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ADA EASD Position Statement Management of Hyperglycemia in T2 DM April 2012
1. Management of Hyperglycemia in Type 2
Diabetes: A Patient-Centered Approach
Position Statement of the American Diabetes Association (ADA) and
the European Association for the Study of Diabetes (EASD)
2. Writing Group
American Diabetes Association European Assoc. for the Study of Diabetes
Richard M. Bergenstal MD Michaela Diamant MD, PhD
Int’l Diabetes Center, Minneapolis, MN VU University, Amsterdam, The Netherlands
John B. Buse MD, PhD Ele Ferrannini MD
University of North Carolina, Chapel Hill, NC University of Pisa, Pisa, Italy
Anne L. Peters MD Michael Nauck MD
Univ. of Southern California, Los Angeles, CA Diabeteszentrum, Bad Lauterberg, Germany
Richard Wender MD Apostolos Tsapas MD, PhD
Thomas Jefferson University, Philadelphia, PA Aristotle University, Thessaloniki, Greece
Silvio E. Inzucchi MD (co-chair) David R. Matthews MD, DPhil (co-chair)
Yale University, New Haven, CT Oxford University, Oxford, UK
3. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM: A Patient-Centered Approach
• PATIENT-CENTERED APPROACH
2. BACKGROUND
• Epidemiology and health care impact
• Relationship of glycemic control to outcomes
• Overview of the pathogenesis of Type 2 diabetes
3. ANTI-HYPERGLYCEMIC THERAPY
• Glycemic targets
• Therapeutic options
- Lifestyle
- Oral agents & non-insulin injectables
- Insulin
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
4. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM: A Patient-Centered Approach
3. ANTIHYPERGLYCEMIC THERAPY
• Implementation Strategies
- Initial drug therapy
- Advancing to dual combination therapy
- Advancing to triple combination therapy
- Transitions to and titrations of insulin
4. OTHER CONSIDERATIONS
• Age
• Weight
• Sex/racial/ethnic/genetic differences
• Comorbidities (Coronary artery disease, Heart failure,
Chronic kidney disease, Liver dysfunction, Hypoglycemia)
5. FUTURE DIRECTIONS / RESEARCH NEEDS
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
5. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
• Patient-Centered Approach
“...providing care that is respectful of and responsive to
individual patient preferences, needs, and values - ensuring
that patient values guide all clinical decisions.”
• Gauge patient’s preferred level of involvement.
• Explore, where possible, therapeutic choices.
• Utilize decision aids.
•Shared decision making – final decisions re: lifestyle choices
ultimately lies with the patient.
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
6. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
2. BACKGROUND
• Epidemiology and health care impact
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
7. Age-adjusted Percentage of U.S. Adults with
Obesity or Diagnosed Diabetes
Obesity (BMI ≥30 kg/m2)
1994 2000 2009
O
B
E
S
I
T
No Data <14.0% 14.0-17.9% 18.0-21.9% 22.0-25.9% >26.0%
Y
Diabetes
D 1994 2000 2009
I
A
B
E
T
E No Data <4.5% 4.5-5.9% 6.0-7.4% 7.5-8.9% >9.0%
S
CDC’s Division of Diabetes Translation. National Diabetes Surveillance System available
at http://www.cdc.gov/diabetes/statistics
9. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
2. BACKGROUND
• Relationship of glycemic control to outcomes
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
11. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
2. BACKGROUND
• Overview of the pathogenesis of T2DM
- Insulin secretory dysfunction
-Insulin resistance (muscle, fat, liver)
-Increased endogenous glucose production
-Deranged adipocyte biology
-Decreased incretin effect
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
12. Main Pathophysiological Defects in T2DM
pancreatic
incretin insulin
effect secretion
pancreatic
glucagon
gut
− secretion ?
carbohydrate
delivery &
absorption HYPERGLYCEMIA
−
+
peripheral
hepatic glucose
glucose uptake
production Adapted from: Inzucchi SE, Sherwin RS in: Cecil Medicine 2011
13. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
3. ANTI-HYPERGLYCEMIC THERAPY
•Glycemic targets
- HbA1c < 7.0% (mean PG ∼150-160 mg/dl [8.3-8.9 mmol/l])
- Pre-prandial PG <130 mg/dl (7.2 mmol/l)
- Post-prandial PG <180 mg/dl (10.0 mmol/l)
- Individualization is key:
Tighter targets (6.0 - 6.5%) - younger, healthier
Looser targets (7.5 - 8.0%+) - older, comorbidities,
hypoglycemia prone, etc.
