Diabetes & ramadan (2)
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Fasting Ramadan carry many hazards to diabetic need to fast. Uncontrolled patients have a liability to some dangerous complications like DKA,HYPOGLYCEMIA,HHS AND thromboembolism
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Diabetes & ramadan (2)
- 1. ALAA WAFA. MD Associate Professor of Internal Medicine PGDIP DM Cardiff University UK Diabetes and Endocrine unit Mansoura university Diabetes and Ramadan (Challenges and Recommendations)
- 3. Blood glucose Insulin and Glucagon Regulate Normal Glucose Homeostasis Glucose output Glucose uptake Glucagon (α cell) Insulin (β cell) Pancreas Liv er Muscle Adipose tissue Fasting state Fed state Porte D Jr, Kahn SE. Clin Invest Med. 1995;18:247–254. Adapted with permission from Kahn CR, Saltiel AR. In: Kahn CR et al, eds. Joslin’s Diabetes Mellitus. 14th ed. Lippincott Williams & Wilkins; 2005:145–168. 4
- 4. Islet dysfunction Adapted from Buse JB et al. In Williams Textbook of Endocrinology. 10th ed. Philadelphia, Saunders, 2003:1427–1483; Buchanan TA Clin Ther 2003;25(suppl B):B32–B46; Powers AC. In: Harrison’s Principles of Internal Medicine. 16th ed. New York: McGraw-Hill, 2005:2152–2180; Rhodes CJ Science 2005;307:380–384. The Pathophysiology of Type 2 Diabetes Includes Multiple Defects Pancreas Insulin deficiency Liver Muscle & Fat Excess glucagon Diminished insulin Beta cell produces less insulin Alpha cell produces excess glucagon Insulin resistance (decreased glucose uptake) Excess Glucose Output HYPERGLYCEMI A
- 5. Time Pancreatic Islet Cells in Type 2 Diabetes B cells α cells B cells α cells
- 6. The Core Defects in type 2 diabetes: Insulin resistance in peripheral tissues Excess Hepatic Glucose Production due to 1)increased glucagon 2)insulin insufficiency 3)insulin resistance Insulin deficiency due to insufficient pancreatic insulin release
- 7. Reprinted from Primary Care, 26, Ramlo-Halsted BA, Edelman SV, The natural history of type 2 diabetes. Implications for clinical practice, 771–789, © 1999, with permission from Elsevier. Development and Progression of Type 2 Diabetes and Related Complications* *Conceptual representation. Insulin level Insulin resistance Hepatic glucose production Postprandial glucose Fasting plasma glucose Beta-cell function Progression of Type 2 Diabetes Mellitus Impaired Glucose Tolerance Diabetes Diagnosis Frank Diabetes 4–7 years Development of Macrovascular Complications Development of Microvascular Complications
- 8. Type 2 diabetes is a progressive disease 8 Conceptual representation adapted from Ramlo-Halsted BA, Edelman SV. Prim Care 1999;26(4):771–789. © 1999 Elsevier Insulin level Insulin resistance Hepatic glucose production Postprandial glucose Fasting plasma glucose Beta-cell function Progression of Type 2 Diabetes Impaired Glucose Tolerance Diabetes Diagnosis Diabetes 4–7 years Development of Macrovascular Complications Development of Microvascular Complications
- 9. New era of treatment of T2DM
- 10. peripheral glucose uptake hepatic glucose production pancreatic insulin secretion pancreatic glucagon secretion gut carbohydrate delivery & absorption incretin effect HYPERGLYCEMIA ? Adapted from: Inzucchi SE, Sherwin RS in: Cecil Medicine 2011 Multiple, Complex Pathophysiological Abnormalities in T2DM _ _ + renal glucose excretion
- 11. peripheral glucose uptake hepatic glucose production pancreatic insulin secretion pancreatic glucagon secretion gut carbohydrate delivery & absorption incretin effect HYPERGLYCEMIA ? Adapted from: Inzucchi SE, Sherwin RS in: Cecil Medicine 2011 Multiple, Complex Pathophysiological Abnormalities in T2DM _ _ + renal glucose excretion DA agonists T Z D sMetformin S U sGlinides DPP-4 inhibitors GLP-1R agonists A G I s Amylin mimetics Insulin Bile acid sequestrants
- 12. Adapted from Riddle MC. Endocrinol Metab Clin North Am. 2005;34:77–98. Diet and Exercise Oral Monotherapy Standard Approach to the Management of T2DM: Treatment Intensification Oral Combination + + Oral + Injectable Incretin Mimetics Oral + Insulin + + Insulin
- 23. Management of Hyperglycemia in Type 2 Diabetes, 2015: A Patient-Centered Approach Update toa Position Statement of theAmericanDiabetesAssociation(ADA) and the EuropeanAssociationfor the Study of Diabetes (EASD) Diabetes Care 2015;38:140–149 Diabetologia 2015;58:429–442
- 24. 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 ADA-EASD Position Statement Update: Management of Hyperglycemia in T2DM, 2015 Diabetes Care 2012;35:1364–1379; Diabetologia 2012;55:1577–1596 Diabetes Care 2015;38:140-149; Diabetologia 2015;58:429-442
- 25. more stringent less stringent Patient attitude and expected treatment efforts highly motivated, adherent, excellent self-care capacities less motivated, non-adherent, poor self-care capacities Risks potentially associated with hypoglycemia and other drug adverse effects low high Disease duration newly diagnosed long-standing Life expectancy long short Important comorbidities absent severefew / mild Established vascular complications absent severefew / mild Readily available limited Usually not modifiable Potentially modifiable HbA1c 7% PATIENT / DISEASE FEATURES Approach to the management of hyperglycemia Resources and support system Diabetes Care 2015;38:140-149; Diabetologia 2015;58:429-442 Figure 1. Modulation of the intensiveness of glucose lowering therapy in T2DM
- 26. Oral Class Mechanism Advantages Disadvantages Cost Biguanides • Activates AMP- kinase (?other) • Hepatic glucose production • Extensive experience • No hypoglycemia • Weight neutral • ? CVD • Gastrointestinal • Lactic acidosis (rare) • B-12 deficiency • Contraindications Low Sulfonylureas • Closes KATP channels • Insulin secretion • Extensive experience • Microvascular risk • Hypoglycemia • Weight • Low durability • ? Blunts ischemic preconditioning Low Meglitinides • Closes KATP channels • Insulin secretion • Postprandial glucose • Dosing flexibility • Hypoglycemia • Weight • ? Blunts ischemic preconditioning • Dosing frequency Mod. TZDs • PPAR-g activator • Insulin sensitivity • No hypoglycemia • Durability • TGs (pio) • HDL-C • ? CVD events (pio) • Weight • Edema/heart failure • Bone fractures • LDL-C (rosi) • ? MI (rosi) Low Table 1. Properties of anti-hyperglycemic agents Diabetes Care 2015;38:140-149; Diabetologia 2015;10.1077/s00125-014-3460-0
