Transcript Insulin Elixir of life

Insulin
Elixir of life
Dr. Sergio Diez Alvarez
Staff Specialist Physician
The Challenge
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Mr XL has type 2 diabetes and has been
on Oral Hypoglycemic Agents (metformin
+ glibenclamide) for 8 months, his HbA1c
is 8.3% and you have decided to offer him
the option of going on to insulin.
In theory, there is no difference between
theory and practice.
In practice, there is a big difference.
-Unknown
Understand the Stakeholders
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The Willing Patient
The Willing Clinician
The Insulin type and Regimen
The Delivery Device
Safety Accessories
Other factors
The Patient
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Insulinopaenia – beta cell reserve
Insulin Resistance – mainly hepatic,
muscle, and adipose tissues
Type 1 – complete insulin deficiency
Type 2 – Insulin dependent (LADA) vs.
insulin requiring
DAWN Study
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Resistance to Insulin Therapy Among
Patients and Providers
Results of the cross-national
Diabetes Attitudes, Wishes, and
Needs (DAWN) study
Diabetes Care November 2005 vol. 28 no. 11 2673-2679
Patients
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Patients rate the clinical efficacy of insulin as low
and would blame themselves if they had to start
insulin therapy.
Self-blame is significantly lower among those
who have better diet and exercise adherence
and less diabetes-related distress.
Patients who are not managing their diabetes
well (poor perceived control, more
complications, and diabetes-related distress) are
significantly more likely to see insulin therapy as
potentially beneficial.
The Clinician
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Most nurses and general practitioners (50–55%) delay
insulin therapy until absolutely necessary, but specialists
and opinion leaders are less likely to do so.
Delay of insulin therapy is significantly less likely when
physicians and nurses see their patients as more
adherent to medication or appointment regimens, view
insulin as more efficacious, and when they are less likely
to delay oral diabetes medications.
Resources were considered barely adequate currently
and there were concerns about worsening problems with
increasing numbers of patients with diabetes, and
increased use of insulin
Clinicians Shifting
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1980s - clinicians tended to be more
pessimistic than patients and overestimate
the barriers complying with treatment.
Insulin was seen as efficacious but there
was resistance because of a lack of
support, a skills deficit, and a lack of
confidence and experience in starting
insulin.
Psychological Resistance
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Remember – at time of Diagnosis 50% of
-cell function is already lost.
Insulin must be regarded as
“expected therapy”.
Not “Failure”
Not “Last Resort”
Not “End-stage therapy”
AND SHOULD BE STARTED MUCH EARLIER
Innovators vs. Conservative Clinicians
History of Insulin
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Insulin first isolated 1921 by Banting and Best
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Insulin first used as a treatment for diabetes in 1922
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Had short duration period and required several daily
injections
Had to be given through reusable glass syringes with
large often blunted needles
The Insulin Types
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Human vs. Analogs
Long Acting Insulin (Basal)
Short Acting Insulin (Bolus)
Pre-mixed Insulins
24-hour plasma glucose and insulin
profiles in healthy individuals
The Lancet, 2001, Vol 358, pages 739–746.
Owens DR et al. Lancet 2001;358:739–746
Insulin Regimens
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There is NO best Insulin – there is
only the Right Insulin for the Right
Patient
Daily Bolus (in combination with OHA's)
Twice daily
Basal bolus
Basal plus 1,2,3
CIIS
These can all be used in combination with OHAs (
especially insulin sensitizing agents)
Delivery Devices
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Syringes
Pen-sets – disposable or Refill
Continuous Insulin Infusion Pump
Glucose Monitoring
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Standard (simplified) Glucometer
Blood Ketone measuring (for Insulin
dependent patients)
Continuous Glucose Monitoring Device
Other (important ) Factors
 Family
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Friends (peers or colleagues)
Co-morbidities
Diabetic Complications e.g. retinopathy
Media (including internet)
After Sales Strategy
Match the regime to the patient
 What is the target HbA1c?
 How avidly should hypos be avoided?
 How many injections is the patient willing
to give?
 Fasting or postprandial the greater
problem?
 What device can the patient use?
Relative contribution of FPG & PPG to hyperglycaemia.
(12 hour profile)
FPG contribution.
PPG contribution.
p=0.048
p=0.001
83
69
65
35
31
17
HbA1c tertiles :
<7.3%
7.3%-8.0%
>8.0%
Peter R, Owens DR et al- Diab Med- 2004
Complications
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Lipodystrophy
Lipoatrophy & lipohypertrophy