Ada 2012
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ACTUALIZACION ADA 2012. NORMAS DE LA ATENCION AL DIABETICO. DR. JUSTO VENEREO.
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Ada 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) Diabetes Care 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 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 1. 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 2012;35:1364– 1379
- 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 2012;35:1364– 1379
- 5. ADA-EASD Position Statement: Management of Hyperglycemia in T2DM 1. 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 lie with the patient. Diabetes Care 2012;35:1364– 1379
- 6. ADA-EASD Position Statement: Management of Hyperglycemia in T2DM 2. BACKGROUND • Epidemiology and health care impact Diabetes Care 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 7. Age-adjusted Percentage of U.S. Adults with Obesity or Diagnosed Diabetes Obesity (BMI ≥30 kg/m2) O 1994 2000 2009 B E S I T Y No Data <14.0% 14.0-17.9% 18.0-21.9% 22.0-25.9% >26.0% Diabetes D 1994 2000 2009 I A B E T E S No Data <4.5% 4.5-5.9% 6.0-7.4% 7.5-8.9% >9.0% CDC’s Division of Diabetes Translation. National Diabetes Surveillance System available at http://www.cdc.gov/diabetes/statistics
- 8. The Diabetes Epidemic: Global Projections, 2010–2030 IDF. Diabetes Atlas 5th Ed. 2011
- 9. ADA-EASD Position Statement: Management of Hyperglycemia in T2DM 2. BACKGROUND • Relationship of glycemic control to outcomes Diabetes Care 2012;35:1364– 1379
- 10. Impact of Intensive Therapy for Diabetes: Summary of Major Clinical Trials Study Microvasc CVD Mortality UKPDS DCCT / EDIC* ACCORD ADVANCE VADT Kendall DM, Bergenstal RM. © International Diabetes Center 2009 Initial Trial UK Prospective Diabetes Study (UKPDS) Group. Lancet 1998;352:854. Holman RR et al. N Engl J Med. 2008;359:1577. DCCT Research Group. N Engl J Med 1993;329;977. Long Term Follow-up Nathan DM et al. N Engl J Med. 2005;353:2643. Gerstein HC et al. N Engl J Med. 2008;358:2545. Patel A et al. N Engl J Med 2008;358:2560. Duckworth W et al. N Engl J Med 2009;360:129. (erratum: Moritz T. N Engl J Med 2009;361:1024) * in T1DM
- 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 2012;35:1364– 1379
- 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 Medici
- 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 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 14. Diabetes Care 2012;35:1364–1379 Figure 1 Diabetologia 2012;55:1577–1596 (Adapted with permission from: Ismail-Beigi 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 Diabetes Care 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 16. ADA-EASD Position Statement: Management of Hyperglycemia in T2DM 3. ANTI-HYPERGLYCEMIC THERAPY • Therapeutic options: Oral agents & non-insulin injectables - Metformin - Meglitinides - Sulfonylureas - Thiazolidinediones - a-glucosidase inhibitors - DPP-4 inhibitors - Bile acid sequestrants - GLP-1 receptor agonists - Dopamine-2 agonists - Amylin mimetics Diabetes Care 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 17. Class Mechanism Advantages Disadvantages Cost Biguanides • Activates AMP- • Extensive experience • Gastrointestinal Low (Metformin kinase • No hypoglycemia • Lactic acidosis ) • Hepatic glucose • Weight neutral • B-12 deficiency production • ? CVD events • Contraindications SUs / • Closes KATP • Extensive experience • Hypoglycemia Low Meglitinide channels • Microvascular risk • Weight gain s • Insulin secretion • Low durability • ? Ischemic preconditioning TZDs • Activates PPAR-g • No hypoglycemia • Weight gain High • Insulin sensitivity • Durability • Edema / heart • TGs, HDL-C failure • ? CVD events (pio) • Bone fractures • ? MI (rosi) • ? Bladder ca (pio) a-GIs • Inhibits a- • No hypoglycemia • Gastrointestinal Mod. glucosidase • Nonsystemic • Dosing frequency • Slows carbohydrate • Post-prandial • Modest A1c absorption glucose • ? CVD events Diabetes Care 2012;35:1364–1379 Table 1. Properties of anti-hyperglycemic agents Diabetologia 2012;55:1577–1596
- 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 • Weight loss • GI High receptor receptor • No hypoglycemia • ? Pancreatitis agonists • Insulin, glucagon • ? Beta cell mass • Medullary ca • gastric emptying • ? CV protection • Injectable • satiety Amylin • Activates amylin • Weight loss • GI High mimetics receptor • Post-prandial • Modest A1c • glucagon glucose • Injectable • gastric emptying • Hypo w/ insulin • satiety • Dosing frequency Bile acid • Binds bile acids • No hypoglycemia • GI High sequestrant • Hepatic glucose • Nonsystemic • Modest A1c s production • LDL-C • TGs • Dosing frequency Dopamine-2 • Activates DA receptor • No hypoglycemia • Modest A1c High agonists • Modulates • ? CVD events • Diabetes Care 2012;35:1364–1379 Table 1. Properties of anti-hyperglycemic agents Diabetologia 2012;55:1577–1596
- 19. Class Mechanism Advantages Disadvantages Cost Insulin • Activates insulin • Universally • Hypoglycemia Variable receptor effective • Weight gain • Glucose disposal • Unlimited efficacy • ? Mitogenicity • Hepatic glucose • Microvascular • Injectable production risk • Training requirements • “Stigma” Diabetes Care 2012;35:1364–1379 Table 1. Properties of anti-hyperglycemic agents Diabetologia 2012;55:1577–1596
