MANEJO ACTUAL DE LA DIABETES MELLITUS

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EL DR MENDOZA HACE UNA DISERTACION MAGISTRAL SOBRE EL MANEJO ACTUAL DE LA DIABETES Y LA FISIOLOGIA DE LAS INCRETINAS.

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  • Good afternoon. It's my pleasure to share with you the overall messages and key findings of this new WHO global report: Preventing chronic diseases: a vital investment. Several misunderstandings about chronic diseases have contributed to their global neglect. This report dispels these misunderstandings with the strongest evidence and proposes a way forward for stopping the rising global epidemic.
  • MANEJO ACTUAL DE LA DIABETES MELLITUS

    1. 1. www.who.int/chp
    2. 2. January 18, 2007 Expanding Priorities—Confronting Chronic Disease in Countries with Low Income Gerard Anderson and Edward Chu argue that international health organizations need to greatly expand their efforts to prevent and treat noncommunicable chronic diseases.
    3. 3. January 18, 2007 Obesity and Diabetes in the Developing World — A Growing Challenge Propelling an upsurge in cases of diabetes and hypertension is the growing prevalence of overweight and obesity. Drs. Parvez Hossain, Bisher Kawar, and Meguid El Nahas write that preventing obesity, diabetes, and hypertension will require fundamental social and political changes.
    4. 4. 8
    5. 5. 07/15/2010 Dr. Enrique Mendoza
    6. 6. 07/15/2010 Dr. Enrique Mendoza
    7. 7. Figure 1—Disorders of glycemia: etiologic types and stages. ∗Even after presenting in ketoacidosis, these patients can briefly return to normoglycemia without requiring continuous therapy (i.e., ―honeymoon‖ remission); ∗∗in rare instances, patients in these categories (e.g., Vacor toxicity, type 1 diabetes presenting in pregnancy) may require insulin for survival.
    8. 8. DCCT Intensive Insulin Treatment in Type 1 Diabetes 11 10 Conventional therapy Median HbA1c (%) 9 8 7 Intensive therapy 6 Normal range 5 0 1 2 3 4 5 6 7 8 9 10 Study Year The Diabetes Control and Complications Trial Research Group. N Engl J Med. 1993;329:977-986, with permission. 07/15/2010 Medical Age Publishing, Division of Snyder Healthcare Communications Worldwide, Stamford, Connecticut. All rights reserved. ©1999, Dr. Enrique Mendoza
    9. 9. DCCT Microvascular Risk Reduction With Intensive Treatment Reduction in Complication Relative Risk Retinopathy 63% Nephropathy 54% Neuropathy 60% Data from the Diabetes Control and Complications Trial Research Group. N Engl J Med. 1993;329:977-986. 07/15/2010 Medical Age Publishing, Division of Snyder Healthcare Communications Worldwide, Stamford, Connecticut. All rights reserved. ©1999, Dr. Enrique Mendoza
    10. 10. DCCT Relationship of HbA1c to Risk of Microvascular Complications 15 Retinopathy 13 Nephropathy Neuropathy 11 Microalbuminuria Relative Risk 9 7 5 3 1 6 7 8 9 10 11 12 HbA1c (%) Skyler. Endocrinol Metab Clin. 1996;25:243-254, with permission. 07/15/2010 Medical Age Publishing, Division of Snyder Healthcare Communications Worldwide, Stamford, Connecticut. All rights reserved. ©1999, Dr. Enrique Mendoza
    11. 11. UKPDS Blood Glucose Control Study: Aims • To determine whether improved glycemic control will prevent clinical complications • To determine whether treatment with a sulfonylurea, insulin, or metformin has specific advantages or disadvantages Adapted from UK Prospective Diabetes Study (UKPDS) Group. Lancet. 1998;352:837-853. 07/15/2010 Medical Age Publishing, Division of Snyder Healthcare Communications Worldwide, Stamford, Connecticut. All rights reserved. ©1999, Dr. Enrique Mendoza
