Download Type 2 Diabetes Management Goals

Glycemic Management in
Type 2 Diabetes
1
AACE Comprehensive Care
Plan
Disease management from
a multidisciplinary team
Antihyperglycemic
pharmacotherapy
Comprehensive
Care Plan
Comprehensive diabetes
self-education for the
patient
Therapeutic lifestyle
change
2
Handelsman Y, et al. Endocr Pract. 2011;17(suppl 2):1-53.
Glycemic Management in
Type 2 Diabetes
Therapeutic Lifestyle Change
3
Components of Therapeutic
Lifestyle Change
•
•
•
•
•
•
Healthful eating
Sufficient physical activity
Sufficient sleep
Avoidance of tobacco products
Limited alcohol consumption
Stress reduction
4
Handelsman Y, et al. Endocr Pract. 2011;17(suppl 2):1-53.
AACE Healthful Eating
Recommendations
Topic
General eating
habits
Recommendation

Regular meals and snacks; avoid fasting to lose weight

Plant-based diet (high in fiber, low calories, low glycemic index, high in phytochemicals/antioxidants)

Understand Nutrition Facts Label information

Incorporate beliefs and culture into discussions

Informal physician-patient discussions

Use mild cooking techniques instead of high-heat cooking
Carbohydrate

Understand health effects of the 3 types of carbohydrates: sugars, starch, and fiber

Target 7-10 servings per day of healthful carbohydrates (fresh fruits and vegetables, pulses, whole
grains)

Lower-glycemic index foods may facilitate glycemic control:* multigrain bread, pumpernickel bread,
whole oats, legumes, apple, lentils, chickpeas, mango, yams, brown rice
Fat

Eat healthful fats: low-mercury/low-contaminant-containing nuts, avocado, certain plant oils, fish

Limit saturated fats (butter, fatty red meats, tropical plant oils, fast foods) and trans fats

Use no- or low-fat dairy products
Protein

Consume protein from foods low in saturated fats (fish, egg whites, beans)

Avoid or limit processed meats
Micronutrients

Routine supplementation not necessary except for patients at risk of insufficiency or deficiency

Chromium; vanadium; magnesium; vitamins A, C, and E; and CoQ10 not recommended for glycemic
control
*Insufficient evidence to support a formal recommendation to educate patients that sugars have both positive and negative
health effects
5
Handelsman Y, et al. Endocr Pract. 2011;17(suppl 2):1-53.
AACE Medical Nutritional
Therapy Recommendations
• Consistency in day-to-day carbohydrate intake
• Adjusting insulin doses to match carbohydrate
intake (eg, use of carbohydrate counting)
• Limitation of sucrose-containing or highglycemic index foods
• Adequate protein intake
• “Heart-healthy” diets
• Weight management
• Exercise
• Increased glucose monitoring
6
Handelsman Y, et al. Endocr Pract. 2011;17(suppl 2):1-53.
AACE Physical Activity
Recommendations
• ≥150 minutes per week
of moderate-intensity
exercise
– Flexibility and strength
training
– Aerobic exercise (eg, brisk
walking)
• Start slowly and build up
gradually
• Evaluate for
contraindications and/or
limitations to increased
physical activity before
patient begins or
intensifies exercise
program
• Develop exercise
recommendations
according to individual
goals and limitations
7
Handelsman Y, et al. Endocr Pract. 2011;17(suppl 2):1-53.
Glycemic Management in
Type 2 Diabetes
Antihyperglycemic Therapy
8
Noninsulin Agents Available for
Treatment of Type 2 Diabetes
Class
Primary Mechanism of Action
 Delay carbohydrate
absorption from intestine
Agent
Acarbose
Miglitol
Available as
Precose or generic
Glyset



Decrease glucagon secretion
Slow gastric emptying
Increase satiety
Pramlintide
Symlin
Biguanide


Decrease HGP
Increase glucose uptake in
muscle
Metformin
Glucophage or generic
Bile acid
sequestrant