- 20. ADA-EASD Position Statement: Management of Hyperglycemia in T2DM 3. ANTI-HYPERGLYCEMIC THERAPY • Therapeutic options: Insulin - Human Neutral protamine Hagedorn (NPH) - Human Regular - Basal analogues (glargine, detemir) - Rapid analogues (lispro, aspart, glulisine) - Pre-mixed varieties Diabetes Care 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 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 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 23. Fig. 2. T2DM Antihyperglycemic Therapy: General Recommendations Care 2012;35:1364–1379 Diabetes Diabetologia 2012;55:1577–1596
- 24. Fig. 2. T2DM Antihyperglycemic Therapy: General Recommendations Care 2012;35:1364–1379 Diabetes Diabetologia 2012;55:1577–1596
- 25. Fig. 2. T2DM Antihyperglycemic Therapy: General Recommendations Care 2012;35:1364–1379 Diabetes Diabetologia 2012;55:1577–1596
- 26. Diabetes Care 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 27. Diabetes Care 2012;35:1364–1379 Fig. 3. Sequential Insulin Strategies in T2DM Diabetologia 2012;55:1577–1596
- 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 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 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 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 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 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 31. Diabetes Care 2012;35:1364–1379 T2DM Anti-hyperglycemic Therapy: General Recommendations Diabetologia 2012;55:1577–1596
- 32. Adapted Recommendations: When Goal is to Avoid Weight Gain Diabetes Care 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 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 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 34. ADA-EASD Position Statement: Management of Hyperglycemia in T2DM 4. OTHER CONSIDERATIONS • Comorbidities Metformin: CVD benefit - Coronary Disease (UKPDS) - Heart Failure Avoid hypoglycemia ? SUs & ischemic - Renal disease preconditioning - Liver dysfunction ? Pioglitazone & CVD events - Hypoglycemia ? Effects of incretin-based therapies Diabetes Care 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 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 - Renal disease Avoid TZDs - Liver dysfunction ? Effects of incretin-based - Hypoglycemia therapies Diabetes Care 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 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: half-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 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 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 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 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 morbidity / mortality Proper drug selection is key in the hypoglycemia prone Diabetes Care 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 39. Diabetes Care 2012;35:1364–1379 T2DM Anti-hyperglycemic Therapy: General Recommendations Diabetologia 2012;55:1577–1596
- 40. Diabetes Care 2012;35:1364–1379 Adapted Recommendations: When Goal is to Avoid Hypoglycemia Diabetologia 2012;55:1577–1596
- 41. Diabetes Care 2012;35:1364–1379 Adapted Recommendations: When Goal is to Minimize Costs Diabetologia 2012;55:1577–1596
- 42. Guidelines for Glucose, BP, & Lipid Control American Diabetes Assoc. Goals HbA1C < 7.0% (individualization) Preprandial 70-130 mg/dL (3.9-7.2 mmol/l) glucose Postprandial < 180 mg/dL glucose Blood pressure < 130/80 mmHg LDL: < 100 mg/dL (2.59 mmol/l) < 70 mg/dL (1.81 mmol/l) (with overt CVD) Lipids HDL: > 40 mg/dL (1.04 mmol/l) > 50 mg/dL (1.30 mmol/l) TG: < 150 mg/dL (1.69 mmol/l) HDL = high-density lipoprotein; LDL = low-density lipoprotein; PG = plasma glucose; TG = triglycerides. ADA. Diabetes Care 2012;35:S11–S63
- 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 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 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.) • Comprehensive CV risk reduction - a major focus of therapy. Diabetes Care 2012;35:1364–1379 Diabetologia 2012;55:1577–1596
- 45. ADA-EASD Position Statement: Management of Hyperglycemia in T2DM Invited Reviewers James Best, The University of Melbourne, Australia Migdalis, NIMTS Hospital, Athens, Greece Ilias Henk Bilo, Isala Clinics, Zwolle, Netherlands 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 Bernard Charbonnel, University of Nantes, France Robert Sherwin, Yale University, New Haven, CT Stephen Colagiuri, The University of Sydney, Australia 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, Greec Andrew Wolf, Univ of Virginia Charlottesville, VA Faramarz Ismail-Beigi, CWR Univ, Cleveland, OH Bernard Zinman, University of Toronto, Ontario, Can Devan Kansagara, Oregon H&S Univ, Portland, OR 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 do Editor
- 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.
- 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 "hidden" 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 "hidden" 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.