Diabetes Current Treatment Guideline 2012

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Oral Therapy for Type 2 Diabetes Dr. Zeeshan Ali MBBS, MCPS, FCPS CONSULTANT PHYSICIAN JINNAH POSTGRADUATE MEDICAL CENTRE KARACHI

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Number of People with Diabetes (20-79 years) 2010 and 2030 IDF Diabetes Atlas, 4th ed. International Diabetes Federation, 2009

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Number of People with Diabetes by Age Group, 2010 and 2030 Millions

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Number of People with Impaired Glucose Tolerance by Age Group, 2010 and 2030 Millions

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Definition of Diabetes

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Definition of Impaired Glucose Tolerance

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Types Of Diabetes Type 1 (Juvenile-Onset) Type 2 (Adult-Onset) Other types including: - Gestational diabetes - MODY (maturity onset diabetes of the young) - LADA (latent auto-immune diabetes of adults) - Others

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Cause of Type 1 DM Auto-immune destruction of insulin-producing ß-cells in the pancreas

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Cause of Type 2 DM Insulin resistance (genetics) - aggravated by obesity - aggravated by lack of exercise “Exhaustion” of insulin-producing ß-cells

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Major Metabolic Defects in Type 2 Diabetes Peripheral insulin resistance in muscle and fat Decreased pancreatic insulin secretion Increased hepatic glucose output Haffner SM, et al. Diabetes Care, 1999

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Development and Progression of Type 2 Diabetes* Relative Activity Glucose Years from Diabetes Diagnosis –10 –5 0 5 10 15 20 25 30 -10 -5 0 5 10 15 20 25 30 *Conceptual representation. NGT=normal glucose tolerance; IGT=impaired glucose tolerance; IFG=impaired fasting glucose. Adapted from Ferrannini E. Presentation at 65th ADA in Washington, DC, 2006.; and Ramlo-Halsted et al. Prim Care. 1999;26:771–789. NGT ® Insulin ® IGT/ IFG ® Type 2 Diabetes Resistance Postprandial glucose Fasting glucose Insulin resistance —hepatic and peripheral Insulin level Beta-cell function

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0 UKPDS: Progressive Deterioration in Glycemic Control Over Time Intensive Conventional Time from randomization (y) 6 3 9 12 15 Median A1C (%) A1C Years from diagnosis b-cell function (%) 100 80 60 40 20 0 UKPDS Group. Lancet. 1998;352:837-853. -12 -10 -8 -6 -4 -2 0 2 4 6 Holman RR. Diabetes Res Clin Pract. 1998;40(suppl):S21-S25. 9 8 7 6 0

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Mechanisms Responsible for Changes in Insulin Levels Normal b-cell adaptation to insulin resistance Increased secretion from each cell Increased b-cell mass Impaired b-cell adaptation in type 2 diabetes result of Decreased secretion from each cell Reduced b-cell mass

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Potential Causes for Declining Insulin Secretion Prentki M et al. Diabetes. 2002;51(suppl 3):s405-s413.

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Abnormalities of a-Cell Function in Type 2 Diabetes Elevated glucagon levels Loss of insulin-induced suppression Loss of glucose-induced suppression Increased stimulatory effect of arginine Dunning BE et al. Diabetologia. 2005;48:1700-1713.

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Summary Islets can adapt to insulin resistance Failure of adaptation results in impaired glucose tolerance and eventually, type 2 diabetes Failure appears to be due to reduced insulin secretion per islet and a reduction in the number of islets Increased glucagon contributes to hyperglycemia in type 2 diabetes

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Global Cardiometabolic Risk* Gelfand EV et al, 2006; Vasudevan AR et al, 2005 * working definition

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Complications of Diabetes Small Blood Vessel - eye (retina) – blindness - kidney failure – dialysis Large Blood Vessel - heart attacks - strokes - peripheral vascular : amputations Neuropathy Erectile dysfunction (both vascular and nerve damage)

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Avoiding Complications - I Diet / exercise ‘Girth’ control Sugar control Lipid (cholesterol) control Blood pressure control Smoking cessation

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Avoiding Complications - II Self-monitoring glucose Visits to PCP – endocrinologist: goals Eye exams Podiatry exams Periodic blood / urine lab testing

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Standards of Care American Diabetes Association Glycemia: HbA1c <7.0%, FPG 90-130 mg/dL, PP <180 mg/dL Blood Pressure: <130/80 mm Hg Lipids: LDL <100 mg/dL; TG <150 mg/dL Yearly Dilated eye exam; urinary protein; foot exam; flu shot Other Aspirin usage; pneumococcal vaccine AACE goals HbA1c 6.5% FPG 110 mg/dL PP 140 mg/dL NCEP LDL =70 mg/dL FPG – fasting plasma glucose PP - Postprandial ADA. Diabetes Care. 2009;32(suppl 1);S13-S61.

