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2012 SEMDSA Guideline for the Management of Type 2 Diabetes Mellitus Aslam Amod 1st FCPSA Congress 19 May 2012, Cape Town.

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Presentation on theme: "2012 SEMDSA Guideline for the Management of Type 2 Diabetes Mellitus Aslam Amod 1st FCPSA Congress 19 May 2012, Cape Town."— Presentation transcript:

1 2012 SEMDSA Guideline for the Management of Type 2 Diabetes Mellitus Aslam Amod 1st FCPSA Congress 19 May 2012, Cape Town

2 Amod A et al. The 2012 SEMDSA guideline for the management of type 2 diabetes. JEMDSA. 2012;17(1):S1-S94. Available at http://www.jemdsa.co.za

3 The Guideline & Steering Committee Chairperson: Aslam Amod Section 1Definition, diagnosis and organisation Ayesha A Motala Definition, classification, diagnosis and screening Naomi S LevittOrganisation of Diabetes Care Section 2 Lifestyle Modification Jeannie Berg, Madelein Young, Natalie Grobler Diabetes self management education, Medical nutrition therapy Andrew HeilbrunnPhysical activity and type 2 diabetes

4 The Guideline & Steering Committee (2) Chairperson: Aslam Amod Section 3Glycaemic Control Larry A DistillerAssessment of Glycaemic Control Aslam Amod, Fraser Pirie, Joel Dave Glycaemic control: Non-insulin therapies Insulin-based therapies The SEMDSA 2012 algorithm Ken HuddleHypoglycaemia, Diabetes in pregnancy Daksha JivanHyperglycaemic emergencies Imran ParukIn-hospital management of type 2 diabetes

5 The Guideline & Steering Committee (3) Chairperson: Aslam Amod Section 4Complications and co-morbidities Wayne MayObesity in type 2 diabetes Derick Raal, Dirk BlomCardiovascular risk and dyslipidaemia Brynne Ascott-EvansAspirin therapy Susan BrownHypertension Willie MollenzeChronic kidney disease and Retinopathy Paul Rheeder, Lynne Tudhope, Gerda van Rensburg Neuropathy and foot problems in type 2 diabetes

6 The Guideline & Steering Committee (4) Chairperson: Aslam Amod Section 5Diabetes in Special Circumstances Yasmin Ganie, Michelle Carrihill Type 2 diabetes in children and adolescents, management of sick days Sophie RauffType 2 diabetes in older persons Danie van ZylType 2 diabetes in high risk ethnic groups Hoosen RandereeType 2 diabetes during Ramadaan Duma KhutsoaneType 2 diabetes in HIV infected individuals Pankaj JoshiPrevention/Delay of Type 2 Diabetes Peter RaubenheimerDiabetes and driving

7 The Advisory Committee SEMDSA / Association of Clinical Endocrinologists (ACE-SA) Members Philip Erasmus, Gregory Arthur Hough, Stanley Landau, Puvanesveri Naiker, MAK Omar, Helena Oosthuizen, William Toet, Carsten Weinreich, Holger Wellmann Department of Health (Chronic Diseases) Anne Croasdale, Melvyn Freeman, Sandhya Singh Society of General / Family Practitioners, Angelique Coetzee, Philip Erasmus Diabetes Education Society of South Africa (DESSA) Jeannie Berg, Gerda van Rensburg, Madelein Young Diabetes South Africa (DSA) Leigh-Ann Bailie, Ranga Kuni Medical Aids Margaret Campbell (Discovery) Council of Medical Schemes (CMS) Selaelo Mametja

8 Introduction Target Audience – All healthcare professionals (medical & allied) – Focus on primary care, but also general physician – Funders of healthcare – Undergraduates and postgraduates Not for “experts ” – Self-proclaimed or otherwise Disclaimer International Diabetes Federation. IDF Diabetes Atlas [cited 2012 Mar 18]. Available from: http:// www.idf.org/diabetesatlas

9 Disclaimer This guideline is not intended to replace professional judgement, experience and appropriate referral. These guidelines are intended to inform general patterns of care, to enhance diabetes prevention efforts and to reduce the burden of diabetes complications in people living with this disease. They reflect the best available evidence at the time, and practitioners are encouraged to keep updated with the latest information in this rapidly changing field. While every care has been taken to ensure accuracy, reference to product information is recommended before prescribing. SEMDSA assumes no responsibility for personal or other injury, loss or damage that may result from the information in this publication. Unless otherwise specified, these guidelines pertain to the care of adults with type 2 diabetes at primary care level.