Decrease HGP?
Increase incretin levels?
Colesevelam
WelChol

Increase glucose-dependent
insulin secretion
Decrease glucagon secretion
Alogliptin
Linagliptin
Saxagliptin
Sitagliptin
Nesina
Tradjenta
Onglyza
Januvia
Activates dopaminergic
receptors
Bromocriptine
Cycloset
-Glucosidase
inhibitors
Amylin analogue
DPP-4 inhibitors

Dopamine-2
agonist

9
HGP, hepatic glucose production.
Inzucchi SE, et al. Diabetes Care. 2012;35:1364-1379.
Noninsulin Agents Available for
Treatment of Type 2 Diabetes
Class
Primary Mechanism of Action
Glinides

Increase insulin secretion

Increase glucose-dependent
insulin secretion
Decrease glucagon secretion
Slow gastric emptying
Increase satiety
Increase urinary excretion of
glucose
GLP-1 receptor
agonists
SGLT2 inhibitor
Sulfonylureas






Thiazolidinediones

Increase insulin secretion
Increase glucose uptake in
muscle and fat
Decrease HGP
Agent
Nateglinide
Repaglinide
Available as
Starlix or generic
Prandin
Exenatide
Byetta
Exenatide XR
Bydureon
Liraglutide
Victoza
Canagliflozin
Invokana
Glimepiride
Glipizide
Amaryl or generic
Glucotrol or generic
Glyburide
Diaeta, Glynase,
Micronase, or generic
Pioglitazone
Actos
Rosiglitazone*
Avandia
*Use restricted due to increased risk of myocardial infarction (MI)
10
HGP, hepatic glucose production.
Inzucchi SE, et al. Diabetes Care. 2012;35:1364-1379.
Insulins Available for the Treatment
of Type 2 Diabetes
Class
Primary Mechanism of Action
Basal
Prandial
Premixed


Increase glucose uptake
Decrease HGP
Agent
Detemir
Glargine
Available as
Levemir
Lantus
Neutral protamine
Hagedorn (NPH)
Generic
Aspart
Glulisine
Lispro
Regular human
Biphasic aspart
Biphasic lispro
NovoLog
Apidra
Humalog
Humulin, generic
NovoLog Mix
Humalog Mix
11
Inzucchi SE, et al. Diabetes Care. 2012;35:1364-1379.
Pharmacokinetics of Insulin
Agent
Onset (h)
Peak (h)
Duration (h)
Considerations
NPH
2-4
4-10
10-16
Glargine
~1-4
No pronounced
peak*
Up to 24
hours†
Less nocturnal hypoglycemia
compared to NPH
~0.5-1
~2-3
Up to 8

Basal
Detemir
Greater risk of nocturnal
hypoglycemia compared to insulin
analogues
Prandial
Regular

