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Type 2 diabetes disease state overview

Type 2 Diabetes: Disease State Overview

AF2086R0


Suggestions for slide deck use

Suggestions for Slide Deck Use

  • The following unbranded slides are provided as a disease state library and may be used as background information at the beginning of any promotional program

  • These slides should always supplement the affirmative deck unless the program is scheduled to be "disease state only"


Diabetes disease state overview

Diabetes Disease State Overview

  • Diabetes: epidemiology/pathophysiology

    • Prevalence and burden of diabetes

    • Core defects of type 2 diabetes

    • Complications and costs associated with type 2 diabetes

    • Predicting and preventing type 2 diabetes

  • Treatment goals and strategies

    • Improving glycemic control

    • Reducing diabetes-related complications

    • Treating the whole patient


Type 2 diabetes disease state overview

Every Day in the United States Approximately…

66 people lose

their eyesight

because of diabetes

128 people begin

treatment for end-stage

renal disease (ESRD)

More than 4000 new

cases* of diabetes will be

diagnosed today

195 lower-limb

amputations are performed

because of diabetes

640 people die from

diabetes and its

complications

*Patients ages ≥20 years.

Centers for Disease Control. National Diabetes Fact Sheet. http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2007.pdf. Accessed March 5, 2009.


23 5 million 10 7 americans 20 years or older have diabetes diagnosed or undiagnosed

≈23.5 Million (10.7%) Americans 20 Years or Older Have Diabetes (Diagnosed or Undiagnosed)*

23.8

Percentage

10.8

2.6

20–39

40–59

60+

Age group

*Data is from 2003–2006, projected to year 2007.

NIDDK. National Diabetes Statistics. 2007. Available at: http://diabetes.niddk.nih.gov/dm/pubs/statistics/#y_people.Accessed February 11, 2009.


Type 2 diabetes disease state overview

Adults Diagnosed with Diabetes in the United States*

1.6 million new cases of diabetes were diagnosed in people aged 20 years or older in 2007

Total economic costs of diabetes estimated to be $174 billion (2007)

819,000

536,000

Number

281,000

20–39

40–59

60+

Age group

*Data is from 2004–2006, projected to year 2007.

NIDDK. National Diabetes Statistics. November 2007. Available at: http://diabetes.niddk.nih.gov/dm/pubs/statistics/#y_people.Accessed February 11, 2009.


Age adjusted total prevalence of diabetes in the united states by race ethnicity age 20

Age-adjusted Total Prevalence of Diabetes in the United States by Race/Ethnicity (Age ≥20)

17

American Indians/Alaska Natives

12

Non-Hispanic Blacks

10

Hispanic/Latino Americans

8

Asian Americans

7

Non-Hispanic Whites

0

2

4

6

8

10

12

14

16

18

20

Percentage

NIDDK. National Diabetes Statistics. November 2007. Available at: http://diabetes.niddk.nih.gov/dm/pubs/statistics/#y_people.Accessed February 11, 2009.


Economic consequences of diabetes

Economic Consequences of Diabetes

Total Annual Cost in 2002: $132 Billion

Indirect costs* = $40 billion

Direct costs† = $92 billion

Disability and early mortality

Diabetes and diabetes supplies

$23 billion

$40 billion

$25 billion

Chronic complications

$44 billion

General medical conditions

*Indirect costs include lost productivity, disability, and premature mortality.

†Direct costs include: hospital inpatient care, nursing home care, physician office visits, total home healthcare costs, costs associated with hospice care, and diabetes supplies.

Stolar MW et al. JMCP. 2008;14:S1–S19.


Annual medical expenditures and length of time with diabetes

0

5

10

15

Annual Medical Expenditures and Length ofTime with Diabetes

Annual cost increases with length of time with diabetes

Diagnosis of diabetes at age 50

Diagnosis of diabetes at age 65

Cost in 2005 (dollars)

Duration of Diabetes (Years)

Adapted from Trogdon JG et al. Diabetes Care. 2008;31:2307–2311.


