Insulin initiation and intensification in the type 2 diabetic patient
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Insulin Initiation and Intensification in the Type 2 Diabetic Patient. Jorge De Jesus MD FACE . Disclosures.

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Insulin Initiation and Intensification in the Type 2 Diabetic Patient

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Insulin Initiation and Intensification in the Type 2 Diabetic Patient

Jorge De Jesus MD FACE


Disclosures

  • Dr Jorge De Jesús has received honorariums as speaker for the following pharmaceutical companies: Bristol Myers-Squibb; Merck; Eli-Lilly; Astra-Zeneca; Boehringer- Ingelheim; Janssen

  • Dr Jorge De Jesús has no conflicts of interests with any entity for the information included in this presentation

Jorge De Jesús MD FACE


What is -cell dysfunction?

Major defect in individuals with type 2 diabetes

Reduced ability of -cells to secrete insulin in response to hyperglycemia

DeFronzo RA, et al. Diabetes Care 1992; 15:318–354.


Why insulin therapy in type 2 diabetes?


Antihyperglycemic Monotherapy Maximum Therapeutic Effect on A1C, dependent upon starting A1C

Baseline A1C

8.51

Acarbose

Nateglinide

8.3-8.52

Sitagliptin

Bromocriptine

7.73

7.8-12.54

Liraglutide

8.2-8.55

8.06

Exenatide

10.0-10.37

Pioglitazone

8.8-9.08

Repaglinide

Glimepiride

7.79

Glipizide GITS

8.3-8.810

9.7-10.111

Metformin

Insulin

0

-1.0

-1.5

-2.0

-0.5

Reduction in A1C Level (%)

1. Precose [PI]. West Haven, CT: Bayer; 2003; 2. Hanefeld M et al. Diabetes Care. 2000;23:202–207; 3. Sitagliptin PI, Merck & Co, Inc, Whitehouse Station, NJ, 2010;1-23; 4. Kerr et al. Ann Pharm. 2010;44:1777-1785; 5. Blonde et al. DiabObesMetab. 2009;11(S3):26-34; 6. Nelson P, et al. Diabetes TechnolTher. 2007;9:317–326; 7. Aronoff S, et al. Diabetes Care. 2000;23:1605–1611; 8. Lebovitz HE, et al. J ClinEndocrinolMetab. 2001;86:280–288; 9. Goldberg RB et al. Diabetes Care. 1996;19(8):849-856; 10. Simonson DC et al. Diabetes Care. 1997;20(4):597-606; 11. Garber AJ, et al. Am J Med. 1997;102:491–497.


Insulin

  • Remains the most powerful tool we have to control blood glucose

  • Dosing potential and A1C reduction only limited by risk of hypoglycemia

    • Patients with type 2 diabetes are at lower risk for hypoglycemia than type 1 patients

Nathan DM, et al. Diabetes Care. 2006;29:1963-1972.


When To Start Insulin in T2DM

  • When combination oral/injectable agents become inadequate

  • Have poor AM or daytime glycemic control

  • Unacceptable side effects of oral/injectable agents

  • Patient wants more flexibility

  • Special circumstances (i.e. steroids, infection, pregnancy)

  • Patients with hepatic or renal disease


Normal Insulin Secretion

75

Bolus or Meal Response

Dawn Phenomenon

Basal or Background

50

Plasma Insulin (U/mL)

Decrease at Night

25

0

4:00

8:00

12:00

16:00

20:00

24:00

4:00

8:00

Time (hrs)

Polonsky W. Diabetes Educ. 2007;33(suppl 3):241S–244S.


Treat to Target StudyInsulin Glargine vs. NPH Insulin Added to Oral Therapy

  • 9

Insulin glargine

NPH insulin

  • 8

Mean A1C(%)

  • 7

Target A1C (%)

60% reach target A1C < 7%

  • 6

  • 0

  • 4

  • 8

  • 12

  • 16

  • 20

  • 24

Weeks

Riddle MC, et al. Diabetes. 2002;51(suppl 2):A113.


Treat to Target Study: Cumulative Incidence of Hypoglycemia (N=756) PG 72 mg/dL ( 4.0 mmol/L)

NPH insulin

Insulin glargine

Insulin Glargine vs. NPH in Overweight Patients with T2DM

Cumulative Hypoglycemic Events

NPH, Neutral protamineHagedorn; PG, plasma glucose.

Riddle MC, et al. Diabetes Care. 2003;26:3080-3086.


Detemir + OAD

NPH + OAD

Risk of Hypoglycemia with Detemir

p < 0.001

18

16

14

12

Hypoglycemic events per patient per year

10

8

p < 0.001

6

4

2

0

Overall

Nocturnal*

* Any episode between 11 pm and 6 am

Please see full prescribing information.

Insulin detemir [package insert]. Bagsvaerd, Denmark; Novo Nordisk; 2009. NPH insulin [package insert]. Bagsvaerd, Denmark; Novo Nordisk; 2009. Hermansen K et al. Diabetes Care. 2006;29:1269-1274.


Insulin Detemir vs. NPH Weight Profile

3

Insulin detemir

*p<0.05, insulin detemir vs NPH insulin

NPH insulin

2.5

2

*

*

*

*

*

*

*

*

*

*

*

*

1.5

1

Weight change (kg)

0.5

0

Studies in type 2 diabetes

-0.5

-1

Hermansen

Standl

Vague

De Leeuw

Pieber

Pieber

Home

Home

Russell-Jones

Hermansen

Rašlová

Haak


  • Long-acting insulin analogs are superior to NPH insulin because they provide a fairly flat response for approximately 24 hours and pro-vide better reproducibility and consistency both between subjects and within subjects, with a corresponding reduction in the risk of hypoglycemia.

  • Rapid-acting insulin analogs are superior to Regular because they are more predictable.


24-Hour Insulin Secretion and Replacement

Aspart

Lispro

Glulisine

Regular

50

Insulin

(µU/mL)

25

Total Daily Dose (TDD)

~50% Bolus Insulin

~50% Basal Insulin

0

Breakfast Lunch Dinner

Detemir Glargine

NPH

Riddle MC et al. The American Journal of Medicine. 2005;118(5A):14S–20S. Tanaka M. et al. The Journal of International Medical Research. 2010;38:674–68.


Example: Starting Multiple Daily Injections in 100-kg Person with Moderate Insulin Resistance

  • Starting dose = 0.5 x wt in kg

    • 0.5 x 100 kg = 50 units

  • Basal dose = 50% of starting dose at bedtime

    • 50% of 50 units = 25 units at bedtime

  • Total bolus dose = 50% of starting dose evenly distributed1/3 at each meal

    • 25 units ÷ by 3 meals = 8 units before meals (TID)


Meal Insulin Rapid-Acting Analogs (Lispro, Aspart, Glulisine) vs Regular

Timing of

food absorbed

Analog insulin

10

8

6

Insulin

Activity

4

Regular Human Insulin

2

0

1

2

3

4

5

6

7

8

9

10

11

12

0

Hours

Howey DC, et al. Diabetes. 1994;43:396–402.


Barriers to insulin initiation

Patients refusal

Insulin costs

Fear of Hypoglycemia

Myths

Medical Inertia

Patient education is time consuming

Sometimes we transmit our concerns to patients even with non-verbal communication


Es mejorprenderunavelitaquemaldecir la oscuridad

Gracias

Agradecer al Dr Harry Jimemnez por la ayuda en algunos visuales de esta presentacion


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