Aspart
<0.5
~0.5-2.5
Glulisine
Lispro
12
~3-5


Must be injected 30-45 min
before a meal
Injection with or after a meal
could increase risk for
hypoglycemia
Can be injected 0-15 min before
a meal
Less risk of postprandial
hypoglycemia compared to
regular insulin
* Exhibits a peak at higher dosages.
† Dose-dependent.
Moghissi E, et al. Endocr Pract. 2013;Feb 20:1-33. [Epub ahead of print].
Combination Agents Available for the
Treatment of Type 2 Diabetes
Class
Metformin + DPP-4 inhibitor
Metformin + glinide
Metformin + sulfonylurea
Metformin + thiazolidinedione
Thiazolidinedione + DPP-4 inhibitor
Thiazolidinedione + sulfonylurea
Added Agent
Available as
Alogliptin
Kazano
Linagliptin
Jentadueto
Sitagliptin
Janumet
Repaglinide
Prandimet
Glipizide
Metaglip and generic
Glyburide
Glucovance and generic
Pioglitazone
ACTOplus Met
Rosiglitazone*
Avandamet
Pioglitazone +
alogliptin
Oseni
Pioglitazone
Duetact
Rosiglitazone*
Avandaryl
*Use restricted due to increased risk of myocardial infarction (MI)
13
Principles of the AACE/ACE
T2DM Algorithm
Glucose Targets
• Ongoing lifestyle optimization essential
– Requires support from full diabetes team
• Set A1C target based on individual
patient characteristics and risk
– ≤6.5% optimal if it can be achieved safely
– Targets may change over time
• FPG and PPG regularly monitored by
patient with SMBG
14
Garber AJ, et al. Endocr Pract. 2013;19:327-336.
Principles of the AACE/ACE
T2DM Algorithm
Antihyperglycemic Medications
•
Choose medications based on
individual patient attributes
– Minimize risk of hypoglycemia
– Minimize risk of weight gain
– Combine agents with
complimentary mechanisms of
action for optimal glycemic
control
•
Prioritize safety and efficacy
over medication cost
– Medication cost small portion of
total cost of diabetes
– Risk of adverse effects
considered part of “cost” of
medication
• Evaluate treatment efficacy
every 3 months
– A1C, FPG, and PPG data
– Hypoglycemia
– Other adverse events (weight
gain; fluid retention; hepatic,
renal, or cardiac disease)
– Comorbidities and
complications
– Concomitant drugs
– Psychosocial factors affecting
patient care
15
Garber AJ, et al. Endocr Pract. 2013;19:327-336.
16
17
18
19
Common Principles in AACE/ACE and
ADA/EASD T2DM Treatment Algorithms
• Individualize glycemic goals based on patient
characteristics
• Promptly intensify antihyperglycemic therapy to maintain
blood glucose at individual targets
– Combination therapy necessary for most patients
– Base choice of agent(s) on individual patient medical history,
behaviors and risk factors, ethno-cultural background, and
environment
• Insulin eventually necessary for many patients
• SMBG vital for day-to-day management of blood sugar
– All patients using insulin
– Many patients not using insulin
20
Inzucchi SE, et al. Diabetes Care. 2012;35:1364-1379.
Garber AJ, et al. Endocr Pract. 2013;19:327-336.
ADA/EASD T2DM Treatment Algorithm
21
Inzucchi SE, et al. Diabetes Care. 2012;35:1364-1379.
ADA/EASD T2DM Treatment Algorithm:
Sequential Insulin Strategies
22
Inzucchi SE, et al. Diabetes Care. 2012;35:1364-1379.
Early Insulin Use in Type 2
Diabetes
Outcome Reduction With an Initial Glargine Intervention
CV risk factors + prediabetes or T2DM (N=12,537)
23
ORIGIN Trial Investigators. N Engl J Med. 2012;367:319-328.
Pipeline Classes and Agents
(2013)
Class
Phase of Development
Dual peroxisome proliferator activated
receptor - (PPAR-) agonist
Phase 3
Short-acting GLP-1 receptor agonist
Description
Lixisenatide
Improve insulin sensitivity in the periphery as well as lipid profiles
Approved agents may reduce both cardiovascular risks and potential for
diabetes complications
Human-derived molecule with effects similar to exenatide
Long-acting GLP-1 receptor agonists
Phase 3
Albiglutide
Taspoglutide
Effects probably similar to currently available GLP-1 receptor agonists
Longer duration of action will permit longer intervals between injections
Insulin
Phase 3
Degludec
Aleglitazar
DegludecPlus
Ultra-long-acting basal insulin (half-life ~25 hours) with low within-subject
variability and potential for reduced incidence of hypoglycemia
Premixed insulin containing degludec plus aspart, providing both fasting
and postprandial glucose control
Generically available anti-inflammatory medication currently approved for
treatment of arthritis; inhibits activity of NF-B, an inflammatory factor
Salicylates
Phase 3
Salsalate
Sodium-dependent glucose
cotransporter 2 (SGLT-2) inhibitors
Phase 3
Dapagliflozin
Empagliflozin
Tofogliflozin
Act in the kidney
Reduce hyperglycemia by inhibiting glucose reabsorption into the
bloodstream from the renal filtrate, increasing urinary excretion of glucose
INCB13739
RG4929
Inhibit 11HSD-1 mediated conversion of low-activity cortisone to cortisol,
which is primarily produced in the liver and adipose tissue
May lessen stress-induced obesity, improve insulin sensitivity, enhance
