorter Duration of Disease UKPDS T2DM, newly diagnosed (N=4209) DCCT T1DM, 5-6 years duration (N=1441) 42% risk reductionP=0.02 15% risk reductionP=0.01 0.12 1.0 Randomized treatment Randomized treatment 0.10 0.8 0.08 Conventional 0.6 CV Outcome Cumulative incidence 0.06 Proportion With MI Conventional 0.4 0.04 0.2 Intensive 0.02 Intensive 0.00 0.0 0 5 10 15 20 0 5 10 15 20 25 Years Years No. at Risk Conventional 714 688 618 92 Intensive 705 683 629 113 11381013857578 221 20 2729248820971459 577 66 CV, cardiovascular; DCCT, Diabetes Control and Complications Trial; MI, myocardial infarction;UKPDS, United Kingdom Prospective Diabetes Study. Nathan DM, et al. N Engl J Med. 2005;353:2643-2653.Holman RR, et al. N Engl J Med. 2008;359:1577-1589.

  36. Intensive Glycemic Control Does Not Reduce MacrovascularRisk in Older Patients With Longer Duration of Disease *Intensive vs standard glucose control. ACCORD Study Group. N Engl J Med. 2008;358:2545-2559.ADVANCE Collaborative Group. N Engl J Med. 2008;358:2560-2572. Duckworth W, et al. N Engl J Med. 2009;360:129-139.

  37. Macrovascular Risk Reduction in T2DM • Individualized glucose control • Hypertension control • Dyslipidemia control • Smoking cessation • Aspirin therapy • Diagnosis and management of: • Autonomic cardiac neuropathy • Kidney disease HandelsmanY, et al. EndocrPract. 2011;17(suppl 2):1-53.

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