Insulin Initiation : When We should Start with Basal Insulin?
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Insulin Initiation : When We should Start with Basal Insulin? Dr. Agus Taolin , SpPD, FINASIM | PAPDI CABANG BOGOR Disampaikan pada acara PIT VI IDI Kota Bogor | 9 Nopember 2013
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Insulin Initiation : When We should Start with Basal Insulin?
- 1. Insulin Initiation : When We should Start with Basal Insulin? Dr. Agus Taolin , SpPD, FINASIM PAPDI CABANG BOGOR PIT IDI Bogor 10 November 2013
- 2. Diabetes is a global disease Estimated global prevalence of diabetes 171 million1 2000 1. 2. 366 million2 2011 2010 Wild. Diabetes Care. 2004. 27:1047-1053. International Diabetes Federation. IDF Diabetes Atlas. Fifth Edition. 2011 552 million2 2030
- 4. DM PREVALENCE BY PROVINCES IN INDONESIA
- 5. Diabetes in Indonesia Laurentia Litbangkes 2008
- 6. Diabetes is a progressive disease ⢠Type 2 diabetes (T2DM) progression is characterised by decline in beta-cell function and worsening insulin resistance1 ⢠Getting to, or maintaining, target HbA1c levels in T2DM requires intensified treatment over time2 1. 2. Fonseca VA. Br J Diab Vasc Dis 2008;8:S3 Nathan DM, et al. Diabetes Care 2009;32:193-203
- 7. 7 papdi.bogor@ya hoo.com Loss of beta cell Pancreas Apoptosis induced by leptin, Autoimmu ne responses Apoptosis by: Sulfonylure as Glucocortic oids Glucotoxi city Oxidative stress Proinflam matory cytokines Loss beta cell Lipotoxicit y: FFA, LDL-C and low HDL-C Wajchenberg BL. Et al.. Endocr. Rev. 28, 187-218 (2007)
- 8. 8 papdi.bogor@ya hoo.com Progressive Loss of β-cell Function in T2DM
- 9. T2DM: Progressive loss of insulin secretion with increasing insulin resistance1 Impaired glucose tolerance Undiagnosed diabetes Known diabetes Insulin resistance Insulin secretion Postprandial glucose Fasting glucose Microvascular complications Macrovascular complications 1. Adapted from: Ramlo-Halsted BA, Edelman SV. Clincial Diabetes 2000;18(2): http://journal.diabetes.org/clinicaldiabetes/v18n22000/pg80.htm
- 10. 10 papdi.bogor@ya hoo.com Modalities in Diabetes Management Diet Management Physical Activity Oral Anti Diabetic Diabetic Patients And or Insulin Injection Education ADA Consensus statement,2010
- 11. New position statement of the ADA and EASD on management of hyperglycemia in type 2 diabetes Basal Insulin Inzucci SE, et al. Diabetologia. 2012 Slide no 11
- 12. Algoritme Pengelolaan DM Tipe 2 Tanpa Disertai Dekompensasi DM Tahap I GHS GHS + Monoterapi Catatan 1. Dinyatakan gagal bila dengan terapi 2-3 bulan tidak mencapai target HbA1c <7% 2. Bila tidak ada pemeriksaan HbA1c dapat digunakan pemeriksaan glukosa darah. Ratarata glukosa darah sehari dikonversikan ke HbA1c menurut kriteria ADA 2010 Jalur alternatif jika tidak terdapat insulin, menolak dan target glukosa belum optimal Tahap II GHS + Kombinasi 2 OHO GHS + Kombinasi 2 OHO + Basal Insulin GHS + Kombinasi 3 OHO Tahap III Insulin Intensif 12 Konsensus Pengelolaan dan pencegahan Diabetus Melitus, PB Perkeni, 2011
- 13. Evolving Treatment Paradigm in T2DM : Delayed Insulin Therapy - 10 Years from Diagnosis 0 -5 +5 +10 13 +15 Amylin ( pramlintide ) Insulin GLP-1 Analogues and DPP-IV inhibitor Oral combination Oral monotherapy Diet management + exercise Pre-diabetes Type 2 Diabetes Joslin Diabetes Centre
- 14. 14 papdi.bogor@ya hoo.com Study to evaluation how many patients move to next step of therapy when A1c > 8 % ⢠Sulfonilurea âŚâŚ..âŚâŚâŚ 35 % ad second drug ⢠Metformin âŚâŚâŚâŚâŚ... 44 % ad other therapy ⢠2 drugs OAD âŚâŚâŚâŚâŚ.. 18 % ( because the next step is insulin ) ⢠Spent 5 years duration before decided to give the next therapy Keiser Permante Group California
- 15. 15 papdi.bogor@ya hoo.com ⢠Most patients with type 2 diabetes require insulin therapy when OAD provide suboptimal glycemic control ⢠Long-term glycemic improvement reduces the risks of vascular complications. ⢠Different insulin regimens have varying effects on glycemic control, weight gain, and the risk of hypoglycemia Holman RR, et al.N Engl J Med 2008;359:1577-89. 2. Turnbull FM, et al. Diabetologia 2009 August 5 3. Lasserson DS, et al. Diabetologiia, 2009;52:1990-2000.