    12. 12. UKPDS Effect of Treatment on HbA1c 9 Conventional (10-y cohort) Intensive (10-y cohort) Median HbA1c (%) 8 ADA action Conventional (all patients) Intensive 7 (all patients) ADA goal 6 6.2% upper limit of normal range 0 0 3 6 9 12 15 Time From Randomization (y) Adapted from UK Prospective Diabetes Study (UKPDS) Group. Lancet. 1998;352:837-853, with permission. 07/15/2010 Medical Age Publishing, Division of Snyder Healthcare Communications Worldwide, Stamford, Connecticut. All rights reserved. ©1999, Dr. Enrique Mendoza
    13. 13. UKPDS Risk Reduction of Microvascular Complications 30 Conventional Intensive % of Patients With an Event Intensive policy group 20 25% overall risk reduction P =.0099 10 0 0 3 6 9 12 15 Time From Randomization (y) UK Prospective Diabetes Study (UKPDS) Group. Lancet. 1998;352:837-853, with permission. 07/15/2010 Medical Age Publishing, Division of Snyder Healthcare Communications Worldwide, Stamford, Connecticut. All rights reserved. ©1999, Dr. Enrique Mendoza
    14. 14. 07/15/2010 Dr. Enrique Mendoza
    15. 15. Volume 359:1577-1589 October 9, 2008 Number 15 10-Year Follow-up of Intensive Glucose Control in Type 2 Diabetes Rury R. Holman, F.R.C.P., Sanjoy K. Paul, Ph.D., M. Angelyn Bethel, M.D., David R. Matthews, F.R.C.P., and H. Andrew W. Neil, F.R.C.P.
    16. 16. Volume 359:1577-1589 October 9, 2008 Number 15 10-Year Follow-up of Intensive Glucose Control in Type 2 Diabetes Rury R. Holman, F.R.C.P., Sanjoy K. Paul, Ph.D., M. Angelyn Bethel, M.D., David R. Matthews, F.R.C.P., and H. Andrew W. Neil, F.R.C.P.
    17. 17. Background During the United Kingdom Prospective Diabetes Study (UKPDS), patients with type 2 diabetes mellitus who received intensive glucose therapy had a lower risk of microvascular complications than did those receiving conventional dietary therapy. We conducted post-trial monitoring to determine whether this improved glucose control persisted and whether such therapy had a long-term effect on macrovascular outcomes.
    18. 18. Methods Of 5102 patients with newly diagnosed type 2 diabetes, 4209 were randomly assigned to receive either conventional therapy (dietary restriction) or intensive therapy (either sulfonylurea or insulin or, in overweight patients, metformin) for glucose control. In post-trial monitoring, 3277 patients were asked to attend annual UKPDS clinics for 5 years, but no attempts were made to maintain their previously assigned therapies. Annual questionnaires were used to follow patients who were unable to attend the clinics, and all patients in years 6 to 10 were assessed through questionnaires. We examined seven prespecified aggregate clinical outcomes from the UKPDS on an intention-to-treat basis, according to previous randomization categories.
    19. 19. Results Between-group differences in glycated hemoglobin levels were lost after the first year. In the sulfonylurea–insulin group, relative reductions in risk persisted at 10 years for any diabetes-related end point (9%, P=0.04) and microvascular disease (24%, P=0.001), and risk reductions for myocardial infarction (15%, P=0.01) and death from any cause (13%, P=0.007) emerged over time, as more events occurred. In the metformin group, significant risk reductions persisted for any diabetes-related end point (21%, P=0.01), myocardial infarction (33%, P=0.005), and death from any cause (27%, P=0.002).