- Avoidance of hypoglycemia
PG = plasma glucose Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
14. Figure 1 Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
(Adapted with permission from: Ismail-Beigi F, et al. Ann Intern Med 2011;154:554)
15. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
3. ANTI-HYPERGLYCEMIC THERAPY
•Therapeutic options: Lifestyle
-Weight optimization
-Healthy diet
- Increased activity level iabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
D
16. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
3. ANTI-HYPERGLYCEMIC THERAPY
• Therapeutic options:
Oral agents & non-insulin injectables
- Metformin - Meglitinides
- Sulfonylureas - α-glucosidase inhibitors
- Thiazolidinediones - Bile acid sequestrants
- DPP-4 inhibitors - Dopamine-2 agonists
- GLP-1 receptor agonists - Amylin mimetics
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
17. Class Mechanism Advantages Disadvantages Cost
Biguanides • Activates AMP-kinase • Extensive experience • Gastrointestinal Low
• ↓ Hepatic glucose • No hypoglycemia • Lactic acidosis
production • Weight neutral • B-12 deficiency
• ? ↓ CVD • Contraindications
SUs / • Closes KATP channels • Extensive experience • Hypoglycemia Low
Meglitinides • ↑ Insulin secretion • ↓ Microvasc. risk • Weight gain
• Low durability
• ? Ischemic
preconditioning
TZDs • PPAR-γ activator • No hypoglycemia • Weight gain High
• ↑ insulin sensitivity • Durability • Edema / heart failure
• ↓ TGs, ↑ HDL-C • Bone fractures
• ? ↓ CVD (pio) • ? ↑ MI (rosi)
• ? Bladder ca (pio)
α-GIs • Inhibits • No hypoglycemia • Gastrointestinal Mod.
α−glucosidase • Nonsystemic • Dosing frequency
• Slows carbohydrate • ↓ Post-prandial • Modest ↓ A1c
absorption glucose
• ? ↓ CVD events
Table 1. Properties of anti-hyperglycemic agents Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
18. Class Mechanism Advantages Disadvantages Cost
DPP-4 • Inhibits DPP-4 • No hypoglycemia • Modest ↓ A1c High
inhibitors • Increases GLP-1, GIP • Well tolerated • ? Pancreatitis
• Urticaria
GLP-1 • Activates GLP-1 R • Weight loss • GI High
receptor • ↑ Insulin, ↓ glucagon • No hypoglycemia • ? Pancreatitis
agonists • ↓ gastric emptying • ? Beta cell mass • Medullary ca
• ↑ satiety • ? CV protection • Injectable
Amylin • Activates amylin • Weight loss • GI High
mimetics receptor • ↓ PPG • Modest ↓ A1c
• ↓ glucagon • Injectable
• ↓ gastric emptying • Hypo w/ insulin
• ↑ satiety • Dosing frequency
Bile acid • Bind bile acids • No hypoglycemia • GI High
sequestrants • ↓ Hepatic glucose • Nonsystemic • Modest ↓ A1c
production • ↓ Post-prandial • Dosing frequency
glucose
Dopamine-2 • Activates DA receptor • ↓ CVD events
• No hypoglyemia • Modest ↓ A1c High
agonists • Modulates hypothalamic • ? ↓ CVD events • Dizziness/syncope
control of metabolism • Nausea
• ↑ insulin sensitivity • Fatigue
Table 1. Properties of anti-hyperglycemic agents Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
19. Class Mechanism Advantages Disadvantages Cost
Insulin • Activates insulin • Universally • Hypoglycemia Variable
receptor effective • Weight gain
• ↑ peripheral glucose • Unlimited efficacy • ? Mitogenicity
uptake • ↓ Microvascular • Injectable
risk • Training
requirements
• “Stigma”
Table 1. Properties of anti-hyperglycemic agents Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
20. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
3. ANTI-HYPERGLYCEMIC THERAPY
•Therapeutic options: Insulin
- Neutral protamine Hagedorn (NPH)
- Regular
- Basal analogues (glargine, detemir)
- Rapid analogues (lispro, aspart, glulisine)
- Pre-mixed varieties
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
21. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
3. ANTI-HYPERGLYCEMIC THERAPY
•Therapeutic options: Insulin
Rapid (Lispro, Aspart, Glulisine)
Insulin level
Short (Regular)
Intermediate (NPH)
Long (Detemir)
Long (Glargine)
0 2 4 6 8
Hours
10 12 14 16 18 20 22 24
Hours after injection
22. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
3. ANTI-HYPERGLYCEMIC THERAPY
•Implementation strategies:
-Initial therapy
-Advancing to dual combination therapy
-Advancing to triple combination therapy
-Transitions to & titrations of insulin
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
23. Diabetes Care, Diabetologia. 19 April 2012
T2DM Antihyperglycemic Therapy: General Recommendations [Epub ahead of print]
24. Diabetes Care, Diabetologia. 19 April 2012