- 16. 16 papdi.bogor@ya hoo.com Intensive diabetes Management ⢠⢠⢠⢠⢠Mode of treatment for person with Diabetes Goal : Euglycemic or near normal glycemic Using all available resources to accomplish this goal Prevent/ delayed loss beta cell pancreas Prevent or delayed chronic complication of diabetes ADA 2011
- 17. 17 papdi.bogor@ya hoo.com Stepwise Intensification of Insulin Therapy FBG at target HbA1c above target FBG above target HbA1c above target Basal bolus Additional prandial doses as needed Basal plus Add prandial insulin at main meal HbA1c above target Basal Add basal insulin and titrate Oral agents Lifestyle changes Progressive deterioration of -cell function Adapted from Raccah D et al. Diabetes Metab Res Rev 2007;23(4):257-64.
- 18. 18 Insulin papdi.bogor@ya hoo.com ⢠A hormone secreted by the beta cells ⢠Secreted in response to glucose or other stimuli, such as amino acids Insulin ⢠Normal response characterized by low basal levels of insulin, with surges of insulin triggered by a rise in blood glucose 60 40 20 0 Breakfast Lunch Supper
- 19. 19 papdi.bogor@ya hoo.com Basal and Prandial Insulin â˘Basal insulin replacement mimics the constant physiologic release of insulin that regulates metabolism and hepatic glucose production. â˘Prandial insulin replacement is intended to mimic the postmeal insulin response to nutrient intake
- 20. Physiologic insulin secretion Analogue insulin mechanisme of action ------- Breakfast Lunch Dinner Insulin endogen Levemir NovoRapid NovoMix Bed time
- 21. 21 Jenis-jenis insulin papdi.bogor@ya hoo.com Aspart, glulisine, lispro (4â6 jam) Kadar insulin plasma Reguler (6â8 jam) NPH (12â20 jam) Ultralente (18â24 jam) Glargine (20-24 jam) Detemir 0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 Jam Hirsh IB, N Eng J Med 2005;352:174-183
- 22. papdi.bogor@ya hoo.com Insulin types and action Onset (hrs) Peak (hrs) Duration (hrs) Rapid Acting analog lispro aspart glulisine <Âź ž-2½ 3½-4½ ½-1 2-4 6-8 1-2 6-12 18-24 Short acting (Human) Regular (soluble) Intermediate acting NPH Long acting(analog) glargine detemir 3-4 1-2 3-24 3-8 âĽ24 12-24
- 23. 23 Insulin therapy ⢠Insulin therapy aims to replicate the normal physiological insulin response ⢠Insulin regimens should be individualized â type of diabetes â willingness to inject â lifestyle â blood glucose monitoring â age â dexterity â glycaemic targets papdi.bogor@ya hoo.com
- 24. Insulin remains the most efficacious glucose lowering agent HbA1c % Decrease in HbA1c: Potency of monotherapy CHOOSING INSULIN EARLIER FOR BETTER EFFICACY Nathan et al., Diabetes Care 2009;32:193-203.