- 27. Oral Class Mechanism Advantages Disadvantages Cost a-Glucosidase inhibitors • Inhibits a-glucosidase • Slows carbohydrate digestion / absorption • No hypoglycemia • Nonsystemic • Postprandial glucose • ? CVD events • Gastrointestinal • Dosing frequency • Modest A1c Mod. DPP-4 inhibitors • Inhibits DPP-4 • Increases incretin (GLP-1, GIP) levels • No hypoglycemia • Well tolerated • Angioedema / urticaria • ? Pancreatitis • ? Heart failure High Bile acid sequestrants • Bind bile acids • ? Hepatic glucose production • No hypoglycemia • LDL-C • Gastrointestinal • Modest A1c • Dosing frequency High Dopamine-2 agonists • Activates DA receptor • Alters hypothalamic control of metabolism • insulin sensitivity • No hypoglyemia • ? CVD events • Modest A1c • Dizziness, fatigue • Nausea • Rhinitis High SGLT2 inhibitors • Inhibits SGLT2 in proximal nephron • Increases glucosuria • Weight • No hypoglycemia • BP • Effective at all stages • GU infections • Polyuria • Volume depletion • LDL-C • Cr (transient) High Table 1. Properties of anti-hyperglycemic agents Diabetes Care 2015;38:140-149; Diabetologia 2015;10.1077/s00125-014-3460-0
- 28. Injectabl e Class Mechanism Advantages Disadvantages Cost Amylin mimetics • Activates amylin receptor • glucagon • gastric emptying • satiety • Weight • Postprandial glucose • Gastrointestinal • Modest A1c • Injectable • Hypo if insulin dose not reduced • Dosing frequency • Training requirements High GLP-1 receptor agonists • Activates GLP-1 R • Insulin, glucagon • gastric emptying • satiety • Weight • No hypoglycemia • Postprandial glucose • Some CV risk factors • Gastrointestinal • ? Pancreatitis • Heart rate • Medullary ca (rodents) • Injectable • Training requirements High Insulin • Activates insulin receptor • Myriad • Universally effective • Unlimited efficacy • Microvascular risk • Hypoglycemia • Weight gain • ? Mitogenicity • Injectable • Patient reluctance • Training requirements Variable Table 1. Properties of anti-hyperglycemic agents Diabetes Care 2015;38:140-149; Diabetologia 2015;10.1077/s00125-014-3460-0
- 29. Healthy eating, weight control, increased physical activity & diabetes education Metformin high low risk neutral/loss GI / lactic acidosis low If HbA1c target not achieved after ~3 months of monotherapy, proceed to 2-drug combination (order not meant to denote any specific preference - choice dependent on a variety of patient- & disease-specific factors): Metformin + Metformin + Metformin + Metformin + Metformin + high low risk gain edema, HF, fxs low Thiazolidine- dione intermediate low risk neutral rare high DPP-4 inhibitor highest high risk gain hypoglycemia variable Insulin (basal) Metformin + Metformin + Metformin + Metformin + Metformin + Basal Insulin + Sulfonylurea + TZD DPP-4-i GLP-1-RA Insulin§ or or or or Thiazolidine- dione + SU DPP-4-i GLP-1-RA Insulin§ TZD DPP-4-ior or or GLP-1-RA high low risk loss GI high GLP-1 receptor agonist Sulfonylurea high moderate risk gain hypoglycemia low SGLT2 inhibitor intermediate low risk loss GU, dehydration high SU TZD Insulin§ GLP-1 receptor agonist + SGLT-2 Inhibitor + SU TZD Insulin§ Metformin + Metformin + or or or or SGLT2-i or or or SGLT2-i Mono- therapy Efficacy* Hypo risk Weight Side effects Costs Dual therapy† Efficacy* Hypo risk Weight Side effects Costs Triple therapy or or DPP-4 Inhibitor + SU TZD Insulin§ SGLT2-i or or or SGLT2-i or DPP-4-i If HbA1c target not achieved after ~3 months of dual therapy, proceed to 3-drug combination (order not meant to denote any specific preference - choice dependent on a variety of patient- & disease-specific factors): If HbA1c target not achieved after ~3 months of triple therapy and patient (1) on oral combination, move to injectables, (2) on GLP-1 RA, add basal insulin, or (3) on optimally titrated basal insulin, add GLP-1-RA or mealtime insulin. In refractory patients consider adding TZD or SGL T2-i: Metformin + Combination injectable therapy‡ GLP-1-RAMealtime Insulin Insulin (basal) + Figure 2. Anti-hyperglycemic therapy in T2DM: General recommendations Diabetes Care 2015;38:140-149; Diabetologia 2015;58:429-442
- 30. Healthy eating, weight control, increased physical activity & diabetes education Metformin high low risk neutral/loss GI / lactic acidosis low If HbA1c target not achieved after ~3 months of monotherapy, proceed to 2-drug combination (order not meant to denote any specific preference - choice dependent on a variety of patient- & disease-specific factors): Metformin + Metformin + Metformin + Metformin + Metformin + high low risk gain edema, HF, fxs low Thiazolidine- dione intermediate low risk neutral rare high DPP-4 inhibitor highest high risk gain hypoglycemia variable Insulin (basal) Metformin + Metformin + Metformin + Metformin + Metformin + Basal Insulin + Sulfonylurea + TZD DPP-4-i GLP-1-RA Insulin§ or or or or Thiazolidine- dione + SU DPP-4-i GLP-1-RA Insulin§ TZD DPP-4-ior or or GLP-1-RA high low risk loss GI high GLP-1 receptor agonist Sulfonylurea high moderate risk gain hypoglycemia low SGLT2 inhibitor intermediate low risk loss GU, dehydration high SU TZD Insulin§ GLP-1 receptor agonist + SGLT-2 Inhibitor + SU TZD Insulin§ Metformin + Metformin + or or or or SGLT2-i or or or SGLT2-i Mono- therapy Efficacy* Hypo risk Weight Side effects Costs Dual therapy† Efficacy* Hypo risk Weight Side effects Costs Triple therapy or or DPP-4 Inhibitor + SU TZD Insulin§ SGLT2-i or or or SGLT2-i or DPP-4-i If HbA1c target not achieved after ~3 months of dual therapy, proceed to 3-drug combination (order not meant to denote any specific preference - choice dependent on a variety of patient- & disease-specific factors): If HbA1c target not achieved after ~3 months of triple therapy and patient (1) on oral combination, move to injectables, (2) on GLP-1 RA, add basal insulin, or (3) on optimally titrated basal insulin, add GLP-1-RA or mealtime insulin. In refractory patients consider adding TZD or SGL T2-i: Metformin + Combination injectable therapy‡ GLP-1-RAMealtime Insulin Insulin (basal) + Figure 2. Anti-hyperglycemic therapy in T2DM: General recommendations Diabetes Care 2015;38:140-149; Diabetologia 2015;58:429-442
