Julie White, MS Administrative Director Boston University School of Medicine Continuing Medical Education

Transcription

1 MENTOR QI Diabetes Performance Improvement Initiative, Getting Patients to Goal in Glycemic Control: Current Data Julie White, MS Administrative Director Boston University School of Medicine Continuing Medical Education

2 Participation 144 clinicians registered for the program 57 have completed their practice assessment 8 have completed their baseline chart reviews 4 have implemented their action plans and are awaiting reassessment

3 About Your Practices You see an average of 230 patients per month 36% of those patients have type 2 diabetes On a 1 to 10 scale (10 = highest), the average confidence level for treating type 2 diabetes is 7 35% (n=21) do not offer/encourage patient education 18% (n=11) do not have access to a Diabetes Educator or Nutritionist for their patients

4 Snapshot of Participants Practices Type 2 Diabetes Patients: # % Taking one oral medication Taking two oral medications Taking 3 or more oral medications Taking insulin alone Taking a combination of oral therapy AND insulin Taking a combination of oral therapy AND a non-insulin injectable Using an insulin pump Not on therapy 3 3.4

5 A1C Levels 47% of patients had A1C >7% at their last visit Therapy was not intensified for 22% of patients who had an A1C >7% at the last visit

6 Initiating and Advancing Oral Diabetes Medications Elliot Sternthal, MD, FACP Clinical Director of Diabetes Services Boston Medical Center Boston, MA

7 Type 2 Diabetes: Expanded Key Concepts Pathophysiology β-cell function: Insulin action: decreased insulin & amylin secretion increased insulin resistance in liver, muscle, & fat α-cell function: increased glucagon secretion ( ( hepatic glucose production) Gut: deficiency of incretin GLP-1 1 (exacerbates insulin deficiency & glucagon excess) Glucotoxicity aggravates both impairments Multiple mechanisms to correct hyperglycemia Most patients require combination therapy

8 Mechanisms to Lower Glucose Correct Insulin Deficiency Stimulate Insulin Secretion Glucose Production Muscle Glucose Uptake Retard Carbohydrate Absorption Insulin or Insulin Analogues Sulfonylureas Glinides X Biguanides X minor Glitazones minor X Alpha- glucosidase Inhibitors (AGIs) X X Pramlintide X X Exenatide* DPP-4 Inhib Inhib X X X* X

9 Oral Antihyperglycemic Monotherapy Maximum Therapeutic Effect on A1C Nateglinide Acarbose Repaglinide Rosiglitazone Pioglitazone Glimepiride Glipizide GITS Metformin Reduction in A1C (%) Hanefeld M, et al. Diabetes Care. 2000;23: ; 207; Precose (acarbose) package insert; Wolffenbuttel BH, van Haeften TW. Drugs ;50: ; 288; Lebovitz HE, et al. J Clin Endocrinol Metab. 2001;86: ; 288; Aronoff S, et al. Diabetes Care. 2000;23: ; 1611; Goldberg RB, et al. Diabetes Care ;19: ; 856; Simonson DC, et al. Diabetes Care. 1997;20: ; Garber AJ, et al. Am J Med ;102:

10 Incretin Deficiency in Type 2 Diabetes GLP-1 1 (glucagon-like like peptide-1) level is reduced by ~30% but sensitivity to it remains near normal. It is the predominant incretin GIP (glucose-dependent insulinotropic polypeptide) level remains normal but there is resistance to its action

11 Exenatide Mimics Many Properties of GLP-1 GLP-1 Exenatide Glucose-dependent insulin secretion Glucagon secretion Hepatic glucose output Hepatic glucose output Regulates gastric emptying Rate of nutrient absorption Rate of nutrient absorption Food intake Plasma glucose acutely to nearnormal levels normal levels Resistant to DPP-IV degradation Duration in plasma following a subcutaneous (SC) injection Short Long

12 Suggested Doses of Medications for Type 2 Diabetes* Medication Sulfonylurea Monotherapy Initial Dose Combination glyburide mg qd mg qd glipizide mg qd mg qd glimepiride Meglitinide 1-22 mg qd 1-22 mg qd repaglinide mg tid mg tid nateglinide mg tid mg tid AGI acarbose miglitol 25 mg qd-tid 25 mg qd-tid 25 mg qd-tid 25 mg qd-tid Maximal Dose/ Optimal Dose Monotherapy Combination 20 mg qd mg qd 40 mg qd mg qd 8 mg qd 4 mg tid-qid 4-88 mg qd 2-44 mg tid-qid 120 mg tid mg tid 100 mg tid 100 mg tid 100 mg tid 100 mg tid

13 Suggested Doses of Medications for Type 2 Diabetes (cont d)* Medication Monotherapy Biguanide metformin TZD rosiglitazone 500 mg qd-bid 2-44 mg qd Initial Dose Combination 500 mg qd-bid 2-44 mg qd pioglitazone mg qd mg qd DPP-IV Inhibitor sitagliptin 100 mg qd 100 mg qd Maximal Dose/ Optimal Dose Monotherapy 2,550 mg qd 8 mg qd 45 mg qd 100 mg qd Combination 2,550 mg 8 mg qd 45 mg qd 100 mg qd exenatide mcg sc bid 10 mcg sc bid 10 mcg sc bid *Dosing assumes normal hepatic and renal function. Reductions and a contraindications apply with hepatic and renal insufficiency.