Pathophysiology of type 2 diabetes

Pathophysiology of Type 2 Diabetes

  • Type 2 diabetes results from a progressive insulin secretory defect on the background of insulin resistance1

  • Key pathophysiologic mechanisms leading to hyperglycemia in type 2 diabetes

    • Insulin resistance2,3

    • Beta-cell dysfunction3

1. American Diabetes Association. Diabetes Care. 2009;32:S13–S61.

2. DeFronzo RA. Med Clin North Am. 2004;88:787–835.

3. Kahn SE. J Clin Endocrinol Metab. 2001;86:4047–4058.


Two defects contributing to type 2 diabetes

Two Defects Contributing to Type 2 Diabetes

Obesity (visceral)2

Obesity (visceral)1

Insulin

resistance

Beta-cell dysfunction

Liver

Muscle tissue

Adipose tissue

Pancreas

Beta-cell

Type 2 Diabetes

1. Buchanan TA. Clin Ther. 2003;25(suppl 2):B32–B46.

2. Kahn SE. J Clin Endocrinol Metab. 2001;86:4047–4058.


Natural progression of insulin resistance in patients with type 2 diabetes 1 2

Natural Progression of Insulin Resistance in Patients with Type 2 Diabetes1,2

Insulin resistance

Insulin production & secretion/ Beta-cell function

Fasting plasma glucose

Normal glycemia

Insulin resistance rises, leading to beta cells working overtime to secrete more insulin

Beta cells are unable to produce the insulin needed to compensate for the increased level of insulin resistance, causing glucose levels to rise, leading to type 2 diabetes*

*Type 2 diabetes is diagnosed when FPG is ≥126 mg/dL.3

Adapted from International Diabetes Center, Minneapolis, MN.1

1. Bergenstal RM et al. Endocrinology. 4th ed. Philadelphia, PA: WB Saunders Company;2001:821–835.

2. Ramlo-Halsted BA, Edelman SV. Clin Diab. 2000;18:80–85.

3. American Diabetes Association. Diabetes Care. 2008;31(suppl1):S12–S54.


Type 2 diabetes associated with serious complications

Type 2 Diabetes Associated with Serious Complications

Stroke

DiabeticRetinopathy

CV Disease & Stroke account for ~65% of deaths in T2D patients

Leading cause

of blindness

in adults

CardiovascularDisease

Diabetic

Nephropathy

DiabeticNeuropathy

Major cause of kidney failure

Major cause of lower extremity amputations

CV = cardiovascular.

National Institute of Diabetes and Digestive and Kidney Diseases. National Diabetes Statistics fact sheet: general information and national estimates on diabetes in the United States, 2005. Bethesda, MD: U.S. Department of Health and Human Services, National Institute of Health, 2005.


Prevalence of multiple complications among people with type 2 diabetes

Prevalence of Multiple Complications Among People with Type 2 Diabetes

American Association of Clinical Endocrinologists. State of Diabetes Complications in America Report. Available at: http://www.aace.com/newsroom/press/2007/images/DiabetesComplicationsReport_FINAL.pdf. Accessed March 5, 2009.


Prevalence of macrovascular and microvascular complications of diabetes

Prevalence of Macrovascular and Microvascular Complications of Diabetes

*

Macrovascular

Microvascular

*In NHANES, “chronic kidney disease" refers to people with microalbuminuria (albumin:creatinine ratio >30 µg/mg).

†In the NHANES analysis, "foot problems" includes foot/toe amputations, foot lesions, and numbness in the feet.

‡"Eye damage" includes a positive response by NHANES participants to the question, "Have you been told diabetes has affected your eyes/had retinopathy?" Retinopathy is damage to the eye's retina. In NHANES, people without diagnosed diabetes were not asked this question, therefore, prevalence information for nondiabetics is not available.

CHD = coronary heart disease; CHF = congestive heart failure.

American Association of Clinical Endocrinologists. State of Diabetes Complications in America Report. Available at: http://www.aace.com/newsroom/press/2007/images/DiabetesComplicationsReport_FINAL.pdf. Accessed March 9, 2009.