insulin-secretory responsiveness, and improve glucose tolerance in
patients with metabolic syndrome and/or type 2 diabetes
11-Hydroxysteroid dehydrogenase
type 1 (11HSD-1) inhibitors
Phase 2
24
Agents
Bakris GL, et al. Kidney Int. 2009;75:1272-1277; Calado J, et al. Kidney Int Suppl. 2011:S7-S13;
Garber AJ. Expert Opin Investig Drugs. 2012;21:45-57; Goldfine AB, et al. Ann Intern Med. 2010;152:346-357;
King A. J Fam Pract. 2012;61:S28-S31; Tahrani AA, et al. Lancet. 2011;378:182-197;
Tahrani AA, et al. Lancet. 2012;379:1465-1467.
Glycemic Management in
Type 2 Diabetes
Technology for Type 2 Diabetes
Management
25
SMBG in Type 2 Diabetes:
AACE/ACE Recommendations
Noninsulin Users
• Introduce at diagnosis
• Personalize frequency of
testing
• Use SMBG results to inform
decisions about whether to
target FPG or PPG for any
individual patient
Testing positively affects glycemia in
T2DM when the results are used to:
• Modify behavior
• Modify pharmacologic treatment
Insulin Users
• All patients using insulin should
test glucose
– ≥2 times daily
– Before any injection of insulin
• More frequent SMBG (after
meals or in the middle of the
night) may be required
– Frequent hypoglycemia
– Not at A1C target
26
SMBG, self-monitoring of blood glucose.
Handelsman Y, et al. Endocr Pract. 2011;17(suppl 2):1-53.
SMBG in Noninsulin Using
Patients With T2DM
Adjusted Mean A1C (%)
9.0
Active control group (n=227)
Structured testing group (n=256)
8.8
8.6
8.4
8.2
8.0
-0.3%
7.8
(P=0.04)
7.6
7.4
7.2
Baseline M1
M3
M6
M9
M12
ACG
8.9%
(0.08)
8.7%
(0.1)
8.2%
(0.1)
7.9%
(0.1)
8.0%
(0.1)
8.0%
(0.1)
STG
8.9%
(0.07)
8.5%
(0.09)
7.9%
(0.09)
7.9%
(0.09)
7.6%
(0.09)
7.7%
(0.09)
27
ACG, active cotnrol group; STG, structured testing group.
Polonsky WH, et al. Diabetes Care. 2011;34:262-267.
CSII in Type 2 Diabetes:
Patient Candidates
• Absolutely insulin-deficient
• Take 4 or more insulin
injections a day
• Assess blood glucose levels 4
or more times daily
• Motivated to achieve tighter
glucose control
• Mastery of carbohydrate
counting, insulin correction, and
adjustment formulas
• Ability to troubleshoot problems
related to pump operation and
plasma glucose levels
• Stable life situation
• Frequent contact with members
of their healthcare team, in
particular their pumpsupervising physician
28
CSII, continuous subcutaneous insulin infusion.
Handelsman Y, et al. Endocr Pract. 2011;17(suppl 2):1-53.
Glycemic Management in
Type 2 Diabetes
Surgical Intervention
29
Surgical Intervention in
Type 2 Diabetes
3.5
3.0
2.5
2.0
1.5
1.0
0.5
0.0
Baseline
P<0.001
P<0.001
3
6
9
12
 FPG (mg/dL)
0.0
0.5
1.0
1.5
2.0
2.5
3.0
3.5
Baseline
Sleeve gastrectomy
Roux-en-Y gastric bypass
20
0
-20
-40
-60
-80
-100
-120
-140
-160
Baseline
P=0.02
P<0.001
3
6
9
12
0
P<0.001
P<0.001
3
6
Months
9
12
 BMI (kg/m2)
Average no. diabetes
medications
 A1C (%)
Intensive medical therapy
-2
-4
-6
P<0.001
-8
-10
-12
Baseline
P<0.001
3
6
9
12
Months
30
Schauer PR, et al. N Engl J Med. 2012;366:1567-1576.
Glycemic Management in
Type 2 Diabetes
Safety Concerns: Hypoglycemia
31
Type 2 Diabetes Pathophysiology:
Origins of Hypoglycemia
Defect
β-cells
Increased insulin availability due to use of secretagogues or exogenous
insulin
Liver
Suppressed hepatic glucose production due to impaired counterregulatory response
Skeletal muscle
Increased glucose uptake due to exercise
α-cells
Suppressed glucagon due to impaired counter-regulatory response
Brain
Hypoglycemia unawareness
32
Cryer PE. Am J Physiol. 1993; 264(2 Pt 1):E149-E155.
Hypoglycemia: Risk Factors
Patient Characteristics
Behavioral and Treatment
Factors
• Older age
• Female gender
• African American
ethnicity
• Longer duration of
diabetes
• Neuropathy
• Renal impairment
• Previous hypoglycemia
• Missed meals
• Elevated A1C
• Insulin or sulfonylurea
therapy
33
Miller ME, et al. BMJ. 2010 Jan 8;340:b5444. doi: 10.1136/bmj.b5444.
Symptoms and Signs with
Progressive Hypoglycemia
Blood Glucose (mg/dL)
100
90
80
70
60
50
40
30
20
10
34
Decreased insulin secretion
Increased glucagon, epinephrine,
ACTH, cortisol, and growth hormone
Palpitation, sweating
Decreased cognition, hunger
Aberrant behavior
Seizures, coma
Neuronal cell death
0
Moghissi E, et al. Endocr Pract. 2013;Feb 20:1-33. [Epub ahead of print].
Hypoglycemia: Clinical
Consequences
Acute
• Symptoms (sweating,
irritability, confusion)
• Accidents
• Falls
Long-term
• Recurrent hypoglycemia
and hypoglycemia
unawareness
• Refractory diabetes
• Dementia (elderly)
• CV events
– Cardiac autonomic
neuropathy
– Cardiac ischemia
– Fatal arrhythmia
– Angina
35
Cryer PE, et al. Diabetes Care. 2003;26:1902-1912.
ADA. Diabetes Care. 2013;36(suppl 1):S11-S66.
Zammit NN, et al. Diabetes Care. 2005;28:2948-2961.
Treatment of Hypoglycemia:
AACE/ACE Recommendations
Blood
Glucose
Level
~50-60
<50
Classification
Typical Signs and
Symptoms
Treatment
Mild hypoglycemia