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Prevention of DM TYPE 1 - Immune modulation TYPE 2 - Diet/exercise - Drugs: Metformin TZD’s Glucosidase inhibitors Others?

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Stamp Out Diabetes!

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Dietary Therapy Best implemented by a registered dietitian experienced in behavioral modification Individualized diet based on weight, lipids, lifestyle Total carbohydrates 45-65% of daily energy intake Avoid sugars, increase complex carbohydrates, 50 gram of fiber daily Fat <30% calories (<7% saturated) Dietary therapy alone can reduce A1C by 0.25-3% or more Diabetes Care, 2010. 33 (Supp 1) S11-S48

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Physical Activity Perform at least 150 minutes of moderate-intensity* aerobic physical activity per week In the absence of contraindications, perform resistance training three times a week Diabetes Care, 2010. 33 (Supp 1) S11-S48 * 50-70% of max heart rate

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Patient Education in Diabetes Mellitus: 10 Content Areas Diabetes Self- Management Education Diabetes Disease Process Physical Activity Utilizing Medication Monitoring Blood Glucose Preventing, Detecting & Treating Acute Complications Preventing, Detecting & Treating Chronic Complications Goal setting for Health & Daily Living Integrating Psychosocial Adjustment To Daily Living Promoting Care prior to and during Pregnancy Nutritional Management Funnell et. al. Diabetes Care 2010:33 (Suppl1) S89-96 tt

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The Current Armamentarium of Oral Agents for Type 2 Diabetes Mellitus—Sequencing Oral Therapy When and Where Do We Start? When Do We Add? How Do The Guidelines Guide Us? Investigations • Innovation • Clinical Application

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Oral Drugs for Rx DM2 Metformin Sulfonylureas (glyburide, gliclizide glimepiride) Thiazolidinediones DPP-IV inhibitors Alpha Glucosidase inhibitors Others: colesevelam ; bromocriptine

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Injectables For RX DM2 Pramlintide (Symlin) Exenatide (Byetta) / liraglutide (Victoza) Insulins Native - Regular (short-acting) - Isophane (NPH : intermediate) - Mixtures Analogues - Glargine / Detemir (long-acting) - Humalog, Novolog, Apidra (rapid) - Mixtures

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Conclusions A1C goal should be individualized <6.5% if healthy, and short duration diabetes and long life expectancy <7% average patient <7.5-8% medically complex, clinical cardiovascular disease, failed to achieve lower target with lifestyle, metformin and adequate doses of insulin The future: continuing surveillance of newer classes of drugs for adverse – or beneficial – cardiovascular effects

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Future Rx DM2 Longer acting GLP-1 analogues More DPP-IV inhibitors More TZD’s Newer drug classes : e.g., SGLT2-inhibitors NOTE : FDA requires longer duration studies in DM2 to better understand risk / benefit before approval

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Type 2 Diabetes Medication Choices Experience and Potency

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Mechanisms of Action of Pharmacologic Agents for Diabetes Improving Outcomes in Patients With Type 2 Diabetes Mellitus: Practical Solutions for Clinical Challenges James R. Gavin, III, MD, PhD; Mark W. Stolar, MD; Jeffrey S. Freeman, DO; Craig W. Spellman, DO, PhD JAOA • Vol 110 • No 5suppl6 • May 2010 • 2-14

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Type 2 Diabetes Medication Choices and Potency Higher baseline A1C levels predict greater drop in A1C Shorter duration of diabetes predicts greater drop in A1C with any oral agent All oral agents require presence of some endogenous b cell function, as they work by either increasing insulin sensitivity or augmenting b cell insulin release Practical Tips! Sherifali et.al. Diabetes Care. 2010; 33: 1859-1864

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Metformin - Drug Profile

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Sulfonylureas - Drug Profile

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Repaglinide and Nateglinide: Drug Profiles