Prevalence of diabetic retinopathy

Prevalence of Diabetic Retinopathy

40.3%*

Prevalence of retinopathy

in diabetics age ≥40 years (%)

8.2%†

§

*95% CI: 38.8%–41.7%

†95% CI: 7.4%–9.1%

‡Diabetic retinopathy defined as a retinal vascular disorder characterized by signs of retinal ischemia and/or signs of increased retinal vascular permeability. Retinopathy severity level ≥14 retinopathy and/or macular edema.

§Vision threatening retinopathy defined as severe retinopathy and/or diabetic macular edema. Retinopathy severity level ≥50 and/or macular edema.

Kempen JH et al. Arch Ophthalmol. 2004;122:552–563.


Number of cases with esrd due to diabetic nephropathy is increasing in the united states

Number of Cases with ESRD Due to Diabetic Nephropathy Is Increasing in the United States

Diabetes is the leading cause of ESRD

50

40

30

Number of cases (thousands)

20

10

0

1990

1991

1992

1993

1994

1995

1996

1997

1998

1999

2000

2001

2002

Year

ESRD = end-stage renal disease.

CDC. Morbidity and Mortality Weekly Report. 2005;54(43)1097–1100.


Cv risk in patients with diabetes and no prior mi is similar to risk in nondiabetics with prior mi

CV Risk in Patients with Diabetes and No Prior MI Is Similar to Risk in Nondiabetics with Prior MI

A population study of 3.3 million people

Men

Women

5-year incidence (%)

CV = cardiovascular. For CV death, the hazard ratio was 2.42 in men with diabetes only and 2.44 in men with a prior MI only (P=0.60). Results for women were 2.45 and 2.62, respectively (P<0.001).

Schramm TK et al. Circulation. 2008; 117:1945–1954.


Annual national cost of type 2 diabetes and related complications

Annual National Cost of Type 2 Diabetes and Related Complications*

Cost in billions

*Cost estimates in this report were adjusted for inflation to reflect 2006 costs.

American Association of Clinical Endocrinologists. State of Diabetes Complications in America Report. Available at: http://www.aace.com/newsroom/press/2007/images/DiabetesComplicationsReport_FINAL.pdf. Accessed March 5, 2009.


Individual costs by complication

Individual Costs by Complication*

$ 1785

Eye damage

Total expenditures

$ 480

Out-of-pocket costs

$ 4687

Foot problems

$ 153

$ 6062

CHD

$ 224

$ 7806

Stroke

$ 448

$ 7932

CHF

$ 510

$ 9002

Chronic kidney disease

$ 439

$ 14,150

Heart attack

$ 574

$

$

$

$

$

$

$

$

$

0

2000

4000

6000

8000

10,000

12,000

14,000

16,000

Annual Healthcare Costs

*Cost estimates in this report were adjusted for inflation to reflect 2006 costs.

American Association of Clinical Endocrinologists. State of Diabetes Complications in America Report. Available at: http://www.aace.com/newsroom/press/2007/images/DiabetesComplicationsReport_FINAL.pdf. Accessed March 5, 2009.


Algorithm to estimate type 2 diabetes risk

Algorithm to Estimate Type 2 Diabetes Risk

According to a study in a middle-aged white population, total points ≥25 corresponds to >35% 8-year risk of type 2 diabetes.

Wilson PW et al. Arch Intern Med. 2007;167:1068–1074.


Preventing development of type 2 diabetes

Preventing Development of Type 2 Diabetes

  • Screening for prediabetes and asymptomatic type 2 diabetes should be considered in adults who are overweight or obese (BMI ≥25 kg/m2)and have additional risk factors

  • In those without risk factors, testing should begin at age 45 years

  • If results are normal, testing should be repeated at least every 3 years

  • Counseling on lifestyle modification is recommended for patients with impaired fasting glucose or impaired glucose tolerance

    • Weight-loss goal of 5%–10% of initial body weight

    • Physical activity with moderate intensity for 150 minutes per week

American Diabetes Association. Diabetes Care. 2009;32(suppl 1):S13–S61.