T2DM Antihyperglycemic Therapy: General Recommendations [Epub ahead of print]
25. Diabetes Care, Diabetologia. 19 April 2012
T2DM Antihyperglycemic Therapy: General Recommendations [Epub ahead of print]
27. e n t i a l I n s u l i n S t r a t e g i e s i n T 2 D M Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
28. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
4. OTHER CONSIDERATIONS
•Age
•Weight
•Sex / racial / ethnic / genetic differences
•Comorbidities
-Coronary artery disease
-Heart Failure
-Chronic kidney disease
-Liver dysfunction
-Hypoglycemia
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
29. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
4. OTHER CONSIDERATIONS
•Age: Older adults
-Reduced life expectancy
-Higher CVD burden
-Reduced GFR
-At risk for adverse events from polypharmacy
-More likely to be compromised from hypoglycemia
Less ambitious targets
HbA1c <7.5–8.0% if tighter
targets not easily achieved
Focus on drug safety
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
30. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
4. OTHER CONSIDERATIONS
•Weight
-Majority of T2DM patients overweight / obese
-Intensive lifestyle program
-Metformin
-GLP-1 receptor agonists
-? Bariatric surgery
-Consider LADA in lean patients
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
31. Diabetes Care, Diabetologia. 19 April 2012
T2DM Anti-hyperglycemic Therapy: General Recommendations [Epub ahead of print]
32. Diabetes Care, Diabetologia. 19 April 2012
Adapted Recommendations: When Goal is to Avoid Weight Gain [Epub ahead of print]
33. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
4. OTHER CONSIDERATIONS
•Sex/ethnic/racial/genetic differences
-Little is known
-MODY & other monogenic forms of diabetes
-Latinos: more insulin resistance
-East Asians: more beta cell dysfunction
-Gender may drive concerns about adverse effects (e.g.,
bone loss from TZDs)
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
34. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
4. OTHER CONSIDERATIONS
•Comorbidities Metformin: CVD benefit (UKPDS)
-Coronary Disease Avoid hypoglycemia
-Heart Failure ? SUs & ischemic
preconditioning
-Renal disease
? Pioglitazone & ↓ CVD events
-Liver dysfunction ? Effects of incretin-based
-Hypoglycemia therapies
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
35. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
4. OTHER CONSIDERATIONS
•Comorbidities
-Coronary Disease Metformin: May use unless
-Heart Failure condition is unstable or severe
Avoid TZDs
-Renal disease
? Effects of incretin-based
-Liver dysfunction therapies
-Hypoglycemia
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
36. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
4. OTHER CONSIDERATIONS
•Comorbidities
-Coronary Disease
-Heart Failure Increased risk of hypoglycemia
-Renal disease Metformin & lactic acidosis
US: stop @SCr ≥ 1.5 (1.4
-Liver dysfunction
women)
-Hypoglycemia UK: ↓ dose @GFR <45 &
stop @GFR <30
Caution with SUs (esp. glyburide)
DPP-4-i’s – dose adjust for most
Avoid exenatide if GFR <30
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
37. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
4. OTHER CONSIDERATIONS
•Comorbidities
-Coronary Disease
-Heart Failure
-Renal disease
Most drugs not tested in
-Liver dysfunction advanced liver disease
-Hypoglycemia Pioglitazone may help steatosis
Insulin best option if disease
severe
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
38. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
4. OTHER CONSIDERATIONS
•Comorbidities
-Coronary Disease
-Heart Failure
-Renal disease
-Liver dysfunction
Emerging concerns regarding
-Hypoglycemia association with increased
mortality
Proper drug selection in the
hypoglycemia prone
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
39. Diabetes Care, Diabetologia. 19 April 2012
T2DM Anti-hyperglycemic Therapy: General Recommendations [Epub ahead of print]
40. Diabetes Care, Diabetologia. 19 April 2012
Adapted Recommendations: When Goal is to Avoid Hypoglycemia[Epub ahead of print]
41. Diabetes Care, Diabetologia. 19 April 2012
Adapted Recommendations: When Goal is to Minimize Costs [Epub ahead of print]
43. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
4. FUTURE DIRECTIONS / RESEARCH NEEDS
•Comparative effectiveness research
Focus on important clinical outcomes
•Contributions of genomic research
•Perpetual need for clinical judgment!