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TZDs - Drug Profile

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Alpha Glucosidase Inhibitor (AGI) - Drug Profile

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DPP4 Inhibitors – Drug Profile

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ADA/EASD Guidelines

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ADA/EASD: Considerations for the Guidelines Use of information from clinical trials that address the efficacy and safety of different modalities of treatment Paucity of high quality evidence was an impediment Clinical judgment of the panel participants Extrapolation of UKPDS data that glucose lowering of drugs (metformin, sulfonylureas, insulin) predicted decrease in complications. Nonglycemic effects of medication, such as effect on CV risk, lipids, hypertension or insulin resistance Safety, side effects, ease of use and expense

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ADA Algorithm for Management of Diabetes Diabetes Care. 2009, 32:193-203 At diagnosis: Lifestyle + Metformin Lifestyle+Metformin + Pioglitazone (No hypoglycemia, edema, CHF, bone loss) Lifestyle+Metformin + Sulfonylurea Lifestyle+Metformin + Intensive insulin Lifestyle+Metformin + Basal Insulin Lifestyle+Metformin + GLP1 (No hypoglycemia, wt loss, Nausea/vomiting) Lifestyle+Metformin + Pioglitazone + Sulfonylurea Lifestyle+Metformin + Basal Insulin Tier 2: less well-validated therapies Tier 1: Well-validated core therapies Step 1 Step 2 Step 3 Amylin agonists, Glinides DPP-4 inhibitors may be appropriate in selected patients *Useful when hypoglycemia is to be avoided

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= alternative approach IDF Treatment Algorithm for Type 2 Diabetes

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Metformin as First Line Therapy Evidence-informed Consensus Effective Favourable effect on weight, low risk of hypoglycaemia, and cost Caution with renal insufficiency CVD benefit

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12 studies; = 52 weeks; at least 1 CVD event CVD outcomes: - fatal / non-fatal MI or stroke PVD other CVD death

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Effect of Metformin on CVD Events

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= alternative approach IDF Treatment Algorithm for Type 2 Diabetes

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= alternative approach IDF Treatment Algorithm for Type 2 Diabetes

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= alternative approach IDF Treatment Algorithm for Type 2 Diabetes

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a-Glucosidase inhibitor or DPP-4 inhibitor, orThiazolidinedione Very few studies have compared these options = alternative approach IDF Treatment Algorithm for Type 2 Diabetes

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a-Glucosidase inhibitor or DPP-4 inhibitor, orThiazolidinedione = alternative approach IDF Treatment Algorithm for Type 2 Diabetes

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a-Glucosidase inhibitor or DPP-4 inhibitor, orThiazolidinedione a-Glucosidase inhibitor or DPP-4 inhibitor,or Thiazolidinedione = alternative approach IDF Treatment Algorithm for Type 2 Diabetes

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Review Annals of Internal Medicine Systematic Review: Comparative Effectiveness and Safety of Oral Medications for Type 2 Diabetes Mellitus Shari Bolen, MD, MPH; Leonard Feldman, MD; Jason Vassy, MD, MPH; Lisa Wilson, BS, ScM; Hsin-Chieh Yeh, PhD; Spyridon Marinopoulos, MD, MBA; Crystal Wiley, MD, MPH; Elizabeth Selvin, PhD; Renee Wilson, MS; Eric B. Bass, MD, MPH; and Frederick L. Brancati, MD, MHS Background: As newer oral diabetes agents continue to emerge on the market, comparative evidence is urgently required to guide appropriate therapy. Purpose: To summarize the English-language literature on the benefits and harms of oral agents (second-generation sulfonylureas, biguanides, thiazolidinediones, meglitinides, and -glucosidase inhibitors) in the treatment of adults with type 2 diabetes mellitus. Conclusions: Compared with newer, more expensive agents (thiazolidinediones, aglucosidase inhibitors, and meglitinides), older agents (second-generation sulfonylureas and metformin) have similar or superior effects on glycemic control, lipids, and other intermediate end points. Large, long-term comparative studies are needed to determine the comparative effects of oral diabetes agents on hard clinical end points. Ann Intern Med. 2007;147:386-399. www.annals.org