Summary of diabetes epidemiology pathophysiology

Summary of Diabetes: Epidemiology/Pathophysiology

Diabetes and diabetes-related complications (eg, heart disease, kidney disease, blindness, amputations) are highly prevalent1

The pathophysiology of diabetes involves the development of insulin resistance and beta-cell dysfunction2

Diabetes is strongly correlated with a number of microvascular risk factors and diseases, and is a contributor to macrovascular disease and mortality1

Routine clinical measures may be used to identify patients at risk of developing type 2 diabetes who may benefit from lifestyle counseling3

1. NIDDK. National Diabetes Statistics. November 2007. Available at: http://diabetes.niddk.nih.gov/dm/pubs/statistics/#y_people.Accessed February 11, 2009.

2. Kahn SE. J Clin Endocrinol Metab. 2001;86:4047–4058.

3. American Diabetes Association. Diabetes Care. 2009;32(suppl 1):S13–S61.


Diabetes disease state overview1

Diabetes Disease State Overview

  • Diabetes: epidemiology/pathophysiology

    • Prevalence and burden of diabetes

    • Core defects of type 2 diabetes

    • Complications and cost associated with type 2 diabetes

    • Predicting and preventing type 2 diabetes

  • Treatment goals and strategies

    • Improving glycemic control

    • Reducing diabetes-related complications

    • Treating the whole patient


Criteria for the diagnosis of diabetes mellitus ada standards of medical care 2009

Criteria for the Diagnosis of Diabetes Mellitus: ADA Standards of Medical Care, 2009

FPG 126 mg/dL (7.0 mmol/L)

Fasting is defined as no caloric intake for at least 8 hours

OR

Symptoms of hyperglycemia plus casual plasma glucose concentration 200 mg/dL (11.1 mmol/L)

Casual is defined as any time of day without regard to time since last meal

The classic symptoms of hyperglycemia include polyuria, polydipsia, and unexplained weight loss

OR

2-h plasma glucose 200 mg/dL (11.1 mmol/L) during an OGTT

The test should be performed as described by WHO, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in water

ADA = American Diabetes Association; OGTT = oral glucose tolerance test, WHO = World Health Organization.

American Diabetes Association. Diabetes Care. 2009;32:S13–S61.


Recommendations for early pharmacologic treatment from aace and ada

Recommendations for Early Pharmacologic Treatment from AACE and ADA

To reduce the risk of serious disease-related complications,1,2AACE recommends

Target A1C goal of ≤6.5%2

Earlier intervention with appropriate therapies and persistent titration to achieve goal2

ADA recommends3

Target A1C goal of <7% “for most patients”

Achieving and maintaining glycemic goals and changing interventions when therapeutic goals are not being met

AACE = American Association of Clinical Endocrinologists.

1. Stratton IM et al. BMJ. 2000;321:405–412.

2. AACE Diabetes Mellitus Clinical Practice Guidelines Task Force. Endocr Pract. 2007;13(suppl 1):4–68.

3. American Diabetes Association. Diabetes Care. 2009;32:S13–S61.


Conventional monotherapies unable to maintain glycemic control over time

Conventional MonotherapiesUnable to Maintain Glycemic Control Over Time

10

Conventional*

9

Insulin

Glibenclamide (glyburide)

8

MET

ADA Goal

7

AACE Goal

6

0

0

3

6

9

12

15

United Kingdom Prospective Diabetes Study (UKPDS)

Median A1C (%)

Time from randomization (years)

FPG = fasting plasma glucose; MET = metformin.*Conventional therapy defined as dietary advice given at 3-month intervals where FPG was targeted at best levels feasible in clinical practice. If FPG exceeded 270 mg/dL, patients were re-randomized to receive nonintensive MET, chlorpropamide, glibenclamide, or insulin. If FPG exceeded 270 mg/dL again, those on SU would have MET added. If FPG exceeded 270 mg/dL after this, insulin was substituted.Adapted from UK Prospective Diabetes Study (UKPDS 34) Group. Lancet. 1998;352:854–865.