10 Epidemiology / Prevalence Type 2 > 90% – Local studies using 1985 WHO criteria Rural African: 3.5% Urban Coloured: 10.8% Urban Indian: 13% 30-85% undiagnosed – >90% are obese IDF Atlas 5 th edition 6.5% of adults aged 20-79 years International Diabetes Federation. IDF Diabetes Atlas [cited 2012 Mar 18]. Available from: http:// www.idf.org/diabetesatlas

11 Diagnosis and screening

12 Diagnosis (WHO criteria) Diagnostic testIFGIGTDiabetes Fasting plasma glucose (FPG) a Two-hour plasma glucose (2-h PG) during oral glucose tolerance test (OGTT) b Glycated haemoglobin A 1c (HbA 1c ) c Random plasma glucose (RPG) d World Health Organization. Definition and diagnosis of diabetes mellitus and intermediate hyperglycaemia [cited 2011 Sep 20]. Available from: http://whqlibdoc.who.int/publications/2006/9241594934_eng.pdf.

13 Diagnosis (WHO criteria) Diagnostic testIFG Fasting plasma glucose (FPG) a 6.1 to 6.9 mmol/L Two-hour plasma glucose (2-h PG) during oral glucose tolerance test (OGTT) b <7.8 mmol/L (if measured) Glycated haemoglobin A 1c (HbA 1c ) c - Random plasma glucose (RPG) d -

14 Diagnosis (WHO criteria) Diagnostic testIGT Fasting plasma glucose (FPG) a <7.0mmol/L (if measured) Two-hour plasma glucose (2-h PG) during oral glucose tolerance test (OGTT) b 7.8 to 11.0 mmol/L Glycated haemoglobin A 1c (HbA 1c ) c - Random plasma glucose (RPG) d -

15 Diagnosis (WHO criteria) Diagnostic testDiabetes Fasting plasma glucose (FPG) a > 7.0 mmol/l, or Two-hour plasma glucose (2-h PG) during oral glucose tolerance test (OGTT) b > 11.1 mmol/l, or Glycated haemoglobin A 1c (HbA 1c ) c > 6.5%, or Random plasma glucose (RPG) d ≥ 11.1 mmol/l if classic symptoms or hyperglycaemic crisis is present

16 Diagnosis (WHO criteria) Diagnostic testIFGIGTDiabetes Fasting plasma glucose (FPG) a 6.1 to 6.9 mmol/L <7.0mmol/L (if measured) > 7.0 mmol/l, or Two-hour plasma glucose (2-h PG) during oral glucose tolerance test (OGTT) b <7.8 mmol/L (if measured) 7.8 to 11.0 mmol/L > 11.1 mmol/l, or Glycated haemoglobin A 1c (HbA 1c ) c --> 6.5%, or Random plasma glucose (RPG) d -- ≥ 11.1 mmol/l if classic symptoms or hyperglycaemic crisis is present

17 Diagnosis (WHO criteria) Diagnostic testIFGIGTDiabetes Fasting plasma glucose (FPG) a 6.1 to 6.9 mmol/L <7.0mmol/L (if measured) > 7.0 mmol/l, or Two-hour plasma glucose (2-h PG) during oral glucose tolerance test (OGTT) b <7.8 mmol/L (if measured) 7.8 to 11.0 mmol/L > 11.1 mmol/l, or Glycated haemoglobin A 1c (HbA 1c ) c --> 6.5%, or Random plasma glucose (RPG) d -- ≥ 11.1 mmol/l if classic symptoms or hyperglycaemic crisis is present For clinical purposes, the diagnosis of diabetes should always be confirmed by repeating the test on another day (preferably the same test), unless there is unequivocal hyperglycaemia with acute metabolic decompensation or obvious symptoms (polyuria, polydipsia and weight loss).