    20. 20. Conclusions Despite an early loss of glycemic differences, a continued reduction in microvascular risk and emergent risk reductions for myocardial infarction and death from any cause were observed during 10 years of post-trial follow-up. A continued benefit after metformin therapy was evident among overweight patients. (UKPDS 80; Current Controlled Trials number, ISRCTN75451837
    21. 21. Volume 359:1618-1620 October 9, 2008 Number 15 UKPDS and the Legacy Effect John Chalmers, M.D., Ph.D., and Mark E. Cooper, M.D., Ph.D.
    22. 22. The United Kingdom Prospective Diabetes Study (UKPDS) continues to produce important evidence concerning the evolution of type 2 diabetes and its management. Two studies published in this issue of the Journal provide some answers to two questions of fundamental importance to patients with diabetes and to physicians alike. In one article, Holman et al. (UKPDS 80)1 provide data that confirm a so-called legacy effect associated with intensive glucose control in patients with type 2 diabetes, long after the cessation of randomized intervention. This finding provides a fitting parallel to the observations of the Diabetes Control and Complications Trial/Epidemiology of Diabetes…
    23. 23. Volume 358:580-591 February 7, 2008 Number 6 Effect of a Multifactorial Intervention on Mortality in Type 2 Diabetes Peter Gæde, M.D., D.M.Sc., Henrik Lund-Andersen, M.D., D.M.Sc., Hans-Henrik Parving, M.D., D.M.Sc., and Oluf Pedersen, M.D., D.M.Sc.
    24. 24. Background Intensified multifactorial intervention — with tight glucose regulation and the use of renin–angiotensin system blockers, aspirin, and lipid-lowering agents — has been shown to reduce the risk of nonfatal cardiovascular disease among patients with type 2 diabetes mellitus and microalbuminuria. We evaluated whether this approach would have an effect on the rates of death from any cause and from cardiovascular causes
    25. 25. Methods In the Steno-2 Study, we randomly assigned 160 patients with type 2 diabetes and persistent microalbuminuria to receive either intensive therapy or conventional therapy; the mean treatment period was 7.8 years. Patients were subsequently followed observationally for a mean of 5.5 years, until December 31, 2006. The primary end point at 13.3 years of follow-up was the time to death from any cause.
    26. 26. Results Twenty-four patients in the intensive-therapy group died, as compared with 40 in the conventional-therapy group (hazard ratio, 0.54; 95% confidence interval [CI], 0.32 to 0.89; P=0.02). Intensive therapy was associated with a lower risk of death from cardiovascular causes (hazard ratio, 0.43; 95% CI, 0.19 to 0.94; P=0.04) and of cardiovascular events (hazard ratio, 0.41; 95% CI, 0.25 to 0.67; P<0.001). One patient in the intensive-therapy group had progression to end-stage renal disease, as compared with six patients in the conventional-therapy group (P=0.04). Fewer patients in the intensive-therapy group required retinal photocoagulation (relative risk, 0.45; 95% CI, 0.23 to 0.86; P=0.02). Few major side effects were reported.
    27. 27. Conclusions In at-risk patients with type 2 diabetes, intensive intervention with multiple drug combinations and behavior modification had sustained beneficial effects with respect to vascular complications and on rates of death from any cause and from cardiovascular causes.
    28. 28. Treatment Options
    29. 29. Lifestyle interventions The major environmental factors that increase the risk of type 2 diabetes are overnutrition and a sedentary lifestyle, with consequent overweight and obesity (39,40). Not surprisingly, interventions that reverse or improve these factors have been demonstrated to have a beneficial effect on control of glycemia in established type 2 diabetes (41). Unfortunately, the high rate of weight regain has limited the role of lifestyle interventions as an effective means of controlling glycemia in the long term. The most convincing long-term data indicating that weight loss effectively lowers glycemia have been generated in the follow-up of type 2 diabetic patients who have had bariatric surgery. In this setting, with a mean sustained weight loss of 20 kg, diabetes is virtually eliminated (42– 45).