Glycemic targets are not being achieved worldwide

Glycemic Targets Are Not Being Achieved Worldwide

EUROPE

(RECAP-DM)3

CANADA

(DICE)1

UNITED STATES

(NHANES)2

HbA1c <6.5%

HbA1c <7%

HbA1c <7%

26%

51%

57%

49%

43%

74%

Patients reaching glycemic target

Patients not reaching glycemic target

DICE = Diabetes in Canada Evaluation; NHANES = National Health and Nutrition Examination Surveys; RECAP-DM = Real-life Effectiveness and Care Patterns of Diabetes Management.

1. Harris SB et al. Diabetes Res Clin Pract. 2005;70:90–97.

2. Ong et al. Ann Epidemol. 2008;18:222–229.

3. Guisasola et al. Diabetes Obes Metab. 2008;10:8–15.


Patients remain on monotherapy 2 years after first a1c 8 0

Patients Remain on Monotherapy >2 Years After First A1C >8.0%*

Length of time between first monotherapy

(A1C >8.0%) and switch/addition in therapy*

35.1

SU Only

26.5

MET Only

0

6

12

18

24

30

36

Months

*May include uptitration.

Based on a prospective, population-based study using retrospective observational data.

Brown JB et al. Diabetes Care. 2004;27:1535–1540.


Risk of cv events or death increased with hba1c level epic norfolk

Risk of CV Events or Death Increased with HbA1c Level (EPIC-Norfolk)

5–5.4%

HbA1c level:

5.5–5.9%

6.0–6.4%

6.5–6.9%

7%

Men

Women

7.96

8

7.07

6.91

7

6

5.01

5

4.73

Age-adjusted relative risk (95% CI)

4

3.49

3.44

3.38

3.03

3.06

3

2.37

2.13

2.29

2.00

1.79

1.80

2

1.63

1.70

1.56

1.57

1.56

1.61

1.23

1.25

1.28

1.04

0.98

1.02

0.96

1

0.89

0

CHD events

CVD events

All-cause

mortality

CHD events

CVD events

All-cause

mortality

P0.001 for linear trend across HbA1c categories for all endpoints.

CHD = coronary heart disease; CI = confidence interval; CVD = cardiovascular disease; EPIC-Norfolk = European prospective investigation into cancer in Norfolk.

  • Khaw KT et al. Ann Intern Med 2004; 141:413–420.


Multifactorial approach strategies for reducing diabetic complications treating the whole patient

Multifactorial Approach: Strategies for Reducing Diabetic Complications—Treating the Whole Patient

  • Strategies for reducing microvascular complications

    • Routine screening for diabetes

    • Optimized glycemic control

    • Optimized BP control

  • Strategies for reducing macrovascular complications

    • Optimized glycemic control

    • Treatment of hypertension and other established cardiovascular risk factors in diabetic and possibly prediabetic subjects*

    • Lipid control*

    • Antiplatelet therapy*

*For appropriate patient population based on treatment guidelines.

American Diabetes Association. Diabetes Care. 2008;31(suppl 1):S12–S54.


Improved glycemic control has been shown to help reduce the risk of complications

Improved Glycemic Control Has Been Shown to Help Reduce the Risk of Complications

According to the United Kingdom Prospective DiabetesStudy (UKPDS) 35, every 1% decrease in A1C resulted in:

21%

37%

Decrease

in risk of microvascular

complications

(P<0.0001)

Decrease in risk of any diabetes-related endpoint

(P<0.0001)

Stratton IM et al. BMJ. 2000;321:405–412.


Ukpds long term intensive glucose control in type 2 diabetes

UKPDS: Long-Term Intensive Glucose Control in Type 2 Diabetes

Multicenter, randomized study with 10-year follow-up1

One of the longest and largest type 2 diabetes trials ever conducted2

4209 patients newly diagnosed with type 2 diabetes1

Study Design

After a 3-month run-in period, patients with FPG >108 mg/dL but <270 mg/dL were randomized to receive either intensive therapy (SU or insulin or, if more than 120% of ideal body weight, MET) or conventional therapy (diet only)1

Primary study objective

To determine whether long-term improved glycemic control was able to sustain risk reductions in microvascular complications, and if intensive therapy had a long-term effect on macrovascular outcomes1

Primary outcome

Prespecified aggregate clinical outcomes were any diabetes-related endpoint, diabetes-related death, death from any cause, myocardial infarction, stroke, peripheral vascular disease, and microvascular disease1

FPG = fasting plasma glucose.