18 Diagnosis (WHO criteria) Diagnostic testIFGIGTDiabetes Fasting plasma glucose (FPG) a 6.1 to 6.9 mmol/L <7.0mmol/L (if measured) > 7.0 mmol/l, or Two-hour plasma glucose (2-h PG) during oral glucose tolerance test (OGTT) b <7.8 mmol/L (if measured) 7.8 to 11.0 mmol/L > 11.1 mmol/l, or Glycated haemoglobin A 1c (HbA 1c ) c --> 6.5%, or Random plasma glucose (RPG) d -- ≥ 11.1 mmol/l if classic symptoms or hyperglycaemic crisis is present a “Fasting” is defined as no caloric intake for at least eight hours b The test should be performed as described by the WHO, using a glucose load containing the equivalent of 75 g anhydrous glucose dissolved in 250 ml water ingested over five minutes

19 Diagnosis (WHO criteria) Diagnostic testIFGIGTDiabetes Fasting plasma glucose (FPG) a 6.1 to 6.9 mmol/L <7.0mmol/L (if measured) > 7.0 mmol/l, or Two-hour plasma glucose (2-h PG) during oral glucose tolerance test (OGTT) b <7.8 mmol/L (if measured) 7.8 to 11.0 mmol/L > 11.1 mmol/l, or Glycated haemoglobin A 1c (HbA 1c ) c --> 6.5%, or Random plasma glucose (RPG) d -- ≥ 11.1 mmol/l if classic symptoms or hyperglycaemic crisis is present d The classic symptoms of hyperglycaemia include polyuria, polydipsia and weight loss. “Hyperglycaemic crisis” refers to diabetic ketoacidosis or hyperosmolar nonketotic hyperglycaemia.

20 Diagnosis (WHO criteria) Diagnostic testIFGIGTDiabetes Fasting plasma glucose (FPG) a 6.1 to 6.9 mmol/L <7.0mmol/L (if measured) > 7.0 mmol/l, or Two-hour plasma glucose (2-h PG) during oral glucose tolerance test (OGTT) b <7.8 mmol/L (if measured) 7.8 to 11.0 mmol/L > 11.1 mmol/l, or Glycated haemoglobin A 1c (HbA 1c ) c --> 6.5%, or Random plasma glucose (RPG) d -- ≥ 11.1 mmol/l if classic symptoms or hyperglycaemic crisis is present c Provided that: -The test method meets stringent quality assurance criteria -The assay is NGSP certified and standardised to the DCCT assay -There are no conditions present which preclude its accurate measurement

21 Use of HbA 1c in the diagnosis of diabetes mellitus For the diagnosis of diabetes HbA 1c > 6.5% HbA 1c < 6.5% does not exclude diagnosis by blood glucose Glucose–based tests (FPG, OGTT) are still valid Interpretation of HbA 1c < 6.5% No recommendation, because of insufficient evidence

22 Use of HbA 1c in the diagnosis of diabetes mellitus Requirements to fulfill (provisos) for use of HbA 1c for diagnosis Stringent quality assurance tests in place a Assays standardised to criteria aligned with international reference values b Low cost and wide availability No conditions present which preclude accurate measurement a Appropriate conditions for assay method: Standardised assay, low coefficient of variability, and calibrated against International Federation of Clinical Chemists (IFCC) standards b DCCT aligned and NGSP certified

23 Use of HbA 1c in the diagnosis of diabetes mellitus Choice between HbA 1c and plasma glucose should be based on local considerations Cost Availability of equipment National quality-assurance system Population characteristics (e.g. prevalence of malaria or haemoglobinopathies) Crucial to ensure that accurate blood glucose measurement be generally available at primary healthcare level before introducing HbA 1c measurement as a diagnostic tool

