Insulin initiation and intensification in the type 2 diabetic patient
Download
1 / 28

Insulin Initiation and Intensification in the Type 2 Diabetic Patient - PowerPoint PPT Presentation


  • 173 Views
  • Uploaded on

Insulin Initiation and Intensification in the Type 2 Diabetic Patient. Jorge De Jesus MD FACE . Disclosures.

loader
I am the owner, or an agent authorized to act on behalf of the owner, of the copyrighted work described.
capcha
Download Presentation

PowerPoint Slideshow about ' Insulin Initiation and Intensification in the Type 2 Diabetic Patient' - gore


An Image/Link below is provided (as is) to download presentation

Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author.While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server.


- - - - - - - - - - - - - - - - - - - - - - - - - - E N D - - - - - - - - - - - - - - - - - - - - - - - - - -
Presentation Transcript
Insulin initiation and intensification in the type 2 diabetic patient

Insulin Initiation and Intensification in the Type 2 Diabetic Patient

Jorge De Jesus MD FACE


Disclosures
Disclosures Diabetic Patient

  • 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
What is  Diabetic Patient-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 Diabetic Patientin type 2 diabetes?


Antihyperglycemic monotherapy maximum therapeutic effect on a1c dependent upon starting a1c
Antihyperglycemic Monotherapy Diabetic PatientMaximum 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 Diabetic Patient

  • 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 Diabetic Patient

  • 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
Normal Insulin Secretion Diabetic Patient

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 study insulin glargine vs nph insulin added to oral therapy
Treat to Target Study Diabetic PatientInsulin 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
Treat to Target Study: Diabetic PatientCumulative 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 Diabetic Patient

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
Insulin Detemir vs. NPH Weight Profile Diabetic Patient

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
24-Hour Insulin Secretion and Replacement 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.

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
Example: 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.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
Meal 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 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
Barriers to insulin initiation 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.

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 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.mejorprenderunavelitaquemaldecir la oscuridad

Gracias

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


ad