    30. 30. FACTORES DE RIESGO
    31. 31. Pharmacological agents
    32. 32. The consensus report concluded that ―Although still limited, early evidence suggests that metformin is associated with a lower risk of cancer and that
    33. 33. exogenous insulin is associated with an increased cancer risk. Further research is needed to clarify these issues and evaluate if insulin glargine is more strongly associated with cancer risk compared with other insulins.‖
    34. 34. Emerging evidence suggests that metformin has a range of biological mechanisms that reduce tumour growth beyond its ability to increase insulin sensitivity. The enhanced binding of insulin glargine to IGF-I receptors is a theoretical concern, but might not translate to an actual increase in cancer risk.
    35. 35. Summary The guidelines and treatment algorithm presented here emphasize the following: ● Achievement and maintenance of near normoglycaemia (A1C 7.0%) ● Initial therapy with lifestyle intervention and metformin ● Rapid addition of medications, and transition to new regimens, when target glycemic goals are not achieved or sustained ● Early addition of insulin therapy in patients who do not meet target goals
    36. 36. A1C 6.5 – 7.5%** A1C 7.6 – 9.0% A1C > 9.0% Drug Naive Under Treatment Symptoms No Symptoms Monotherapy Dual Therapy 8 MET † DPP4 1 GLP-1 TZD 2 AGI 3 GLP-1 or DPP4 1 GLP-1 or TZD 2 INSULIN or DPP4 1 SU 7 INSULIN 2 - 3 Mos.*** MET + Other MET + TZD 2 Other SU or Glinide 4,5 Agent(s) 6 Agent(s) 6 Dual Therapy GLP-1 TZD 2 GLP-1 or DPP4 1 2 - 3 Mos.*** or DPP4 1 MET + TZD 2 Triple Therapy 9 * May not be appropriate for all patients Glinide or SU 5 ** For patients with diabetes and A1C < 6.5%, GLP-1 pharmacologic Rx may be considered + TZD 2 TZD + GLP-1 or DPP4 1 or DPP4 1 *** If A1C goal not achieved safely † Preferred initial agent Colesevelam MET + 1 DPP4 if  PPG and  FPG or GLP-1 if  PPG MET + GLP-1 AACE/ACE Algorithm for Glycemic 3 or DPP4 1 Control Committee 2 TZD if metabolic syndrome and/or AGI + SU 7 *** Cochairpersons: nonalcoholic fatty liver disease (NAFLD) 2 - 3 Mos. TZD 2 Helena W. Rodbard, MD, FACP, MACE 3 AGI if  PPG Paul S. Jellinger, MD, MACE Triple Therapy 4 Glinide if  PPG or SU if  FPG 2 - 3 Mos.*** Zachary T. Bloomgarden, MD, FACE Jaime A. Davidson, MD, FACP, MACE 5 Low-dose secretagogue recommended TZD 2 Daniel Einhorn, MD, FACP, FACE 6 a) Discontinue insulin secretagogue MET + with multidose insulin Alan J. Garber, MD, PhD, FACE b) Can use pramlintide with prandial insulin GLP-1 or + James R. Gavin III, MD, PhD 7 Decrease secretagogue by 50% when added DPP4 1 Glinide or SU 4,7 INSULIN George Grunberger, MD, FACP, FACE to GLP-1 or DPP-4 *** Yehuda Handelsman, MD, FACP, FACE 2 - 3 Mos. Other Edward S. Horton, MD, FACE 8 If A1C < 8.5%, combination Rx with agents Agent(s) 6 Harold Lebovitz, MD, FACE that cause hypoglycemia should be used Philip Levy, MD, MACE with caution INSULIN Etie S. Moghissi, MD, FACP, FACE 9 If A1C > 8.5%, in patients on Dual Therapy, Stanley S. Schwartz, MD, FACE insulin should be considered Other Agent(s) 6 Available at www.aace.com/pub © AACE December 2009 Update. May not be reproduced in any form without express written permission from AACE