- 31. Healthy eating, weight control, increased physical activity & diabetes education Metformin high low risk neutral/loss GI / lactic acidosis low If HbA1c target not achieved after ~3 months of monotherapy, proceed to 2-drug combination (order not meant to denote any specific preference - choice dependent on a variety of patient- & disease-specific factors): Metformin + Metformin + Metformin + Metformin + Metformin + high low risk gain edema, HF, fxs low Thiazolidine- dione intermediate low risk neutral rare high DPP-4 inhibitor highest high risk gain hypoglycemia variable Insulin (basal) Metformin + Metformin + Metformin + Metformin + Metformin + Basal Insulin + Sulfonylurea + TZD DPP-4-i GLP-1-RA Insulin§ or or or or Thiazolidine- dione + SU DPP-4-i GLP-1-RA Insulin§ TZD DPP-4-ior or or GLP-1-RA high low risk loss GI high GLP-1 receptor agonist Sulfonylurea high moderate risk gain hypoglycemia low SGLT2 inhibitor intermediate low risk loss GU, dehydration high SU TZD Insulin§ GLP-1 receptor agonist + SGLT-2 Inhibitor + SU TZD Insulin§ Metformin + Metformin + or or or or SGLT2-i or or or SGLT2-i Mono- therapy Efficacy* Hypo risk Weight Side effects Costs Dual therapy† Efficacy* Hypo risk Weight Side effects Costs Triple therapy or or DPP-4 Inhibitor + SU TZD Insulin§ SGLT2-i or or or SGLT2-i or DPP-4-i If HbA1c target not achieved after ~3 months of dual therapy, proceed to 3-drug combination (order not meant to denote any specific preference - choice dependent on a variety of patient- & disease-specific factors): If HbA1c target not achieved after ~3 months of triple therapy and patient (1) on oral combination, move to injectables, (2) on GLP-1 RA, add basal insulin, or (3) on optimally titrated basal insulin, add GLP-1-RA or mealtime insulin. In refractory patients consider adding TZD or SGL T2-i: Metformin + Combination injectable therapy‡ GLP-1-RAMealtime Insulin Insulin (basal) + Figure 2. Anti-hyperglycemic therapy in T2DM: General recommendations Diabetes Care 2015;38:140-149; Diabetologia 2015;58:429-442
- 32. Healthy eating, weight control, increased physical activity & diabetes education Metformin high low risk neutral/loss GI / lactic acidosis low If HbA1c target not achieved after ~3 months of monotherapy, proceed to 2-drug combination (order not meant to denote any specific preference - choice dependent on a variety of patient- & disease-specific factors): Metformin + Metformin + Metformin + Metformin + Metformin + high low risk gain edema, HF, fxs low Thiazolidine- dione intermediate low risk neutral rare high DPP-4 inhibitor highest high risk gain hypoglycemia variable Insulin (basal) Metformin + Metformin + Metformin + Metformin + Metformin + Basal Insulin + Sulfonylurea + TZD DPP-4-i GLP-1-RA Insulin§ or or or or Thiazolidine- dione + SU DPP-4-i GLP-1-RA Insulin§ TZD DPP-4-ior or or GLP-1-RA high low risk loss GI high GLP-1 receptor agonist Sulfonylurea high moderate risk gain hypoglycemia low SGLT2 inhibitor intermediate low risk loss GU, dehydration high SU TZD Insulin§ GLP-1 receptor agonist + SGLT-2 Inhibitor + SU TZD Insulin§ Metformin + Metformin + or or or or SGLT2-i or or or SGLT2-i Mono- therapy Efficacy* Hypo risk Weight Side effects Costs Dual therapy† Efficacy* Hypo risk Weight Side effects Costs Triple therapy or or DPP-4 Inhibitor + SU TZD Insulin§ SGLT2-i or or or SGLT2-i or DPP-4-i If HbA1c target not achieved after ~3 months of dual therapy, proceed to 3-drug combination (order not meant to denote any specific preference - choice dependent on a variety of patient- & disease-specific factors): If HbA1c target not achieved after ~3 months of triple therapy and patient (1) on oral combination, move to injectables, (2) on GLP-1 RA, add basal insulin, or (3) on optimally titrated basal insulin, add GLP-1-RA or mealtime insulin. In refractory patients consider adding TZD or SGL T2-i: Metformin + Combination injectable therapy‡ GLP-1-RAMealtime Insulin Insulin (basal) + Diabetes Care 2015;38:140-149; Diabetologia 2015;58:429-442
- 33. Healthy eating, weight control, increased physical activity & diabetes education Metformin high low risk neutral/loss GI / lactic acidosis low If HbA1c target not achieved after ~3 months of monotherapy, proceed to 2-drug combination (order not meant to denote any specific preference - choice dependent on a variety of patient- & disease-specific factors): Metformin + Metformin + Metformin + Metformin + Metformin + high low risk gain edema, HF, fxs low Thiazolidine- dione intermediate low risk neutral rare high DPP-4 inhibitor highest high risk gain hypoglycemia variable Insulin (basal) Metformin + Metformin + Metformin + Metformin + Metformin + Basal Insulin + Sulfonylurea + TZD DPP-4-i GLP-1-RA Insulin§ or or or or Thiazolidine- dione + SU DPP-4-i GLP-1-RA Insulin§ TZD DPP-4-ior or or GLP-1-RA high low risk loss GI high GLP-1 receptor agonist Sulfonylurea high moderate risk gain hypoglycemia low SGLT2 inhibitor intermediate low risk loss GU, dehydration high SU TZD Insulin§ GLP-1 receptor agonist + SGLT-2 Inhibitor + SU TZD Insulin§ Metformin + Metformin + or or or or SGLT2-i or or or SGLT2-i Mono- therapy Efficacy* Hypo risk Weight Side effects Costs Dual therapy† Efficacy* Hypo risk Weight Side effects Costs Triple therapy or or DPP-4 Inhibitor + SU TZD Insulin§ SGLT2-i or or or SGLT2-i or DPP-4-i If HbA1c target not achieved after ~3 months of dual therapy, proceed to 3-drug combination (order not meant to denote any specific preference - choice dependent on a variety of patient- & disease-specific factors): If HbA1c target not achieved after ~3 months of triple therapy and patient (1) on oral combination, move to injectables, (2) on GLP-1 RA, add basal insulin, or (3) on optimally titrated basal insulin, add GLP-1-RA or mealtime insulin. In refractory patients consider adding TZD or SGL T2-i: Metformin + Combination injectable therapy‡ GLP-1-RAMealtime Insulin Insulin (basal) + Diabetes Care 2015;38:140-149; Diabetologia 2015;58:429-442 HbA1c ≥9% Metformin intolerance or contraindication Uncontrolled hyperglycemia (catabolic features, BG ≥300-350 mg/dl, HbA1c ≥10-12%)