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
44. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
KEY POINTS
• Glycemic targets & BG-lowering therapies must be individualized.
• Diet, exercise, & education: foundation of any T2DM therapy
program
• Unless contraindicated, metformin = optimal 1st-line drug.
•After metformin, data are limited. Combination therapy with 1-2
other oral / injectable agents is reasonable; minimize side effects.
•Ultimately, many patients will require insulin therapy alone / in
combination with other agents to maintain BG control.
•All treatment decisions should be made in conjunction with the
patient (focus on preferences, needs & values.)
Diabetes Care, Diabetologia. 19 April 2012 [Epub ahead of print]
45. ADA-EASD Position Statement: Management of
Hyperglycemia in T2DM
Invited Reviewers
James Best, The University of Melbourne, AU Ilias Migdalis, NIMTS Hospital, Athens, Greece
Henk Bilo, Isala Clinics, Zwolle, NL Donna Miller, Univ of So California, LA, CA
John Boltri, Wayne State University, Detroit, MI Robert Ratner, MedStar/Georgetown Univ, DC
Thomas Buchanan, Univ of So California, LA, CA Julio Rosenstock, Dallas Diab/Endo Ctr, Dallas, TX
Paul Callaway, University of Kansas,Wichita, KS Guntram Schernthaner, Rudolfstiftung Hosp, Vienna, AT
Bernard Charbonnel, University of Nantes, France
Robert Sherwin, Yale University, New Haven, CT
Stephen Colagiuri, The University of Sydney, AS
Jay Skyler, University of Miami, Miami, FL
Samuel Dagogo-Jack, Univ of Tenn, Memphis, TN
Geralyn Spollett, Yale University,New Haven, CT
Margo Farber, Detroit Medical Center, Detroit, MI
Ellie Strock, Int’l Diabetes Center, Minneapolis, MN
Cynthia Fritschi, University of Illinois, Chicago, IL
Rowan Hillson, Hillingdon Hospital, Uxbridge, U.K. Agathocles Tsatsoulis, University of Ioannina, GR
Faramarz Ismail-Beigi, CWR Univ, Cleveland, OH Andrew Wolf, Univ of Virginia Charlottesville, VA
Devan Kansagara, Oregon H&S Univ, Portland, OR Bernard Zinman, University of Toronto, CA
Professional Practice Committee, American Diabetes Association
Panel for Overseeing Guidelines and Statements, European Association for the Study of Diabetes
American Association of Diabetes Educators
The Endocrine Society
Notas del editor
Changes in obesity and diabetes rates in the United States over a 15 year period.
Figures given are: number of people with diabetes in 2011 and predicted number of people that will have diabetes in 2030 according to IDF estimates. Percentage is the increase in diabetes from 2011 to 2030. “World” box acts as the legend. The burden of diabetes is one of the greatest challenges of the 21st century, as seen in the global incidence and projections of diabetes epidemic worldwide. 366 million people have diabetes in 2011 and this is predicted to rise to 552 million by 2030. Diabetes caused at least $465 billion in healthcare expenditure in 2011 – 11% of the total expenditure, and is expected to exceed $595 billion by 2030.
Overview of the microvascular, macrovascular and mortality outcomes from large T2DM and T1DM randomized clinical trials that focused on the relationship between glycemic control and complications.
Depiction of the elements of decision-making used to determine appropriate efforts to achieve glycaemic targets. Greater concerns about a particular domain are represented by increasing height of the ramp. Thus, characteristics/predicaments towards the left justify more stringent efforts to lower HbA1c, whereas those towards the right are compatible with less stringent efforts. Where possible, such decisions should be made in conjunction with the patient, reflecting his or her preferences, needs and values. This ‘scale’ is not designed to be applied rigidly but to be used as a broad construct to help guide clinical decisions. Adapted with permission from Ismail-Beigi et al [ref 20]
Diagrammatic representation of the approximate pharmacokinetic properties of various insulin formulations.
Moving from the top to the bottom of the figure, potential sequences of anti-hyperglycaemic therapy. In most patients, begin with lifestyle changes; metformin monotherapy is added at, or soon after, diagnosis (unless there are explicit contraindications).