Moderate
hypoglycemia

Severe
hypoglycemia


Neurogenic:
palpitations, tremor,
hunger, sweating,
anxiety, paresthesia
Neuroglycopenic:
behavioral changes,
emotional lability,
difficulty thinking,
confusion
Severe confusion,
unconsciousness,
seizure, coma, death
Requires help from
another individual




Consume glucose-containing
foods (fruit juice, soft drink,
crackers, milk, glucose tablets);
avoid foods also containing fat
Repeat glucose intake if SMBG
result remains low after 15 minutes
Consume meal or snack after
SMBG has returned to normal to
avoid recurrence
Glucagon injection, delivered by
family member or other close
associate
Victim should be taken to hospital
for evaluation and treatment after
any severe episode
36
Cryer PE, et al. Diabetes Care. 2003;26:1902-1912.
Elements of Hypoglycemia
Prevention

Set appropriate
glycemic targets for
individual patients



More stringent goals: young, newly diagnosed, no comorbidities, no micro- or
macrovascular disease, strong and effective self-care skills
Less stringent goals: older, limited life expectancy, history of hypoglycemia, longer
disease duration, established comorbidities, established vascular disease, limited selfcare skills




Signs and symptoms of hypoglycemia
Dietary education for improved glycemic control and appreciation of triggers for
hypoglycemia
Avoiding missed or delayed meals
Appropriate self-treatment
Understanding of hypoglycemia unawareness
Importance of reporting hypoglycemia
Use self-monitoring
of blood glucose




Patient education: technique and action
Observation of patient’s procedure and reaction
Patient access to providers for purposes of reporting results and for providing guidance
Provider reaction to results increases effectiveness of SMBG
Hold a high index
of suspicion for
hypoglycemia



Understand patients may not report “typical” symptoms
When hypoglycemia is suspected, adjust therapy
Consider use of continuous glucose monitoring to detect unrecognized hypoglycemia
Choose appropriate
therapy