1. Holman et al. N Engl J Med. 2008;359:1577–1589.

2. Lawton J et al. Br J Gen Pract. 2003;53:394–398.


Sustained intensive glycemic control can reduce diabetes related complications

Sustained Intensive Glycemic Control Can Reduce Diabetes-Related Complications

Risk Reductions for Intensive-Therapy Regimens at 10-Year Follow-up

  • Long-term intensive glycemic control is associated with a significantly decreased risk of MI or death from any cause, in addition to known risk reductions in microvascular disease

SU-

insulin

SU-

insulin

SU-

insulin

SU-

insulin

MET

MET

MET

MET

-9%

-13%

-16%

-15%

-21%

-24%

-27%

-33%

Any diabetes-related

endpoint

(P = 0.04 for SU-insulin;

P = 0.01 for MET)

Microvascular

disease

(P = 0.001 for SU-insulin;

P = 0.31 for MET)

Myocardial

infarction

(P = 0.01 for SU-insulin;

P = 0.005 for MET)

Death from

any cause

(P = 0.007 for SU-insulin;

P = 0.002 for MET)

Holman et al. N Engl J Med. 2008;359:1577–1589.


Treating the whole patient statin therapy in patients with diabetes reduced cv risk cards

Treating the Whole Patient: Statin Therapy in Patients with Diabetes Reduced CV Risk (CARDS)

1410

1351

1306

1022

651

305

Placebo

1428

1392

1361

1074

694

328

Atorvastatin

Relative CV Risk Reduction 37% (95% CI: –52 to –17)

15

P = 0.001

Placebo

127 CV events*

10

Atorvastatin

83 CV events*

Cumulative hazard (%)

5

0

0

1

2

3

4

4.75

Years

*CV events included stroke.

CARDS = Collaborative Atorvastatin Diabetes Study.

Colhoun HM et al. Lancet. 2004;364:685–696.


Treating the whole patient patients reaching intensive treatment goals at 7 8 years steno 2

Treating the Whole Patient: Patients Reaching Intensive Treatment Goals at 7.8 Years* (Steno-2)

80

P<0.001

P = 0.21

70

P = 0.19

60

50

P = 0.001

40

Patients (%)

30

20

P = 0.06

10

0

A1C

<6.5%

Diastolic BP

<80 mmHg

Cholesterol

<175 mg/dL

Triglycerides

<150 mg/dL

Systolic BP

<130 mmHg

Intensivetherapy (n = 80)†

Conventionaltherapy (n = 80)‡

*Mean.

†Intensive treatment included stepwise implementation of behavior modification and pharmacologic therapy that targeted hyperglycemia, hypertension, dyslipidemia, and microalbuminuria, along with secondary prevention of cardiovascular disease with aspirin.

‡Conventional treatment was based on the Danish Medical Association guidelines.

Gæde et al. N Engl J Med. 2003;348:383–393.


Treating the whole patient intensive therapy reduced composite macrovascular endpoints steno 2

Treating the Whole Patient: Intensive Therapy Reduced Composite Macrovascular Endpoints (Steno-2)

60

Conventional therapy

50

HR† = 0.47 (95% CI, 0.24-0.73)

53%

40

Primary composite endpoint* (%)

30

20

Intensive therapy

10

0

72

0

12

24

36

48

60

84

96

Months of Follow-up

*Composite endpoint of death from cardiovascular causes, nonfatal myocardial infarction, coronary-artery bypass grafting, percutaneous coronary intervention, nonfatal stroke, amputation, or surgery for peripheral atherosclerotic artery disease, P=0.007; †Unadjusted HR.

CI = confidence interval; HR = hazard ratio.