    37. 37. LIFESTYLE MODIFICATION AACE/ACE DIABETES ALGORITHM A1C 6.5 – 7.5%** FOR GLYCEMIC CONTROL Monotherapy MET † DPP4 1 GLP-1 TZD 2 AGI 3 2 - 3 Mos.*** Dual Therapy GLP-1 or DPP4 1 MET + TZD 2 Glinide or SU 5 TZD + GLP-1 or DPP4 1 Colesevelam *** If A1C goal not achieved safely MET + 3 † Preferred initial agent AGI 1 DPP4 if  PPG and  FPG or GLP-1 *** if  PPG 2 - 3 Mos. 2 TZD if metabolic syndrome and/or Triple Therapy nonalcoholic fatty liver disease (NAFLD) 3 AGI if  PPG TZD 2 MET + 4 Glinide if  PPG or SU if  FPG GLP-1 or + 5 Low-dose secretagogue Glinide or SU 4,7 recommended DPP4 1 6 a) Discontinue insulin 2 - 3 Mos.*** secretagogue with multidose insulin b) Can use pramlintide with INSULIN prandial insulin 7 Decrease secretagogue by 50% Other when added to GLP-1 or DPP-4 Agent(s) 6 Available at www.aace.com/pub © AACE December 2009 Update. May not be reproduced in any form without express written permission from AACE
    38. 38. LIFESTYLE MODIFICATION AACE/ACE DIABETES ALGORITHM A1C 7.6 – 9.0% FOR GLYCEMIC CONTROL Dual Therapy 8 GLP-1 or DPP4 1 MET + or TZD 2 SU or Glinide 4,5 2 - 3 Mos.*** *** If A1C goal not achieved safely Triple Therapy 9 † Preferred initial agent 1 DPP4 if  PPG and  FPG or GLP-1 GLP-1 if  PPG + TZD 2 2 TZD if metabolic syndrome and/or or DPP4 1 nonalcoholic fatty liver disease MET + GLP-1 (NAFLD) 4 Glinide if  PPG or SU if  FPG or DPP4 1 + SU 7 5 Low-dose secretagogue TZD 2 recommended 6 a) Discontinue insulin *** secretagogue with multidose 2 - 3 Mos. insulin b) Can use pramlintide with prandial insulin 7 Decrease secretagogue by 50% INSULIN when added to GLP-1 or DPP-4 8 If A1C < 8.5%, combination Rx with Other agents that cause hypoglycemia Agent(s) 6 should be used with caution 9 If A1C > 8.5%, in patients on Dual Therapy, insulin should be considered Available at www.aace.com/pub © AACE December 2009 Update. May not be reproduced in any form without express written permission from AACE
    39. 39. LIFESTYLE MODIFICATION AACE/ACE DIABETES ALGORITHM A1C > 9.0% FOR GLYCEMIC CONTROL Drug Naive Under Treatment Symptoms No Symptoms GLP-1 or DPP4 1 INSULIN SU 7 INSULIN Other MET + TZD 2 Other Agent(s) 6 Agent(s) 6 GLP-1 or DPP4 1 TZD 2 1 DPP4 if  PPG and  FPG or GLP-1 if  PPG 2 TZD if metabolic syndrome and/or nonalcoholic fatty liver disease (NAFLD) 6 a) Discontinue insulin secretagogue with multidose insulin b) Can use pramlintide with prandial insulin 7 Decrease secretagogue by 50% when added to GLP-1 or DPP-4 Available at www.aace.com/pub © AACE December 2009 Update. May not be reproduced in any form without express written permission from AACE
    40. 40. Rosiglitazone and IHD Risk
    41. 41. Pioglitazone and IHD Risk
    42. 42. Pioglitazone vs Rosiglitazone and IHD Risk
    43. 43. Thiazolidinediones and Heart Failure Risk
    44. 44. Recommendations to Reduce Vascular Disease in Patients with Type 2 Diabetes Mellitus

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