24 Factors which influence HbA 1c measurement Erythropoiesis Increased HbA 1c : Iron deficiency, vitamin B 12 deficiency, decreased erythropoiesis Decreased HbA 1c : Administration of erythropoietin, iron or vitamin B 12, reticulocytosis, chronic liver disease Altered haemoglobin Genetic or chemical alterations in haemoglobin may increase or decrease HbA 1c : Haemoglobinopathies, HbF, methaemoglobin Glycation Increased HbA 1c : Alcoholism, chronic renal failure Decreased HbA 1c : Aspirin, vitamins C and E, certain haemoglobinopathies, increased intra-erythrocyte pH Erythrocyte destruction Increased HbA 1c with increased erythrocyte life span: Splenectomy Decreased HbA 1c with decreased erythrocyte life span: Haemoglobinopathies, splenomegaly, rheumatoid arthritis, drugs (e.g. antiretrovirals, ribavirin, dapsone) Assays Increased HbA 1c : Hyperbilirubinaemia, carbamylated haemoglobin, alcoholism, large doses of aspirin, chronic opiate use Decreased HbA 1c : Hypertriglyceridaemia Variable HbA 1c : Haemoglobinopathies Note: Some of these factors cannot be detected by certain assays

25 Screening Diagnosis vs. screening Targeted screening advocated – High rate of undiagnosed diabetes – Age > 45 or any age with multiple risk factors – Repeat every 3 yrs or more frequently – Use FPG, OGTT or HbA1C Exclude diabetes – FPG < 5.6 mmol/L; if not do OGTT – RPG < 5.6 mmol/L; if not do FPG or OGTT – HbA1C – do OGTT if 6.0 to 6.4%

26 Random PG <5.6 mmol/L <5.6 mmol/L 5.6 – 11.0 mmol/L 5.6 – 11.0 mmol/L ≥ 11.1 mmol/L + Symptoms Diabetes excluded Inconclusive Do FPG or OGTT Inconclusive Do FPG or OGTT Diabetes

27 Fasting PG <5.6 mmol/L <5.6 mmol/L 6.0 – 6.9 mmol/L 6.0 – 6.9 mmol/L 5.6 – 5.9 mmol/L 5.6 – 5.9 mmol/L ≥ 7.0 mmol/L ≥ 7.0 mmol/L Diabetes excluded IFG (Repeat) IFG (Repeat) Inconclusive Do OGTT Inconclusive Do OGTT Diabetes (Repeat) Diabetes (Repeat)

28 HbA 1C Normal 6.0 – 6.4 % 6.0 – 6.4 % Normal – 5.9 % Normal – 5.9 % ≥ 6.5 % ≥ 6.5 % Diabetes excluded Inconclusive Do FPG/OGTT Inconclusive Do FPG/OGTT Clinical judgement Diabetes (Repeat) Diabetes (Repeat)

29 2hr OGTT < 7.8 mmol/L < 7.8 mmol/L 7.8 – 11.0 mmol/L 7.8 – 11.0 mmol/L ≥ 11.1 mmol/L Diabetes excluded IGT (Repeat) IGT (Repeat) Diabetes (Repeat) Diabetes (Repeat)

30 Glycaemic targets

31 Individualised glycaemic targets Patient typeTarget HbA 1c Target FPGTarget PPG Young Newly diagnosed No cardiovascular disease Low CV risk < 6.5% 4.0 - 7.0 mmol/l 4.4 - 7.8 mmo/l Majority of patients< 7% 4.0 - 7.0 mmol/l 5.0 -10.0 mmol/l Elderly Hypoglycaemic unaware Poor short-term prognosis Established CV disease High CV risk < 7.5% (< 8.0%) 5.0 - 8.0 mmol/l < 12.0 mmol/l

32 Translating HbA1C into estimated average glucose (eAG) HbA 1c (%) Estimated average glucose (mmol/L) 67.0 78.6 810.2 911.8 1013.4 1114.9 1216.5 Nathan DM et al for the A1c-Derived Average Glucose (ADAG) Study Group. Translating the A1C assay into estimated average glucose values. Diabetes Care 2008; 31: 1473– 1478