- 34. Healthy eating, weight control, increased physical activity & diabetes education Metformin high low risk neutral/loss GI / lactic acidosis low If HbA1c target not achieved after ~3 months of monotherapy, proceed to 2-drug combination (order not meant to denote any specific preference - choice dependent on a variety of patient- & disease-specific factors): Metformin + Metformin + Metformin + Metformin + Metformin + high low risk gain edema, HF, fxs low Thiazolidine- dione intermediate low risk neutral rare high DPP-4 inhibitor highest high risk gain hypoglycemia variable Insulin (basal) Metformin + Metformin + Metformin + Metformin + Metformin + Basal Insulin + Sulfonylurea + TZD DPP-4-i GLP-1-RA Insulin§ or or or or Thiazolidine- dione + SU DPP-4-i GLP-1-RA Insulin§ TZD DPP-4-i GLP-1-RA high low risk loss GI high GLP-1 receptor agonist Sulfonylurea high moderate risk gain hypoglycemia low SGLT2 inhibitor intermediate low risk loss GU, dehydration high SU TZD Insulin§ GLP-1 receptor agonist + SGLT-2 Inhibitor + SU TZD Insulin§ Metformin + Metformin + or or or or SGLT2-i or or or SGLT2-i Mono- therapy Efficacy* Hypo risk Weight Side effects Costs Dual therapy† Efficacy* Hypo risk Weight Side effects Costs Triple therapy or or DPP-4 Inhibitor + SU TZD Insulin§ SGLT2-i or or or SGLT2-i or DPP-4-i If HbA1c target not achieved after ~3 months of dual therapy, proceed to 3-drug combination (order not meant to denote any specific preference - choice dependent on a variety of patient- & disease-specific factors): If HbA1c target not achieved after ~3 months of triple therapy and patient (1) on oral combination, move to injectables, (2) on GLP-1 RA, add basal insulin, or (3) on optimally titrated basal insulin, add GLP-1-RA or mealtime insulin. In refractory patients consider adding TZD or SGL T2-i: Metformin + Combination injectable therapy‡ GLP-1-RAMealtime Insulin Figure 2A. An -hyperglycemic therapy in T2DM: Avoidance of hypoglycemia or or or Insulin (basal) + Diabetes Care 2015;38:140-149; Diabetologia 2015;10.1077/s00125-014-3460-0
- 35. Healthy eating, weight control, increased physical activity & diabetes education Metformin high low risk neutral/loss GI / lactic acidosis low If HbA1c target not achieved after ~3 months of monotherapy, proceed to 2-drug combination (order not meant to denote any specific preference - choice dependent on a variety of patient- & disease-specific factors): Metformin + Metformin + Metformin + Metformin + Metformin + high low risk gain edema, HF, fxs low Thiazolidine- dione intermediate low risk neutral rare high DPP-4 inhibitor highest high risk gain hypoglycemia variable Insulin (basal) Metformin + Metformin + Metformin + Metformin + Metformin + Basal Insulin + Sulfonylurea + TZD DPP-4-i GLP-1-RA Insulin§ or or or or Thiazolidine- dione + SU DPP-4-i GLP-1-RA Insulin§ TZD DPP-4-i GLP-1-RA high low risk loss GI high GLP-1 receptor agonist Sulfonylurea high moderate risk gain hypoglycemia low SGLT2 inhibitor intermediate low risk loss GU, dehydration high SU TZD Insulin§ GLP-1 receptor agonist + SGLT-2 Inhibitor + SU TZD Insulin§ Metformin + Metformin + or or or or SGLT2-i or or or SGLT2-i Mono- therapy Efficacy* Hypo risk Weight Side effects Costs Dual therapy† Efficacy* Hypo risk Weight Side effects Costs Triple therapy or or DPP-4 Inhibitor + SU TZD Insulin§ SGLT2-i or or or SGLT2-i or DPP-4-i If HbA1c target not achieved after ~3 months of dual therapy, proceed to 3-drug combination (order not meant to denote any specific preference - choice dependent on a variety of patient- & disease-specific factors): If HbA1c target not achieved after ~3 months of triple therapy and patient (1) on oral combination, move to injectables, (2) on GLP-1 RA, add basal insulin, or (3) on optimally titrated basal insulin, add GLP-1-RA or mealtime insulin. In refractory patients consider adding TZD or SGL T2-i: Metformin + Combination injectable therapy‡ GLP-1-RAMealtime Insulin Insulin (basal) + or or or Diabetes Care 2015;38:140-149; Diabetologia 2015;10.1077/s00125-014-3460-0 Figure 2B. An -hyperglycemic therapy in T2DM: Avoidance of weight gain
- 36. Healthy eating, weight control, increased physical activity & diabetes education Metformin high low risk neutral/loss GI / lactic acidosis low If HbA1c target not achieved after ~3 months of monotherapy, proceed to 2-drug combination (order not meant to denote any specific preference - choice dependent on a variety of patient- & disease-specific factors): Metformin + Metformin + Metformin + Metformin + Metformin + high low risk gain edema, HF, fxs low Thiazolidine- dione intermediate low risk neutral rare high DPP-4 inhibitor highest high risk gain hypoglycemia variable Insulin (basal) Metformin + Metformin + Metformin + Metformin + Metformin + Basal Insulin + Sulfonylurea + TZD DPP-4-i GLP-1-RA Insulin§ or or or or Thiazolidine- dione + SU DPP-4-i GLP-1-RA Insulin§ TZD DPP-4-ior or or GLP-1-RA high low risk loss GI high GLP-1 receptor agonist Sulfonylurea high moderate risk gain hypoglycemia low SGLT2 inhibitor intermediate low risk loss GU, dehydration high SU TZD Insulin§ GLP-1 receptor agonist + SGLT-2 Inhibitor + SU TZD Insulin§ Metformin + Metformin + or or or or SGLT2-i or or or SGLT2-i Mono- therapy Efficacy* Hypo risk Weight Side effects Costs Dual therapy† Efficacy* Hypo risk Weight Side effects Costs Triple therapy or or DPP-4 Inhibitor + SU TZD Insulin§ SGLT2-i or or or SGLT2-i or DPP-4-i If HbA1c target not achieved after ~3 months of dual therapy, proceed to 3-drug combination (order not meant to denote any specific preference - choice dependent on a variety of patient- & disease-specific factors): If HbA1c target not achieved after ~3 months of triple therapy and patient (1) on oral combination, move to injectables, (2) on GLP-1 RA, add basal insulin, or (3) on optimally titrated basal insulin, add GLP-1-RA or mealtime insulin. In refractory patients consider adding TZD or SGL T2-i: Metformin + Combination injectable therapy‡ GLP-1-RAMealtime Insulin Insulin (basal) + Diabetes Care 2015;38:140-149; Diabetologia 2015;10.1077/s00125-014-3460-0 Figure 2C. An -hyperglycemic therapy in T2DM: Minimiza on of costs