Gæde et al. N Engl J Med. 2003;348:383–393.


Type 2 diabetes disease state overview

Treating the Whole Patient: a 5.5-Year* Follow-up (Steno-2) Intensive Therapy Sustains Cardiovascular Benefits

80

HR 0.41

(95% CI, 0.25 to 0.67; P<0.001)

70

Conventional therapy

60

59%

50

Cumulative Incidence of Any Cardiovascular Event† (%)

40

30

Intensive therapy

20

10

0

0

1

2

3

4

5

6

7

8

9

10

11

12

13

Years of Follow-up

*Mean. †Secondary composite endpoint of cardiovascular events, including death from cardiovascular causes, nonfatal stroke, nonfatal myocardial infarction, coronary-artery bypass grafting, percutaneous coronary intervention, revascularization for peripheral atherosclerotic artery disease, and amputation.

Gæde et al. N Engl J Med. 2008;358:580–591.


Management of type 2 diabetes

Management of Type 2 Diabetes

  • Type 2 diabetes requires a multifactorial approach for the management of glucose levels, blood pressure, and lipids to reduce complications1

  • Recommendations for type 2 diabetes:

*High risk patients are those with acute coronary syndromes or previous cardiovascular events.

AACE = American Association of Clinical Endocrinologists; ACE = American College of Endocrinology; ADA = American Diabetes Association; EASD = European Association for the Study of Diabetes; HDL = high-density lipoprotein; LDL = low-density lipoprotein.

1. ADA Standards of Medical Care in Diabetes – 2009. Diabetes Care. 2009;32:S13–S61.

2. American Association of Clinical Endocrinologists. Endocrine Practice. 2007;13(suppl 1):3–68.


Summary of treatment goals and strategies

Summary of Treatment Goals and Strategies

  • Glycemic control is fundamental to the management of diabetes1

  • The UKPDS demonstrated significant risk reductions in microvascular complications in type 2 diabetes with more intensive glycemic control. The benefit of A1C–lowering to reduce CVD in type 2 diabetes is supported by UKPDS data2

  • There is a need to treat the whole patient, including management of hyperglycemia, CV risk factors and other comorbidities. This is key in reducing diabetes-related complications3

1. AACE. Endocr Pract. 2007;13(suppl 1):4–68.

2. Stratton IM et al. BMJ. 2000;321:405–412.

3. American Diabetes Association. Diabetes Care. 2008;31(suppl 1):S12–S54.


Conclusions management of type 2 diabetes

Conclusions:Management of Type 2 Diabetes

  • Diabetes is a major clinical problem

    • Pathophysiology involves insulin resistance and beta-cell dysfunction1

  • Diabetes is correlated with increased risk of microvascular and macrovascular diseases and events

    • Microvascular complications are predominately driven by hyperglycemia2,3

    • Macrovascular complications are multifactorial and complex4

1. Kahn SE. J Clin Endocrinol Metab. 2001;86:4047–4058.

2. AACE. Endocr Pract. 2007;13(suppl 1):4–68.

3. Stratton IM et al. BMJ. 2000;321:405–412.

4. American Diabetes Association. Diabetes Care. 2008;31(suppl 1):S12–S54.


Conclusions management of type 2 diabetes cont

Conclusions:Management of Type 2 Diabetes (cont)

  • A1C reduction has been shown to reduce the risk of microvascular complications and may contribute to risk reduction of macrovascular endpoints1

  • Early intervention is needed to get A1C to goal (diet and exercise should always be recommended)2

  • It is challenging to maintain A1C control over time with traditional monotherapies3

  • AACE and ADA* guidelines recommends use of combination therapy to achieve and sustain glycemic goals2,4

*ADA guidelines recommend that a second medication should be added within 3 months if patients are not at goal.

1. Stratton IM et al. BMJ. 2000;321:405–412; 2. American Diabetes Association. Diabetes Care. 2008;31(suppl 1):S12–S54; 3. UKPDS. Lancet. 1998;352:854–865; 4. AACE. Endocr Pract. 2007;13(suppl 1):4–68.


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