Use agents with a low risk of hypoglycemia
Be aware of additive effects of combination therapies on hypoglycemia risk
Recognize that long-term costs of hypoglycemia may offset the cost of using older, less
physiologic medications
Educate patients
37
Moghissi E, et al. Endocr Pract. 2013;Feb 20:1-33. [Epub ahead of print].
Hypoglycemia Risk With
Antihyperglycemic Agents Added
to Metformin
Initial Treatment
Additional Treatment
DPP-4 inhibitors
Less
Hypoglycemia
GLP-1 receptor agonists
TZDs
Metformin
More
Hypoglycemia
Sulfonylureas
Insulin (basal, basal-plus, premixed)
38
Moghissi E, et al. Endocr Pract. 2013;Feb 20:1-33. [Epub ahead of print].
Frequency of Severe Hypoglycemia
With Antihyperglycemic Agents
Percentage of Patients Treated in 1 Year
6%
Mixtures, Rapid-acting, Basal-bolus
5%
Insulin
4%
Basal
3%
2%
1%
0
Sulfonylureas
Meglinitides
DPP-4 inhibitors, GLP-1 receptor agonists,
Metformin, TZDs
39
Moghissi E, et al. Endocr Pract. 2013;Feb 20:1-33. [Epub ahead of print].
Relative Rates of Severe
Hypoglycemia with Insulin
Increasing rates
of hypoglycemia
Most
frequent
Prandial
and
premixed
Human insulin
Analogue insulins
Premixed (70/30, 75/25)
More
frequent
Basal +
Basal plus 2-3 prandial
Basal plus one prandial
Basal
only
NPH
Basal analogues (glargine, detemir)
Pipeline basal analogues
(degludec, pegylated lispro)
Less
frequent
40
Moghissi E, et al. Endocr Pract. 2013;Feb 20:1-33. [Epub ahead of print].
Glycemic Management in
Type 2 Diabetes
Safety Concerns: Weight
41
Antidiabetic Agents and Weight
Class
Amylin analog
Biguanide
GLP-1 receptor agonists
SGLT-2 inhibitor
-Glucosidase inhibitors
Bile acid sequestrant
DPP-4 inhibitors
Dopamine-2 agonist
Glinides
Sulfonylureas
Agent(s)
Pramlintide
Metformin
Exenatide, exenatide XR, liraglutide
Canagliflozin
Acarbose, miglitol
Colesevelam
Alogliptin, linagliptin, saxagliptin, sitagliptin
Bromocriptine
Nateglinide, repaglinide
Glimepiride, glipizide, glyburide
Insulin
Aspart, detemir, glargine, glulisine, lispro, NPH, regular
↑↑
Thiazolidinediones
Pioglitazone, rosiglitazone
↑↑
•
Weight Effect
↓
↓
↓
↓
↔
↔
↔
↔
↑
↑
Risk of additional weight gain must be balanced against the benefits of
the agent
– Sulfonylureas may negate weight loss benefits of GLP-1 receptor agonists
or metformin
– Insulin should not be withheld because of the risk of weight gain
42
Inzucchi SE, et al. Diabetes Care. 2012;35:1364-1379. Garber AJ, et al. Endocr Pract. 2013;19:327-336.
Handelsman Y, et al. Endocr Pract. 2011;17(suppl 2):1-53. Stenlof K, et al. Diabetes Obes Metab 2013;15:372-382.
Glycemic Management in
Type 2 Diabetes
Safety Concerns: Cancer Risk
43
Insulin and Cancer Risk
Study
Hazard Ratio (95% CI)
Outcome Reduction With an Initial
Glargine Intervention (ORIGIN)
N=12,537; prospective RCT
Median follow-up: 6.2 years
Any cancer: 1.00 (0.88-1.13); P=0.97
Death from cancer: 0.94 (0.77-1.15); P=0.52
Northern European Database Study
N=447,821; observational
Mean follow-up:
Glargine users: 3.1 years
Other insulin users: 3.5 years
Breast cancer (women): 1.12 (0.99-1.27)
Prostate cancer (men): 1.11 (1.00-1.24)
Colorectal cancer (men and women): 0.86 (0.76-0.98)
Kaiser-Permanente Collaboration
N=115,000; observational
Median follow-up:
Glargine users: 1.2 years
NPH users: 1.4 years
Breast cancer (women): 1.0 (0.9-1.3)
Prostate cancer (men): 0.7 (0.6-0.9)
Colorectal cancer (men and women): 1.00 (0.8-1.2)
All cancers (men and women): 0.9 (0.9-1.0)
MedAssurant Database Study
N=52,453; observational
Mean follow-up:
Glargine users: 1.2 years
NPH users: 1.1 years
No increased risk for breast cancer
44
ORIGIN Trial Investigators. N Engl J Med. 2012;367:319-328. Kirkman MS, et al. Presented at the American Diabetes
Association 72nd Scientific Sessions. June 11, 2012. Session CT-SY13. Philadelphia, PA.
Glycemic Management in
Type 2 Diabetes
Special Populations and
Situations
45
Management Considerations
for Elderly Patients with
Diabetes
Increased risk of and
from falling
• Impaired vision
• Reduced strength and
stamina
• Sensitivity to
medication side effects
• Frailty
• Susceptibility to
hypoglycemia
Hypoglycemia
unawareness and
recurrent
hypoglycemia
• Impaired counterregulatory mechanisms
Other complicating
factors
• Diminished kidney
function
• Urinary incontinence
• Status of social support
and/or caregiver
• Drug-drug interactions
Consider risks before prescribing:
• Sulfonylureas and glinides (hypoglycemia risk)
• Thiazolidinediones (fracture risk)
• Metformin (risk of lactic acidosis with decreased kidney function)
Impaired capacity,
understanding, and/or
motivation for proper
self-care
• Cognitive decline and
dementia
• Depression
• Impaired vision
Consider when establishing
treatment goals
• Patient overall health and well-being
• Self-care capacities
• Social/family support
46
Bourdel Marchasson I, et al. J Nutr Health Aging. 2009;13:685-691. Handelsman Y, et al. Endocr Pract. 2011;17(suppl
2):1-53. Schwartz AV, et al. Diabetes Care. 2008;31:391-396. Zammitt NN, Frier BM. Diabetes Care. 2005;28:2948-2961.
Risk Considerations for
Religious/Cultural Fasting
Main Risks of Fasting
•
•
•
•
Risk Category
Low
Moderate
High
Very high
47
Hypoglycemia
Hyperglycemia
Diabetic ketoacidosis
Dehydration and thrombosis
Features