- 37. • Start: 10U/day or 0.1-0.2 U/kg/day • Adjust: 10-15% or 2-4 U once-twice weekly to reach FBG target. • For hypo: Determine & address cause; ê dose by 4 units or 10-20%. Basal Insulin (usually with metformin +/- other non-insulin agent) Figure 3. Approach to starting & adjusting insulin in T2DM Diabetes Care 2015;38:140-149; Diabetologia 2015;58:429-442
- 38. Add ≥2 rapid insulin* injections before meals ('basal-bolus’† ) Change to premixed insulin* twice daily Add 1 rapid insulin* injections before largest meal • Start: Divide current basal dose into 2/3 AM, 1/3 PM or 1/2 AM, 1/2 PM. • Adjust: é dose by 1-2 U or 10-15% once- twice weekly until SMBG target reached. • For hypo: Determine and address cause; ê corresponding dose by 2-4 U or 10-20%. • Start: 10U/day or 0.1-0.2 U/kg/day • Adjust: 10-15% or 2-4 U once-twice weekly to reach FBG target. • For hypo: Determine & address cause; ê dose by 4 units or 10-20%. Basal Insulin (usually with metformin +/- other non-insulin agent) If not controlled after FBG target is reached (or if dose > 0.5 U/kg/day), treat PPG excursions with meal-time insulin. (Consider initial GLP-1-RA trial.) If not controlled, consider basal- bolus. If not controlled, consider basal- bolus. • Start: 4U, 0.1 U/kg, or 10% basal dose. If A1c<8%, consider ê basal by same amount. • Adjust: é dose by 1-2 U or 10-15% once- twice weekly until SMBG target reached. • For hypo: Determine and address cause; ê corresponding dose by 2-4 U or 10-20%. • Start: 4U, 0.1 U/kg, or 10% basal dose/meal.‡ If A1c<8%, consider ê basal by same amount. • Adjust: é dose by 1-2 U or 10-15% once-twice weekly to achieve SMBG target. • For hypo: Determine and address cause; ê corresponding dose by 2-4 U or 10-20%. Figure 3. Approach to starting & adjusting insulin in T2DM Diabetes Care 2015;38:140-149; Diabetologia 2015;58:429-442
- 39. Add ≥2 rapid insulin* injections before meals ('basal-bolus’† ) Change to premixed insulin* twice daily Add 1 rapid insulin* injections before largest meal • Start: Divide current basal dose into 2/3 AM, 1/3 PM or 1/2 AM, 1/2 PM. • Adjust: é dose by 1-2 U or 10-15% once- twice weekly until SMBG target reached. • For hypo: Determine and address cause; ê corresponding dose by 2-4 U or 10-20%. • Start: 10U/day or 0.1-0.2 U/kg/day • Adjust: 10-15% or 2-4 U once-twice weekly to reach FBG target. • For hypo: Determine & address cause; ê dose by 4 units or 10-20%. Basal Insulin (usually with metformin +/- other non-insulin agent) If not controlled after FBG target is reached (or if dose > 0.5 U/kg/day), treat PPG excursions with meal-time insulin. (Consider initial GLP-1-RA trial.) low mod. high more flexible less flexible Complexity # Injections Flexibility 1 2 3+ If not controlled, consider basal- bolus. If not controlled, consider basal- bolus. • Start: 4U, 0.1 U/kg, or 10% basal dose. If A1c<8%, consider ê basal by same amount. • Adjust: é dose by 1-2 U or 10-15% once- twice weekly until SMBG target reached. • For hypo: Determine and address cause; ê corresponding dose by 2-4 U or 10-20%. • Start: 4U, 0.1 U/kg, or 10% basal dose/meal.‡ If A1c<8%, consider ê basal by same amount. • Adjust: é dose by 1-2 U or 10-15% once-twice weekly to achieve SMBG target. • For hypo: Determine and address cause; ê corresponding dose by 2-4 U or 10-20%. Figure 3. Approach to starting & adjusting insulin in T2DM Diabetes Care 2015;38:140-149; Diabetologia 2015;58:429-442
- 40. DOSING SEE REVERSE FOR TIPS CHOOSE AN INSULIN CATEGORY CHOOSE A BRAND
- 41. ADA-EASD Position Statement Update: Management of Hyperglycemia in T2DM, 2015 Long (Detemir) Rapid (Lispro, Aspart, Glulisine) Hours Long (Glargine) 0 2 4 6 8 10 12 14 16 18 20 22 24 Short (Regular) Hours after injection Insulinlevel (Degludec) 3. ANTI-HYPERGLYCEMIC THERAPY • Therapeutic options: Insulins
- 42. Lifestyle changes plus metformin (± other agents) Basal Add basal insulin Basal Plus Add prandial insulin at main meal Basal Bolus Add prandial insulin before each meal Progressive deterioration of -cell function Basal Plus: once-daily basal insulin plus once-daily* rapid-acting insulin Matching treatment to disease progression using a stepwise approach *As the disease progresses, a second daily injection of glulisine may be added Adapted from Raccah D, et al. Diabetes Metab Res Rev 2007;23:257–64 Proper Basal titration Titrate insulin
- 43. Clinical challenge: Selecting the appropriate treatment for your patient Adapted from Nathan DM. N Engl J Med. 2007;356:437-40 and Nathan et al. Diabetes Care. 2009;32:193-203 0.5-1.01.5 1.5 1.0-1.5 0.5-1.0 0.8-1.0 ≥2.5 Sulfonylureas Biguanides (metformin) Glinides DPP-IV inhibitors TZDs Insulin 0.0 0.5 1.0 1.5 2.0 2.5 3.0 HbA1creduction (%) Efficacy as mono therapy Anti diabetic agents GLP-1 agonist s Insulin is the most effective glucose-lowering agent
- 45. 45 (183)اَيِالص ُمُكْيَلَع َبِتُكْاوُنَآم َينِذَّلا اَهَُّيأَينِذَّلا ىَلَع َبِتُكاَمَكُامَيْمُكِلْبَق نِم َنوُقَّتَت ْمُكَّلَعَل (184)َْوأ اًضيِرَّم مُكنِم َناَكنَمَف ٍاتَودُدْعَّم اًامَّيَأَأ ْنِم ٌةَّدِعَف ٍرَفَس ىَلَعَرَخُأ ٍامَّي ٍيِكْسِم ُامَعَط ٌةَيْدِف ُهَنوُقيِطُي َينِذَّلا ىَلَعَوْيَخ َوُهَف اًرْيَخ َعَّوَطَت نَمَفْاوُومُصَت َنأَو ُهَّل ٌر َنوُمَلْعَت ْمُنتُكنِإ ْمُكَّل ٌرْيَخ (185)ُه ُنآْرُقْلا ِيهِف َلِزُنأ َيِذَّلا َناَضَمَر ُرْهَشا َنِم ٍاتَنِيَبَو َِّاسنلِل ىًدىَدُْْل ْمُصَْيلَف َرْهَّالش ُمُكنِم َدِهَش نَمَف ِانَقْرُفْلاَوَفَس ىَلَع َْوأ اًضيِرَم َناَكنَمَو ُهْنِم ٌةَّدِعَف ٍر يِرُي َالَو َرْسُْيلا ُمُكِب ُاّلل ُديِرُي َرَخُأ ٍامَّيَأِْعلا ْاوُلِمْكُتِلَو َرْسُْعلا ُمُكِب ُدَاّلل ْاوُِّبَكُتِلَو َةَّدىَلَع َنوُرُكْشَت ْمُكَّلَعَلَو ْمُكاَدَه اَم
- 46. 46 The Current decade… Over the current decade, the number of fasting hours will progressively increase in the northern hemisphere as Ramadan falls in the summer months. This will have important implications for Muslims with diabetes who wish to fast.
