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Diabetes: The Burden of Disease

Diabetes: The Burden of Disease. Fall, 2007 NUR464. 1990. 1995. No Data. < 4%. 4%-6%. 6%-8%. 8%-10%. > 10% . Prevalence of Diabetes Is Escalating . 2001. (Includes Gestational Diabetes).

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Diabetes: The Burden of Disease

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  1. Diabetes: The Burden of Disease Fall, 2007 NUR464

  2. 1990 1995 No Data < 4% 4%-6% 6%-8% 8%-10% > 10% Prevalence of Diabetes Is Escalating 2001 (Includes Gestational Diabetes) Source: Mokdad A, et al. Diabetes Care. 2000;23:1278-1283; Mokdad A, et al. J Am Med Assoc. 2001;286:10; Mokdad A, et al. JAMA. 2003;289:76-79.

  3. Diabetes Mortality Continues Unabated Age­AdjustedDeath RateRelative to 1980 Year Freid VM, et al. National Center for Health Statistics, 2003.

  4. Type 2 Accounts for the Vast Majority of Diabetes Mellitus Cases • Type 2 diabetes • About 90% of the diabetes population • Dual impairment: Insulin deficiency & Insulin resistance • No longer a disease of adults only • Obesity • Genetic link • Type 1 diabetes • Approximately 10% of diabetes population • Absolute insulin requirement • Autoimmune mediated CDC. National Diabetes Fact Sheet. 2003; Atlanta, GA. US Dept. HHS, Center for Disease Control and Prevention 2003.

  5. Link Between Obesity and Type 2 Diabetes: Harvard Nurses’ Health Study 120 100 80 60 Age­Adjusted Relative Risk for Diabetes Mellitus 40 20 0 < 22 22­ 23­ 24­ 25­ 27­ 29­ 31­ 33­ > 35 22.9 23.8 24.9 26.9 28.9 30.9 32.9 34.9 BMI (kg/m2) Colditz GA, et al. Ann Intern Med. 1995;122:481-486.

  6. 2002 — Total Per Capita Health Care Expenditures ADA. Diabetes Care. Mar. 2003;26(3):917-932.

  7. Physiologic Blood Insulin Secretion Profile 75 Breakfast Lunch Dinner 50 Plasma Insulin (µU/mL) 25 4:00 8:00 12:00 16:00 20:00 24:00 4:00 8:00 Time Adapted from White JR, Campbell RK, Hirsch I. Postgraduate Medicine. June 2003;113(6):30-36.

  8. Normal Physiologic Insulin Sensitivity and ­Cell Function Produce Euglycemia Normal Insulin Sensitivity Normal ­Cell Function Decreased Lipolysis Pancreas Liver Decreased Plasma FFA ↑ Glucose Uptake ↓ Glucose Production Islet ­Cell Degranulation;Insulin Released in Response to Elevated Plasma Glucose Muscle Adipose Tissue Decreased Glucose Output Normal Physiologic Plasma Insulin Increased Glucose Transport Euglycemia

  9. ­Cell Dysfunction and Insulin Resistance Produce Hyperglycemia in Type 2 Diabetes Insulin Resistance ­Cell Dysfunction Increased Lipolysis Pancreas Liver Elevated Plasma FFA ↓Glucose Uptake ↑Glucose Production Islet ­Cell Degranulation;Reduced Insulin Content Muscle Adipose Tissue Increased Glucose Output Reduced Plasma Insulin Decreased Glucose Transport & Activity (expression) of GLUT4 Hyperglycemia

  10. Usually slow onset May be asymptomatic 3 P’s: polyuria, polydipsia, polyphagia Weakness/fatigue Glycosuria Dry, itchy skin Visual changes Skin and mucous membrane infections Frequent Symptoms of Type 2 Diabetes

  11. Stages of Type 2 Diabetes Related to Beta-Cell Function 100 75 Beta­Cell Function (%) 50 Type 2Phase 1 IGT Type 2Phase 3 25 PostprandialHyperglycemia Type 2Phase 2 0 ­12 ­10 ­6 ­2 0 2 6 10 14 Years from Diagnosis Adapted from Lebovitz HE. Diabetes Reviews. 1999;7(3).

  12. Significant Loss of Beta­Cell Function at Diagnosis • UKPDS • At the time diabetes was diagnosed, 50% of beta­cell function was lost • Beta­cell function continued to decline over the 10-year course of the study • Correlated with loss of response to oral therapy • Secondary failure (progressive loss of beta cell) UKPDS 16. Diabetes. 1995;44:1249-1258 Turner RC, et al. JAMA. 1999 Jun 2;281(21):2005-2012.