- 25. 25 papdi.bogor@ya hoo.com Goal Insulin Therapy ⢠Administration of exogenous insulin to approximate the normal physiologic patterns of pancreatic insulin secretion ⢠Reduce A1c, fasting, and postprandial plasma glucose concentrations to recommended target level
- 26. What is the optimal target HbA1c level? EASD/ADA1 HbA1c <7.0% IDF2 HbA1c <7.0% EMA3 HbA1c <7.0% ⢠Goals of optimum HbA1c levels: ⢠Good glycaemic control ⢠Minimise development and progression of microvascular and macrovascular complications 1. 2. 3. Inzucchi et al. Diabetes care. Published online 19Apr2012. IDF Treatment Algorithm. International Diabetes Federation 2011. http://www.idf.org/treatment-algorithm-people-type-2-diabetes EMA Draft guidance on clinical investigation in DM Jan 2010
- 27. Treat T2DM early for long-term benefits1 ⢠Long-term benefits in reducing cardiovascular risk can be achieved with good control from diagnosis1 50% of patients with T2DM with complications already have them at diagnosis2 Each HbA1c percentage point reduction counts3 HbA1c -1% 1. 2. 3. Holman, et al. NEJM 2008;359:1577â89 UKPDS 6. Diabetes Res 1990;13(1):1-11 Stratton, et al. BMJ 2000;321(7258):405-12 -14% -37% -21% Myocardial infarction Microvascular complications Death related to diabetes
- 28. New ADA/EASD Position on Sequential Insulin Strategy in Type 2 Diabetes Non-Insulin Regimes Number of Injections Regimen Complexity Basal Insulin Only Usually with OAD 1 Low 2 Mod. +3 High Basal Insulin + 1 mealtime rapid-acting injection Pre-mixed Insulin twice-daily Basal Insulin + ⼠2 mealtime rapid-acting injection More Flexible Less Flexible Less Convenient More Convenient Inzucci SE, et al. Diabetologia. 2012. * Gumprecht et al. Intensification to to biphasic insulin aspart 30/70. Int J Clin Pract 2009 Flexibility Convenience*
- 29. Insulin can be initiated at any time ⢠Traditionally, insulin has been reserved as the last line of therapy⌠⢠âŚHowever, considering the benefits of normal glycemic status, Insulin can be initiated earlier and as soon as possible Inadequate Lifestyle + 1 OAD + 2 OAD INITIATE INSULIN + 3 OAD
- 30. How to start Basal Insulin ⢠Start with basal insulin (Insulin Detemir) 10 U or 0,1-0,2 U per Kg BB ⢠Once daily injection, anytime injection but in same time per each day
- 31. LevemirÂŽ Dose Titration Guidelines: 3-0-3 Algorithm Start with Levemir 10 U or 0,1-0,2 U per Kg BB Simple Dose titration with Levemir Mean 3-day FPG (mg/dL) Increase FPG>90 mg/dl (5.0 mm/L) FPG target range 70-90 mg/dL FPG <70 mg/dL (3.8 mmol/L) 3units units Maintain dose Decrease 3 units FPG>110 mg/dL (6.1 mmol/L) FPG target range 80-110 mg/dL FPG <80 mg/dL (4.4 mmol/L) Patients who experienced hypoglycemia reduced their daily dose by 3 units Blonde L et al. Diabetes Obes Metab. 2009; 11(6):623-631.
- 32. LevemirÂŽ/Glargine Head-to-Head: Similar Profiles in Type 2 Diabetes Insulin detemir 2.5 (mg/kg/min) Glucose infusion rate 3.0 0.4 U/kg 0.8 U/kg Insulin glargine 2.0 1.5 1.0 0.5 0 0 2 4 6 8 10 12 14 16 18 Time (h) Klein O et al. Diab Obes Metab 2007; 9:290-299 20 22 24
- 34. Levemir reduces nocturnal hypoglycaemia by up to 65% compared to NPH NPH vs. glargine -44% -53% -65% Relative Risk -29% NPH vs. detemir Insulin Determir Insulin NPH Insulin glargine Riddle et al., 2003 Phillis-Tsimikas et al., 2006 Phillis-Tsimikas. Clin Ther 2006;28(10):1569â81; Riddle et al 2003. Diabetes Care; 26 (11): 30806; Asakura T et al, 2008. Expert Opin Pharmacother; 10 (9): 1-5; Hanel H et al 2008. J Diabetes
- 35. A1chieve study overview and design ⢠Observational study of people with T2DM in routine clinical practice Start a study insulin ⢠Biphasic insulin aspart 30 ⢠Insulin detemir ⢠Insulin aspart BASELINE Week 0 ⢠INTERIM Week 12 FINAL Week 24 Study objectives ⢠Primary: number of attributed adverse drug reactions (includes major hypoglycaemia) ⢠Secondary: other safety and effectiveness measures