- 48. Ramadan Between Diabetes and Fasting Although the Koran exempts sick people from the duty of fasting, many Muslims with diabetes may not perceive themselves as sick and are keen to fast. 43% of patients with type 1 and 86% of those with type 2 diabetes fasted during Ramadan. 1-IBRAHIM SALTI, et al . Diabetes Care 27:2306–2311, 2004 2-E Hui et al , BMJ, 26 june 2010 , Volume 340
- 49. 49 During Ramadan about 60% of patients change their antidiabetic drug intake: 35% stop treatment 8% change the dosage schedule 25% decrease the drug dose. Importantly, this is done at the patients’ own initiative without medical supervision. Salti I, Benard E, Detournay B et al. A population-based study of diabetes and its characteristics during the fasting month of Ramadan in 13 countries. Diabetes Care 2004; 27: 2306–11. Aslam M, Healey MA. Compliance and drug therapy in Moslem patients. J Clin Hosp Pharm 1986; 11: 321–5. Aslam M, Assad A. Drug regimens and fasting during Ramadan: a survey in Kuwait. Public Health 1986; 100: 49–53.
- 50. The Risks of Fasting Include: Hypoglycemia Hyperglycemia Diabetic ketoacidosis Dehydration and thrombosis M. al-Arouj et al, “Recommendations for management of diabetes during Ramadan,” Diabetes Care, 28(2005), 2305-2311.
- 51. 12,243 subjects, in 13 countries including Egypt 1 Almost 90% was T2DM The important finding was: 5 folds Increase in severe hyperglycemia with Ketoacidosis that required hospital admission 7.5 folds increase in the risk of severe hypoglycemia during Ramadan 2% Of fasting patients experienced at least one episode of sever hypoglycemia requiring hospitalization 1-IBRAHIM SALTI, et al . Diabetes Care 27:2306–2311, 2004 2- E Hui et al , BMJ 2010;340:c3053;
- 52. Classification of hypoglycemia according to severity: American Diabetes Association 1- Documented symptomatic hypoglycemia. An event during which typical symptoms of hypoglycemia are accompanied by a measured plasma glucose concentration ≤ 70 mg/dl (3.9 mmol/l). 2- Asymptomatic hypoglycemia. An event not accompanied by typical symptoms of hypoglycemia but with a measured plasma glucose concentration ≤ 70 mg/dl (3.9 mmol/l). 3- Probable symptomatic hypoglycemia. An event during which symptoms of hypoglycemia are not accompanied by a plasma glucose determination. 4- Relative hypoglycemia. An event during which the person with diabetes reports any of the typical symptoms of hypoglycemia, and interprets those as indicative of hypoglycemia, but with a measured plasma glucose concentration >70 mg/dl (3.9 mmol/l). 5- Severe An event requiring assistance of another person to actively administer carbohydrate, glucagons, or other resuscitative actions. 52 American Diabetes Association Workgroup on Hypoglycemia. Defining and Reporting Hypoglycemia in Diabetes. Diabetes Care . 2005;28 (5):1245– 1249.This material can only be shown reactively to answer specific questions from physicians.
- 53. Hypoglycemic Events Increased by 84% During Ramadan Significant increasing in hypoglycemic events during Ramadan mainly with patients ＞60 years old Fatima J et al , Indian J Endocrinol Metab. 2012 Mar;16(2):323-4. 164 NumberofHypoglycemicevents 302 147 N= 179 84%
- 54. Pathophysiological cardiovascular consequences of hypoglycaemia CRP=C-reactive protein; IL-6=interleukin 6; VEGF=vascular endothelial growth factor. Desouza CV, et al. Diabetes Care. 2010; 33: 1389–1394. VEGF IL-6 CRP Neutrophil activation Platelet activation Factor VII Blood coagulation abnormalities Sympathoadrenal response Inflammation Endothelial dysfunction Vasodilation Heart rate variability Rhythm abnormalities Haemodynamic changes Adrenaline Contractility Oxygen consumption Heart workload HYPOGLYCAEMIA 54
- 55. Health and economical consequences of hypoglycemia 55 This material can only be shown reactively to answer specific questions from physicians. Hypoglycemia CV complications2 Weight gain by defensive eating3 Coma2 Car accident4 Hospitalization costs1 Dizzy turn unconsciousness2 Seizures2 Death6 Increased risk of dementia5 Quality of Life7 1. Jönsson L, et al. Cost of Hypoglycemia in Patients with Type 2 Diabetes in Sweden. Value In Health. 2006;9:193–198 2. Barnett AH. CMRO. 2010;26:1333–1342 3. Foley J & Jordan. J. Vasc Health Risk Manag. 2010;6:541–548 4. Canadian Diabetes Association’s Clinical Practice Guidelines for Diabetes and Private and Commercial Driving. CanJ Diabetes. 2003;27(2):128 –140. 5. Whitmer RA, et al. JAMA. 2009;301:15655–1572 6. Zammitt NN, et al. Diabetes Care. 2005;28:2948–2961 7. McEwan P, et al. Diabetes Obes Metab. 2010;12:431–436
- 56. Hypoglycemia and Treatment Adherence Patients’ reports of hypoglycemic symptoms are associated with significantly lower treatment satisfaction and with barriers to adherence. Alvarez Guisasola F, et al. Diabetes Obes Metab. 2008 Jun;10 Suppl 1:25-32.
- 57. Diabetic Ketoacidosis Patients with type 1 diabetes and severe insulin deficiency may have excessive glycogenolysis, gluconeogenesis and ketogenesis. All of this may lead to hyperglycemia and ketoacidosis that may be life- threatening. Karamat et al, J R Soc Med 2010: 103: 139–147.