14 Initiating and Advancing Treatment of Type 2 Diabetes: Use of Metabolic Staging

15 Progression to Type 2 Diabetes Genes Obesity, β-cell mass, insulin resistance Environment Inactivity, excessive calories Insulin Resistance & Hyperinsulinemia β-cell compensation β-cell decompensation - Prediabetes Postprandial Postprandial Hyperglycemia Decreased β-cell mass Fasting hyperglycemia Hypoinsulinemia Hyperglucagonemia Glucotoxicity + lipotoxicity Type 2 Diabetes

16 Efficacy of Oral Antihyperglycemics Declines With Time A1C rises ~0.2% to 0.3% yearly on stable therapy This rate is the same as for diet alone, sulfonylureas, and metformin β-cell function declines at the same rate with all these treatments Combination treatments are routinely needed UKPDS Group. Diabetes ;44: ; 1258; Turner RC, et al. JAMA ;281:

17 Metabolic Staging of Type 2 DM Early Type 2 DM Later Type 2 DM FPG >140 PP PG >250 A1C 6%-7% >7% 1st-phase insulin secretion Lost Lost 2nd-phase insulin secretion Hepatic gluconeogenesis Insulin resistance Above normal or normal Elevated (glucagon excess) Increased (no worsening) Reduced Very elevated (glucagon excess) Increased (no worsening)

18 Mild Hyperglycemia: (A1C 6%-7%) Key Concepts β-cell function and mass, although reduced, may be adequate Reducing demand on β-cell function may be sufficient to restore near-normal normal glycemia via: Increasing insulin sensitivity in liver (metformin( metformin) and muscle & fat (TZDs( TZDs) Delaying and prolonging glucose entry into the circulation (AGIs( AGIs) Enhancing glucose-dependent, 1st-phase insulin secretion and glucagon suppression (incretin( mimetic or enhancer)

19 Mild Hyperglycemia (A1C 6%-7%) Key Concepts (cont d) Targeting postprandial hyperglycemia has greater influence on A1C <7.3% than reducing fasting glycemia Correction of glucotoxicity further improves β-cell cell performance and insulin action No risk of hypoglycemia Monotherapy may be adequate

20 Moderate Hyperglycemia (A1C 7%-8%) Key Concepts Greater β-cell cell deficiency exists Need for combination therapy may be necessary when A1C remains >7.5% Insulin secretagogue (meglitinide or sulfonylurea) may be needed for A1C 7.5%-8%

21 Moderately Severe Hyperglycemia (A1C 8%-9%) Key Concepts Moderately severe reduction in β-cell function and mass Usually will need to initiate treatment with combination therapy if only sensitizers used A more potent secretagogue such as a sulfonylurea is often necessary at initiation and always necessary with advancing therapy Adding insulin +/- amylinomimetic (pramlintide)) is an option when advancing therapy

22 Severe Hyperglycemia (A1C >9%) Key Concepts Severe reduction in β-cell cell function and mass with insulinopenia and expansion of α-cell mass with hyperglucagonemia Combination therapy, almost always with a sulfonylurea, is necessary from the start Insulin +/- oral agents is an option for initiation of therapy and a necessity if other combination therapy is inadequate

23 Suggested Treatment Schema for Type 2 DM* Mild hyperglycemia: A1C 6%-7% Initiating therapy Alpha-glucosidase inhibitor (AGI) Metformin Thiazolidinedione (TZD) Sitagliptin Advancing therapy Metformin + TZD Metformin +/- TZD + exenatide AGI + TZD Sitagliptin + metformin or TZD *Choice of agent will be influenced by body mass index (BMI), fasting blood sugar, 2-hr postprandial blood sugar, age, renal and hepatic status.

24 Suggested Treatment Schema for Type 2 DM (cont d) Moderate Hyperglycemia: A1C 7-8% 7 Initiating therapy AGI Metformin Thiazolidinedione (TZD + metformin combination) Sitagliptin (sitagliptin + metformin combination) Meglitinide Sulfonylurea (low dose)

25 Suggested Treatment Schema for Type 2 DM (cont d) Advancing therapy Metformin + TZD Metformin +/- TZD + exenatide AGI + TZD Sitagliptin + metformin or TZD Meglitinide + metformin +/- TZD Sulfonylurea + metformin +/- TZD Sulfonylurea +/- metformin + sitagliptin Sulfonylurea +/- metformin + exenatide

26 Suggested Treatment Schema for Type 2 DM (cont d) Moderately Severe Hyperglycemia: A1C 8%-9% Initiating therapy Sulfonylurea (high dose) Metformin Metformin + TZD combination Metformin +/- TZD + exenatide Metformin or TZD + sitagliptin (sitagliptin + metformin combination) Meglitinide + metformin +/- TZD Sulfonylurea + metformin or TZD Sulfonylurea + exenatide Sulfonylurea + sitagliptin