If the A1c target is not achieved after ~3 months, consider one of the 5 treatment options combined with metformin (dual combination): a sulfonylurea, TZD, DPP-4 inhibitor, GLP-1 receptor agonist or basal insulin. Note that the order in the chart is determined by historical introduction andr oute of administration and is not meant to denote any specific preference. Choice is based on patient and drug characteristics, with the over-riding goal of improving glycemic control while minimizing side effects. Shared decision-making with the patient may help in the selection of therapeutic options. Rapid-acting secretagogues (meglitinides) may be used in place of sulfonylureas. Consider in patients with irregular meal schedules or who develop late postprandialhypoglycemia on sulfonylureas. Other drugs not shown (α-glucosidase inhibitors, colesevelam, dopamine agonists, pramlintide) may be used where available in selected patients but have modest efficacy and/or limiting side effects. In patients intolerant of, or with contraindications for, metformin, select initial drug from other classes depicted, and proceed accordingly. Consider starting with 2-drug combinations in patients with very high HbA1c (e.g. ≥9%).
Further progression to 3-drug combinations are reasonable if 2-drug combinations do not achieve target. If metformin contraindicated or not tolerated, while published trials are generally lacking, it is reasonable to consider 3-drug combinations other than metformin. Insulin is likely to be more effective than most other agents as a third-line therapy, especially when HbA1c is very high (e.g. ≥9.0%). The therapeutic regimen should include some basal insulin before moving to more complex insulin strategies (see Fig. 3)
Ultimately, more intensive insulin regimens may be required (see Figure 3.) Dashed arrow line on the left-hand side of the figure denotes the option of a more rapid progression from a 2-drug combination directly to multiple daily insulin doses, in those patients with severe hyperglycaemia (e.g. HbA1c ≥10.0-12.0%). Consider beginning with insulin if patient presents with severe hyperglycemia (≥300-350 mg/dl [≥16.7-19.4 mmol/l]; HbA1c ≥10.0-12.0%) with or without catabolic features (weight loss, ketosis, etc).
Basal insulin alone is usually the optimal initial regimen, beginning at 0.1-0.2 U/kg body weight, depending on the degree of hyperglycemia. It is usually prescribed in conjunction with 1-2 non-insulin agents. In patients willing to take >1 injection and who have higher A1c levels (≥9.0%), BID pre-mixed insulin or a more advanced basal plus mealtime insulin regimen could also be considered (curved dashed arrow lines). When basal insulin has been titrated to an acceptable FPG but A1c remains above target, consider proceeding to basal + meal-time insulin, consisting of 1-3 injections of rapid-acting analogues. A less studied alternative—progression from basal insulin to a twice daily pre-mixed insulin—could be also considered (straight dashed arrow line); if this is unsuccessful, move to basal + mealtime insulin. The figure describes the number of injections required at each stage, together with the relative complexity and flexibility. Once a strategy is initiated, titration of the insulin dose is important, with dose adjustments made based on the prevailing BG levels as reported by the patient. Non-insulin agents may be continued, although insulin secretagogues (sulfonylureas, meglitinides) are typically stopped once more complex regimens beyond basal insulin are utilized. Comprehensive education regarding self-monitoring of BG, diet, exercise, and the avoidance of, and response to, hypoglycemia are critical in any patient on insulin therapy.
Overview of anti-hyperglycemic therapy in T2DM (Figure 2.) What follows are variations of this figure to help guide the clinician in choosing agents which may be most appropriate under certain situations: to avoid weight gain, to avoid hypoglycemia, and to minimize costs.
Fig. 2A should be considered when the goal is to avoid hypoglycemia. Note that &quot;hidden&quot; agents may obviously still be used when required, but additional care is needed to avoid adverse events. Here, the risk of hypoglycemia when using the hidden agents will be, in part, dependent on the baseline degree of hyperglycemia, the treatment target, and the adequacy of patient education.
Overview of anti-hyperglycemic therapy in T2DM (Figure 2.) What follows are variations of this figure to help guide the clinician in choosing agents which may be most appropriate under certain situations: to avoid weight gain, to avoid hypoglycemia, and to minimize costs.
Fig. 2B should be considered when the goal is to avoid weight gain. Note that &quot;hidden&quot; agents may obviously still be used when required, but additional care is needed to avoid adverse events. Here, the chances of weight gain when using the hidden agents will be mitigated by more rigorous adherence to dietary recommendations and optimal dosing.
Fig. 2C should be considered when the goal is to minimize costs. This reflects prevailing costs in the North America and Europe in early 2012; costs of certain drugs may vary considerably from country to country and as generic formulations become available.
Avoiding ‘glucocentricity’ is key in the comprehensive management of the patient with T2DM. Cardiovascular risk factor reduction must incorporate blood pressure and lipid control, in addition to, where indicated, anti-platelet therapy.