- 36. Levemir Âą OAD: Indonesia efficacy results HbA1c (%) Insulin naĂŻve FPG (mg/dl) PPG (mg/dl) Baseline values 9.5 219 263 n 147 317 295 -80 Change from baseline to week 24 0.0 -1.0 -100 -101* -2.0 -2.2* -115* -3.0 -120 *p<0.001
- 37. Levemir Âą OAD: Indonesia hypoglycaemia results Overall Major Insulin naĂŻve No. of pt w/hypo 19 Nocturnal Insulin naĂŻve 0 1 Insulin naĂŻve 0 18 0 Percent with at least one event 6,0 5,0 5,10 4,80 4,0 3,0 2,0 1,0 0,0 0,00 0,30 0,00 0,00 Baseline 24 weeks
- 38. A1chieve: Self-rated health in insulin naive patients (Levemir) Patients on Best imaginable LevemirÂŽ health 100 90 80 70 60 50 40 24 weeks Baseline 30 20 Worst imaginable health 10 0 Baseline 24 weeks
- 39. Slide no 39
- 40. Slide 40 SURVEI 30 peserta simposium IDI Bogor 2013 Tgl.9 nov 2013
- 41. Slide 41 Apakah dokter tahu tentang Insulin Basal dan Prandial
- 42. Slide 42 Apakah dokter menggunakan Insulin pada pasien Rawat Jalan
- 43. Slide 43 Apaka dokter pernah menggunakan Insulin basal (mis.levemir) pada Pasien Diabetes
- 44. Slide 44 Apakah dokter Pernah menggunakan Insulin Prandial (misalnya Novorapid)
- 45. Slide 45 Apakah dokter tahu tentang Insulin Basal dan Prandial
- 46. Slide 46 Apakah dokter menggunakan Insulin saja atau Kombinasi dengan diabetes oral
- 47. Conclusion ⢠Diabetes is a progressive disease that is increasing in prevalence in the world ⢠Starting with basal insulin detemir is easy way to reach better glycemic control ⢠In Indonesia, in real life clinical practice (A1chieve study) Levemir show significant improvements in overall glycaemic control in terms of HbA1c, FPG and PPG.
Hinweis der Redaktion
- In the first edition of the IDF Diabetes Atlas, released in 2000, the estimated global diabetes prevalence was 151 million. In the newest 5th edition, the estimated diabetes prevalence for 2011 has risen to 366 million, representing 8.3% of the worldâs adult population, with a prediction that by 2030 the number of people with diabetes will have risen to 552 million.
- IDF juga memperkirakan bahwa 60% dari kasus diabetes tersebut ada di Asia.
- -The prevalence of diabetes varies in different regions of Indonesia â it is higher in urban versus nonurban/outlying provinces and regions-According to the DiabCare Asia 2008 study, the prevalence of diabetes in Jakarta is 3.7%Riskedas 2007 (Cross sectional sampling for a registry conducted across Indonesia)Soewondo et al. DiabCare Asia 2008 Study. Med J Indones 2010.
- Penelusuran Litbangkes menunjukkan bahwa prevalensi diabetes tertinggi di daerah di Indonesia adalah sebesar 11,1%, yaitu di Pontianak (Kalimantan Barat) dan Ternate (Maluku Utara).
- On this slide we can see the usual pattern of insulin intensification in T2DM, moving from lifestyle interventions, the addition of OADs such as metformin, through to a regimen combining the OAD therapies with basal insulin, which has become a popular way to initiate insulin. When this combined BOT fails to control blood glucose levels, further intensification, to basalâbolus therapy, is recommended.
- In the UKPDS study, the incidence of clinical complications was significantly associated with glycaemia3. Each 1% reduction in updated mean HbA1c was associated with reductions in risk of 21% for any end point related to diabetes (95% CI 17% to 24%, P < 0.0001), 21% for deaths related to diabetes (15% to 27%, P < 0.0001), 14% for myocardial infarction (8% to 21%, P < 0.0001), and 37% for microvascular complications (33% to 41%, P < 0.0001). No threshold of risk was observed for any end point.
- Speaker Notes:[Click 1]: Detemir OD reduced the risk of hypoglycaemia by 53% versus NPH OD and reduced the risk of nocturnal hypoglycaemia by 65%