- 58. DKA:Pathophysiology beta- cell alpha- cell Loss of beta cell function is gradual over time
- 59. DKA:Pathophysiology Normal – glucose in blood
- 61. 1. Insulin deficiency *lack of glucose in muscle 2. glucagon excess *increase in gluconeogenesis Diabetic Ketoacidosis:Pathophysiology
- 62. Diabetic Ketoacidosis:Pathophysiology 3. Rapid lipolysis into free fatty acids and ketone bodies release of Beta-hydroxybutyrate ketones resoposible for all s&s
- 63. Diabetic Ketoacidosis:Pathophysiology 4. Hypovolaemia – vomitting + osmotic diuresis Increases concentration of ketones + glucose
- 64. Dehydration and Thrombosis Limitation of fluid intake Hot and humid climates Hard physical labor Excessive perspiration. Hyperglycemia •Osmotic diuresis & •Volume and electrolyte depletion. Adapted from : M. al-Arouj et al, “Recommendations for management of diabetes during Ramadan,” Diabetes Care,
- 65. Dehydration and Thrombosis • Patients with diabetes exhibit a hypercoagulable state due to an increase in clotting factors, a decrease in endogenous anticoagulants, and impaired fibrinolysis. • Increased blood viscosity secondary to dehydration may enhance the risk of thrombosis. • A report from Saudi Arabia suggested an increased incidence of retinal vein occlusion in patients who fasted during Ramadan M. al-Arouj et al, “Recommendations for management of diabetes during Ramadan,” Diabetes Care, 28(2005),
- 66. Patients who insist on fasting need to be aware of the associated risks and be ready to adhere to the recommendations of their health care providers to achieve a safer fasting experience. Al-Arouj M, et al. Diabetes Care. 2005;28(9):2305-11. For Safer Fasting
- 69. High Moderate Low risk of adverse events Categories of risks for patients fasting Ramadan E Hui et al , BMJ 2010;340:c3053; Al-Arouj M. et al, Recommendations for management of diabetes during Ramadan. Diabetes Care. 2010;33: 1895-
- 70. High Moderate Low risk of adverse events •Poor glycemic control, Severe and recurrent episodes of hypoglycemia. • Experience ketoacidosis three months before Ramadan. • Elderly and Pregnant women • Advanced complications • Well controlled patients treated with short acting insulin secretogogue, sulphonylurea, insulin, or taking combination oral or oral plus insulin • Well controlled patients treated with Metformin, Dipeptidyl peptidase-4 inhibitors, or thiazolidinediones who are otherwise healthy E Hui et al , BMJ 2010;340:c3053; Al-Arouj M. et al, Recommendations for management of diabetes during Ramadan. Diabetes Care. 2010;33: 1895-1902. Categories of risks for patients fasting Ramadan
- 71. Diabetic patients at risks during fasting: Acute Peptic Ulcer Pulmonary Tuberculosis Bronchial Asthma Cancer Diabetes –Type 1 and 2 who have poor glycemic control (HbA1c >12%), non compliant with diet or drug/oral regimes, four OR more episodes of hypoglycemia AND/OR hyperglycemia during preceding month, on 2 and MORE insulin injection/day. ESRD Cardiovascular disease Psychiatry Liver disorder, hepatic dysfunction where the liver enzyme is >> 2 x Upper Normal Limit. Intercurrent infections
- 73. Management of Diabetic Patients During Ramadan Patients Education T2DM Pharmaceutical Management in Ramadan
- 74. Four key areas in Ramadan focused education 1-Meal planning and dietary advice 2-Exercise 3-Blood glucose monitoring 4-Recognizing and managing complications E Hui et al , BMJ 2010;340:c3053;
- 75. Breaking the Fast All patients must always and immediately end their fast if: 1. Hypoglycaemia (blood glucose of <60mg/dl). 2. Blood glucose reaches <70 mg in the first few hours after the start of the fast, especially if insulin, sulfonylurea drugs, or neglitinide are taken at predawn. 3. Blood glucose exceeds 300 mg with symptoms of hyperglycaemia. Recommendations for Diabetic Individuals during Ramadan, Diabetes Care , vol 33, num. 8, August2010
- 76. Oral hypoglycaemic agents Short acting insulin Sus Take twice daily at suhur and iftar TZDs No treatment adjustment required 2–4 weeks to exert substantial antihyperglycemic effects DPP4 inhibitors The best tolerated drugs, Consider DPP4i if the risk of hypoglycemia is high. SUs . Consider dose adjustment. Metformin Modify timing of doses: • Two thirds of dose at iftar • One third at suhur. T2DM Pharmaceutical Management in Ramadan E Hui et al , BMJ 2010;340:c3053; Al-Arouj M. et al, Recommendations for management of diabetes during Ramadan. Diabetes Care. 2010;33: 1895- 1902.
- 77. 77 Fasting during Ramadan in patients on insulin therapy
- 78. 78 Plasmainsulin(µU/ml) Aly A. Abdel-Rahim. 4:00 25 50 8:00 12:00 16:00 20:00 24:00 4:00 Breakfast Lunch Dinner Time 8:00 Physiological Serum Insulin Secretion Profile
- 79. 79 Human Insulins and Analogues Typical Times of Action Insulin Preparations Onset of Action Peak Duration of Action Aspart, glulisine, lispro ~15 minutes 1–2 hours 4–6 hours Human regular 30–60 minutes 2–4 hours 6–8 hours Human NPH, lente 2–4 hours 4–10 hours 12–20 hours Premixed insulin ½ -1 hour 6-8hours 10-12 hours Glargine Detemir 2–4 hours Flat ~24 hours 12-20 hs (0.2- 0.4 U/kg/d)
- 80. 80 Action Profiles of Insulin Analogues 0 1 2 53 4 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 Plasma insulin levels Regular 6–8 hours NPH 12–20 hours Hours Glargine or detemir 24 hours Aspart, glulisine, lispro 4–6 hours
- 81. 81 Plasmainsulin(µU/ml) Aly A. Abdel-Rahim. 4:00 8:00 12:00 16:00 20:00 24:00 4:00 Breakfast Lunch Dinner Time 8:00 Basal/ Oral regimen Bedtime NPH 50 Oral agents 25
- 82. 82 Time of day 20 40 60 80 100 B L D Split-Mixed Regimen Human Insulins B=breakfast; L=lunch; D=dinner 0600 06000800 18001200 2400 NPH Regular NPH Regular Normal pattern U/mL
- 83. 83 Plasmainsulin(µU/ml) Aly A. Abdel-Rahim. 4:00 25 50 8:00 12:00 16:00 20:00 24:00 4:00 Breakfast Lunch Dinner Time 8:00 Twice daily premixed
- 84. 84 Time of day 20 40 60 80 100 B L D Multiple Daily Injections MDI Human Insulins B=breakfast; L=lunch; D=dinner 0600 06000800 18001200 2400 Regular NPH NPH Regular Normal pattern U/mL Regular
- 85. 85 0600 0800 18001200 2400 0600 Time of day 20 40 60 80 100 B L D Basal-Bolus Insulin Treatment With Insulin Analogues B=breakfast; L=lunch; D=dinner Glargine/ detemir Lispro, glulisine, or aspart Normal pattern U/mL