  13. Glucose Excursions in Type 2 Diabetes Meal Meal Meal 400 Diabetic 300 Glucose(mg/dL) 200 100 Normal 0 0600 1000 1400 1800 2200 0200 0600 Time of Day Polonsky KS, et al.NEJM. 1988;21;318(19):1237-1239.

  14. Insulin Secretion in Type 2 Diabetes Meal Meal Meal 800 Normal Type 2 diabetes 600 Insulin Secretion (pmol/min) 400 200 0 0600 1000 1400 1800 2200 0200 Time (24­hour clock) Polonsky KS, et al.N Engl J Med. 1996 Mar 21;334(12):777-783.

  15. Normal A1C < 6.0% A1C = + PPG FPG CDC. National Diabetes Fact Sheet. 2003; Atlanta, GA. US Dept. HHS, Center for Disease Control and Prevention 2003.

  16. 110-125 Relative Risk for Death Increases with 2­hour Blood Glucose Regardless of the FPG Level 2.4 2.0 Relative Risk of Death* 1.6 1.2 > 199 1.0 140-198 < 110 < 140 2-h Postprandial Glucose (mg/dL) 126- 139 >140 Fasting Plasma Glucose (mg/dL) *Adjusted for age, sex, study center Adapted from DECODE Study Group. Lancet. 1999;354:617-621.

  17. 100 80 60 40 20 0 As Patients Get Closer to A1C Goal, the Need to Manage PPG Significantly Increases Increasing Contribution of PPG as A1C Improves % Contribution A1C Range (%) Adapted from Monnier L, Lapinski H, Collette C. Contributions of fasting and postprandial plasma glucose increments to the overall diurnal hyperglycemia of Type 2 diabetic patients: variations with increasing levels of HBA(1c). Diabetes Care. 2003;26:881-885.

  18. Blood Glucose Control Guidelines American College of Endocrinology (ACE) American Diabetes Association (ADA) American Diabetes Association. Diabetes Care. 2003;26(suppl 1):S33-S50. American College of Endocrinology. Endocr Pract. 2002;8(suppl 1):40-82.

  19. 60 Chlorpropamide Glipizide 40 20 0 1 2 3 4 5 6 Years from Randomization UKPDS 57: Over Time Increasing Numbers of Patients Require Insulin Patients Requiring Additional Insulin (%) Adapted from: Wright A, et al. Diabetes Care. 2002;25:330–336.

  20. Insulin is Associated with the Most Profound Effects on A1C Nathan DM. NEJM. Oct 24, 2002;347(17):1342-1349.

  21. Human Insulins • Regular • Neutral Protamine Hagedorn (NPH) • Premix 70/30 (70% NPH / 30% Regular)

  22. Human Insulin Time-Action Patterns Normal insulin secretion at mealtime Change in serum insulin Theoretical representation of expected insulin release in nondiabetic subjects Baseline Level Time (hours) SC injection

  23. Normal insulin secretion at mealtime Human Insulin Time-Action Patterns Regular insulin (human) Change in serum insulin Theoretical representation of profile associated with Regular Insulin (human) Baseline Level Time (hours) SC injection

  24. Normal insulin secretion at mealtime Human Insulin Time-Action Patterns NPH insulin (human) Change in serum insulin Theoretical representation of profile associated with NPH Insulin Baseline Level Time (hours) SC injection

  25. Normal insulin secretion at mealtime Human Premix 70/30 (70% NPH & 30% Regular) Human Insulin Time-Action Patterns Theoretical representation of profile associated with Human Premix 70/30 Change in serum insulin Baseline Level Time (hours) SC injection

  26. Analog Insulins • Rapid-acting • Basal • Premix

  27. Normal insulin secretion at mealtime Analog Insulin Time-Action Patterns Change in serum insulin Theoretical representation of expected insulin release in nondiabetic subjects Baseline Level Time (hours) SC injection

  28. Normal insulin secretion at mealtime Analog Insulin Time-Action Patterns Rapid-Acting Insulin Analog Change in serum insulin Theoretical representation of profile associated with rapid-acting Insulin Analog Baseline Level Time (hours) SC injection

  29. Normal insulin secretion at mealtime Analog Insulin Time-Action Patterns QD (basal) Analog Insulin Change in serum insulin Theoretical representation of profile associated with Basal Analog Insulin Baseline Level Time (hours) SC injection

  30. Normal insulin secretion at mealtime Analog Insulin Time-Action Patterns Insulin Analog Premix Change in serum insulin Theoretical representation of profile associated with Insulin Analog Premix Baseline Level Time (hours) SC injection

  31. “Although insulin therapy has not traditionally been implemented early in the course of Type 2 diabetes, there is no reason why it should not be…” Nathan DM. NEJM. Oct 24, 2002;347(17):1342-1349.

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