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Figure 4 Events per 1000 patient-years for representative endpoints. Black bars indicate excess risk of events in diabetes patients relative to nondiabetic subjects;19,75,85,86 gray bars indicate excess risk of events in patients treated with specific glucose- lowering medications relative to diabetic patients on other agents;2,25,41,54,60,61,74 and white bars indicate the decreased risk of events in patients undergoing intensive glucose control policies. Foley RN et al. J Am Soc Nephrol. 2005;16(2):489-495; b = 19Haffner SM et al. N Engl J Med.1998;339(4)229-234; c = 75Noel RA et al. Diabetes Care. 2009;32(5):834-838;d = 86Trautner C et al. Diabetes Care. 1997;20(7):1147-1153; e = 60,61HamptonT. JAMA. 2007;297(15):1645 and Meier C et al. Arch Intern Med. 2008;168(8):820-825; f = 41Lago RM et al. Lancet. 2007;370(9593):1129-1136; g = 25Patel A et al. N Engl J Med. 2008;358(24):2560-2572; h = 2Nissen SE, Wolski K. N Engl J Med. 2007;356(24)2457-2471; i = 54Glucophage [package insert]. Princeton, NJ: Bristol-Myers Squibb Company; 2006; j = 74Dore DD et al. Type 2 Diabetes: Assessing the Relative Risks and Benefits of Glucose-lowering Medications Richard M. Bergenstal, MD, Clifford J. Bailey, PhD David M. Kendall, MD International Diabetes Center, Minneapolis, Minn; Diabetes Research, Life and Health Sciences, Aston University, Birmingham, UK. The American Journal of Medicine (2010) 123, 374.

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Type 2 Diabetes: Assessing the Relative Risks and Benefits of Glucose-lowering Medications Glucose-lowering medications have a favorable risk-benefit profile The most common adverse event is hypoglycemia, particularly among patients receiving sulfonylureas or insulin. Metformin-associated lactic acidosis, exenatide-associated pancreatitis, and sitagliptin-associated hypersensitivity reactions appear to be rare. Increased risks of congestive heart failure and bone fractures in thiazolidinedione-treated patients, and reports of increased cardiovascular events in rosiglitazone-treated patients remain an issue. Richard M. Bergenstal, MD, Clifford J. Bailey, PhD David M. Kendall, MD International Diabetes Center, Minneapolis, Minn; Diabetes Research, Life and Health Sciences, Aston University, Birmingham, UK.

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Figure 2. Kaplan–Meier Estimates of the Cumulative Incidence of Monotherapy Failure at 5 Years. Treatment was considered to have failed if a patient had a confirmed or adjudicated level of fasting plasma glucose of more than 180 mg per deciliter. Risk reduction is listed for comparisons of pairwise groups from a baseline covariateadjusted Cox proportionalhazards model. Gray’s estimates of cumulative incidence adjusted for all deaths were smaller than Kaplan–Meier estimates of treatment failure: 10% in the rosiglitazone group, 15% in the metformin group, and 25% in the glyburide group. I bars indicate 95% CIs. Cumulative Incidence of Monotherapy Failure Hazard ratio (95% CI) Rosiglitazone vs. metformin, 0.68 (0.55–0.85); P<0.001 Rosiglitazone vs. glyburide, 0.37 (0.30–0.45); P<0.001 Years 1 2 3 4 5 Glyburide Metformin Rosiglitazone 10 20 30 40 Glycemic Durability of Rosiglitazone, Metformin, or Glyburide Monotherapy N Engl J Med 2006;355:242743 Steven E. Kahn, M.B., Ch.B., Steven M. Haffner, M.D., Mark A. Heise, Ph.D., William H. Herman, M.D., M.P.H., Rury R. Holman, F.R.C.P., Nigel P. Jones, M.A., Barbara G. Kravitz, M.S., John M. Lachin, Sc.D., M. Colleen O’Neill, B.Sc., Bernard Zinman, M.D., F.R.C.P.C., and Giancarlo Viberti, M.D., F.R.C.P., for the ADOPT Study Group *

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AACE/ACE: Considerations for the Guidelines Minimizing risk and severity of hypoglycemia Minimizing weight gain Inclusion of all major classes of FDA-approved glycemic medications Selection of therapy stratified by hemoglobin A1C (A1C) and based on documented A1C lowering potential Consideration of both fasting and postprandial glucose levels as end points Consideration of total cost of therapy to individual and society - includes cost of medication, glucose monitoring, hypoglycemic events, drug adverse events, and treatment of complications

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