- 86. 86 Recommendations for Management of Diabetes During Ramadan for Patients on Insulin The major objective of insulin therapy during Ramadan is to provide adequate insulin to prevent the post meal hyperglycemia and also prevent hypoglycemia during the period of fasting The choice of insulin therapy is decided by the previous therapy that the patient is taking and also the blood glucose profiles. Ensure adequate fluid intake
- 87. 87Aly A. Abdel-Rahim. Bed time insulin
- 88. 88 Plasmainsulin(µU/ml) Aly A. Abdel-Rahim. 4:00 8:00 12:00 16:00 20:00 24:00 4:00 Breakfast Lunch Dinner Time 8:00 Basal/ Oral regimen Bedtime NPH 50 Oral agents 25
- 89. 89 Plasmainsulin(µU/ml) Aly A. Abdel-Rahim. 4:00 25 50 8:00 12:00 16:00 20:00 24:00 4:00 Time 8:00 Oral agents Can NPH be used in Ramadan •Peak at a time which is not needed. NPH at breakfast •Will not cover breakfast. •Poor coverage of day time
- 90. 90 Plasmainsulin(µU/ml) Aly A. Abdel-Rahim. 4:00 25 50 8:00 12:00 16:00 20:00 24:00 4:00 Time 8:00 Oral agents Can NPH be used in Ramadan •Dangerous time of peak NPH after sohour
- 91. 91 Plasmainsulin(µU/ml) Aly A. Abdel-Rahim. 4:00 8:00 12:00 16:00 20:00 24:00 4:00 Time 8:00 Can peakless insulin replace NPH in Ramadan ?? •No peak, no hypoglycaemia. •Control meals with oral •Free time of injection 50 Oral agents 25 basal insulin
- 92. 92 Plasmainsulin(µU/ml) Aly A. Abdel-Rahim. 4:00 25 50 8:00 12:00 16:00 20:00 24:00 4:00 Time 8:00 Peakless insulin+ once daily oral secretagogue basal insulin 8-12 pm Oral agent once
- 93. 93 4:00 25 50 75 8:00 12:00 16:00 18:00 22:00 4:0 0 PlasmaInsulinµU/ml) Time 8:0 0 One peakless Insulin + One Oral OAD e.g DPP-4inhibitors Glargine Detemir 8-12PM •No Peak •No Hypoglycemia •Control Iftar meal with OAD
- 94. 94 Plasmainsulin(µU/ml) Aly A. Abdel-Rahim. 4:00 50 25 8:00 12:00 16:00 20:00 24:00 4:00 Time 8:00 Peakless insulin+ premeal short acting oral secretagogue •Glinides offers ideal combination •Similar to intensive insulin therapy when there is beta cell reserve •Adjust the dose according to the time and size of meal Short acting secretagogues basal insulin 8-12 pm
- 95. 95 Plasmainsulin(µU/ml) Aly A. Abdel-Rahim. 4:00 25 50 8:00 12:00 16:00 20:00 24:00 4:00 Time 8:00 Short acting Oral agents Once daily premixed in Ramadan: once daily+ oral •50/50 is better to control breakgast. •Short acting secretagogues additional control on sohour •Not suitable for exhausted beta cells
- 96. 96Aly A. Abdel-Rahim. Premixed insulin
- 97. 97 4:00 25 50 75 8:00 12:00 16:00 18:00 22:00 4:0 0 PlasmaInsulinµU/ml) Time 8:0 0 Twice Premix in Ramadan
- 98. 98 Plasmainsulin(µU/ml) Aly A. Abdel-Rahim. 4:00 25 50 8:00 12:00 16:00 20:00 24:00 4:00 Time 8:00 Twice daily premixed in Ramadan •Fear of daytime hypoglycaemia •Overlap between sohour short acting and iftar intermediate acting
- 99. 99 Plasmainsulin(µU/ml) Aly A. Abdel-Rahim. 4:00 25 50 8:00 12:00 16:00 20:00 24:00 4:00 Time 8:00 Twice daily premixed in Ramadan Dangerous even if dose size changed
- 100. 100100 Ensure adequate fluid intake. 70/30 premixed insulin twice daily, e.g., 30 units in morning and 20 units in evening…… In Ramadan,,,,,Use the usual morning dose at the sunset meal (Iftar) and half the usual evening dose at predawn (Suhur), e.g., 70/30 premixed insulin, 30 units at Iftar and 10 units at suhur. Diabetes Care September 2005 , pages 2305-11 Premixed insulin :
- 101. 101 Premixed insulins Mix insulin 50/50 at iftar instead of Mix30 reduced postprandial glucose excursions and reduced hypoglycemia Consider changing premixed insulin preparations to glargine or detemir plus lispro or aspart . Mattoo V, Diabetes Res Clin Pract 2003;59:137-43
- 102. 102 Time of day 20 40 60 80 100 B L D Multiple Daily Injections MDI Human Insulins B=breakfast; L=lunch; D=dinner 0600 06000800 18001200 2400 Regular NPH NPH Regular Normal pattern U/mL Regular
- 103. 103 Plasmainsulin(µU/ml) Aly A. Abdel-Rahim. 4:00 25 50 8:00 12:00 16:00 20:00 24:00 4:00 Time 8:00 Peakless insulin+ premeal rapid acting insulin basal insulin 8-12 pm Rapid acting insulin
- 104. 104104 MOST patients will require short-acting insulin administered in combination with the intermediate, or long-acting insulin at the sunset meal to cover the large caloric load of Iftar & an additional dose of short-acting insulin at predawn. 1. ADA. Diabetes Care 2006;29(suppl 1):S4–S42.
- 105. 105 Patients on Basal insulin analogue glargine or detemir It is advised that patients who take long acting basal insulin, such as glargine, to reduce the dose by 20% to avoid hypoglycemia. Continue taking the same doses of repaglinide or short acting insulin
- 106. 106Aly A. Abdel-Rahim. Advantages of rapid acting insulins
- 107. 107 PLEASE REMEMBER
- 108. 108Aly A. Abdel-Rahim. Patient education regarding fasting during the holy month of Ramadan is badly needed. Diabetic patients with established renal disease are high-risk category. Fasting for prolonged periods, especially in hot climates, may impose negative impacts on renal function from hypovolemia and dehydration. The mainstay of management of those patients is targeted toward arresting the progression of their underlying renal disease, and fasting during Ramadan should not be recommended.
- 109. 109
- 110. 110 Remember Careful use of intermediate- or long-acting insulin preparations plus a short-acting insulin administered before meals would be an effective strategy. Adjustment to treatment necessary: e.g. Reduce the dose of Basal insulin by 20% Use Mix 50 in the evening instead of Mix 30 to avoid post prandial hyperglycemia Diabetes Care 28.9 (Sept 2005): p2305(7).
- 111. 111Aly A. Abdel-Rahim. Treatment should be tailored and adjusted
- 112. 112 Some Parting Thoughts “Fasting is for Me and I (Allah) only will reward it” (Hadith Qudsi) “While fasting , if one does not give up falsehood in words and actions , then Allah has no need of him giving up food and drink (saying of Prophet Muhammad-pbuh)” HAVE A BLESSED RAMADAN
- 113. How to Help Patients Fast Safely ?? Patient Education Program. Individualization of anti diabetic drugs Select more safe drugs. Adjust dose if needed Ensure good non – sugar fluid intake. Avoid heavy physical exercise at afternoon. Ensure good calorie distribution. Summary