27 Suggested Treatment Schema for Type 2 DM (cont d) Advancing therapy Sulfonylurea + metformin + TZD Sulfonylurea + metformin + exenatide Sulfonylurea + metformin + sitagliptin Insulin (use with exenatide or sitagliptin not yet established) HS NPH or glargine or detemir Bid 70/30 or analog 75/25 or 70/30 (d/c( meglitinide or SU) Mealtime analog lispro or aspart or glulisine (d/c secretagogue) Basal-bolus insulin (d/c( secretagogue) Pramlintide added to mealtime insulin

28 Suggested Treatment Schema for Type 2 DM (cont d) Severe hyperglycemia : A1C >9% Initiating therapy Metformin + thiazolidinedione + exenatide Metformin + thiazolidinedione + sitagliptin Sulfonylurea + metformin + thiazolidinedione Sulfonylurea +/- metformin + exenatide Sulfonylurea +/- metformin + sitagliptin Insulin initiated as below +/- metformin +/- thiazolidinedione

29 Suggested Treatment Schema for Type 2 DM (cont d) Advancing therapy Insulin added (use with exenatide or sitagliptin not yet established) HS NPH or glargine or detemir Bid 70/30 or analog 75/25 or 70/30 (d/c( SU) Mealtime analog lispro or aspart or glulisine (d/c SU) Basal-bolus insulin (d/c( SU) Pramlintide added to mealtime insulin

30 Prediabetes DM 2 (early) PP hyperglycemia DM 2 (late) fasting hyperglycemia Insulin Resistance Contribution β-cell Defect Contribution? Metformin? TZD? AGI? PP secretagogues? Exenatide/DPP-4 Inhib SU Insulin Pramlintide

31 Clinical Inertia: A Barrier to Improved Glycemic Control Knowledge Deficit Until 1995, only sulfonylureas and insulin Now many new agents, with uncertainty as to how they fit into a treatment plan Niche agents that address postprandial hyperglycemia are not optimally used Inadequate attention to & control of postprandial hyperglycemia Failure to understand metabolic staging of decompensation in type 2 DM

32 Clinical Inertia Pragmatic Issues Acceptance of fair-poor A1C due to staying in comfort zone with familiar agents Inordinate fear of hypoglycemia Non-adherence to guidelines advocating treatment modification every 3 months when A1C >7% Formulary restrictions and need for prior approval Lack of time/resources to initiate new treatments

33 Promoting Self-Care Jane Jeffrie Seley, GNP, MPH, MSN, CDE Diabetes Nurse Practitioner Weill Cornell Medical Center New York, NY

34 Is Your Patient Noncompliant?

35 Barriers to Self-Care Fear of treatment, complications Shock, denial, a little sugar Unrelated life stresses Lack of family support High cost of care, poor reimbursement Comorbidities Complexity of regimen

36 Compliance vs Concordance Patient & Provider are equals Provider assists patient in making informed decisions Build relationships over time Set mutually agreed upon goals Promote partnerships in care Chatterjee JS. J Med Ethics. 2006;32:

37 Strategies for Success: Clear Health Communication Teach back Have patient repeat instructions in their own words Ask Me 3 1 What is my main problem? What do I need to do? Why is it important for me to do this? 1. Available at: Accessed August 4, 2008.

38 Strategies for Success: Clear Health Communication (cont d) Diabetes Self-Care Regimen Includes: Meal Planning Physical Activity Blood Glucose Monitoring Medication Taking Generic vs brand name When to take Dose & when to adjust Mechanism of action When to call the office Risk of hypoglycemia

39 Strategies for Success: Clear Health Communication (cont d) More information is not better Use simple & same language Example: sugar OR glucose Limit to no more than 3 health messages per visit Be specific: Delineate steps to behavior change Practice skills, difficult situations Provide written instructions, toll-free #s

40 Meet John 46-year year-old Caucasian man Construction worker Type 2 diabetes x 8 years Wt 216 lbs, Ht 5 10 Followed by PCP, never saw educator A1C 8.2%, stopped monitoring blood glucose Failing (?) triple therapy + exenatide

41 John s Current Meds Metformin 500 mg daily Pioglitazone 30 mg daily Glipizide 10 mg XL daily Exenatide 5 mcg bid Simvastatin 20 mg qpm Enalapril 10 mg daily

42 Assessment Taking morning meds after breakfast, including glipizide and exenatide Risk of hypoglycemia with these medications On sub-therapeutic doses of metformin, exenatide Was injecting 5 mcg exenatide in forearm post-meals, stopped because it wasn t working Stopped monitoring blood glucose due to > levels

43 Getting John Back on Track Re-evaluate evaluate & prioritize medications Review BG targets and request information Review meals and physical activity Set short-term term goals Discuss steps to achieve goals Remember teach back Provide take-home resources

44 Knowledge Is Power Assess language skills, literacy Ask preferences for learning: written, audio, video Improve self-efficacy: efficacy: demonstration, practice, teach back

45 Timing Is Everything!

46 Q&A