Glycemia well-controlled with antihyperglycemic agent that does not cause
hypoglycemia (eg, metformin, thiazolidinedione, DPP-4 inhibitor, GLP-1 receptor
agonist)

Otherwise healthy

Glycemia well-controlled with glinides

Moderate hyperglycemia (A1C 7.5-9.0%), renal insufficiency, cardiovascular
complications, and/or other comorbid conditions

Living alone, especially if taking sulfonylureas, insulin, or drugs that affect mentation

Elderly, especially with poor health

History of recurrent hypoglycemia, hypoglycemia unawareness, or episode of severe
hypoglycemia within 3 months prior to Ramadan

Poor glycemic control

Ketoacidosis or hyperosmotic hyperglycemic coma within 3 months prior to Ramadan

Acute illness or chronic dialysis

Intense physical labor

Pregnancy
Al-Arouj M, et al. Diabetes Care. 2005;28:2305-2311.
Glycemic Management During
Religious/Cultural Fasting
• Frequent glucose monitoring—break fast immediately if patient
has:
– Hypoglycemia
• SMBG <70 mg/dL while taking insulin or sulfonylureas
• SMBG <60 mg/dL while on other therapies
– Hyperglycemia: >300 mg/dL
• Healthful eating before and after each fasting period
– Complex carbohydrates prior to fast
– Avoid ingesting high-carbohydrate, high-fat foods when breaking
fast
• Avoid excessive physical activity but maintain normal exercise
routines
• Avoid fasting while ill
48
Al-Arouj M, et al. Diabetes Care. 2005;28:2305-2311.