33 Glycaemic control: Pharmacological therapy

34 General Considerations Type 2 diabetes is not a homogeneous disease – Try to understand the pathophysiology in each individual patient Majority of patients treated at PHC level – Poor access to / use of laboratory testing esp. HbA 1C and renal function – Increase number of agents that can be prescribed safely by PHC doctors and nurses without complex monitoring Accumulating data on dangers of hypoglycaemia as a risk marker for CV death Potential remission / cure in obese patients with substantial weight loss

35 Alternative therapies for special circumstances c Preferred therapies SU = sulphonylurea. Not glibenclamide ; DPP-4i = Dipeptidyl peptidase inhibitor; eGFR = estimated glomerular filtration rate a Severe decompensation includes any of: FPG > 15mmol/L, HbA1C > 11%, marked polyuria & polydipsia, weight loss > 5% or ketoacidosis. Refer the patient for specialist care (Step 4). b Refer to Table I for expected HbA1C reductions. c Refer to text d If at diagnosis, the patient’s HbA1C is >9% without features of severe decompensation, consider initiating therapy at STEP 2. Use this algorithm only if the patient does NOT have features of severe decompensation a. Progress down this algorithm within 3 months if HbA1C remains above 7% (or individualised target). Choose therapies that are likely to produce the HbA1c reduction required to achieve the target b Do not proceed with drug therapy without annual serum eGFR measurement Incretin Acarbose STEP 2: COMBINE ANY 2 DRUGS d STEP 3: COMBINE 3 DRUGS Basal Insulin Metformin + SU + Acarbose Metformin + SU + Incretin STEP 4: MORE ADVANCED THERAPIES SU DPP-4i Acarbose Metformin + Pre-mix insulin (if not used yet) SU Metformin + SU + Basal Insulin (or Metformin + Pre-mix) Metformin Refer to specialist for Basal + mealtime insulin ± Metformin ± Acarbose ± Incretin Refer to specialist for Basal + mealtime insulin ± Metformin ± Acarbose ± Incretin Metformin Lifestyle measures plus STEP 1: INITIATE AT LEAST ONE ORAL DRUG AT DIAGNOSIS Glycaemic control: SEMDSA 2012 algorithm for type 2 diabetes

36 Use this algorithm only if the patient does NOT have features of severe decompensation a. Progress down this algorithm within 3 months if HbA1C remains above 7% (or individualised target). Choose therapies that are likely to produce the HbA1c reduction required to achieve the target b Do not proceed with drug therapy without annual serum creatinine / eGFR measurement a Severe decompensation includes any of: FPG > 15mmol/L, HbA1C > 11%, marked polyuria & polydipsia, weight loss > 5% or ketoacidosis. Refer the patient for specialist care (Step 4). b Refer to Table for expected HbA1C reductions.

37 Alternative therapies for special circumstances Preferred therapies Glycaemic control: SEMDSA 2012 algorithm STEP 1: INITIATE AT LEAST ONE ORAL DRUG AT DIAGNOSIS SU DPP-4i Acarbose Metformin Lifestyle measures plus

38 Alternative therapies for special circumstances Preferred therapies Glycaemic control: SEMDSA 2012 algorithm STEP 1: INITIATE AT LEAST ONE ORAL DRUG AT DIAGNOSIS SU DPP-4i Acarbose Metformin Lifestyle measures plus Incretin Acarbose STEP 2: COMBINE ANY 2 DRUGS d Basal Insulin SU Metformin d If at diagnosis, the patient’s HbA1C is >9% (but without features of severe decompensation), consider initiating therapy at STEP 2

39 Alternative therapies for special circumstances Preferred therapies Glycaemic control: SEMDSA 2012 algorithm STEP 1: INITIATE AT LEAST ONE ORAL DRUG AT DIAGNOSIS SU DPP-4i Acarbose Metformin Lifestyle measures plus Incretin Acarbose STEP 2: COMBINE ANY 2 DRUGS d Basal Insulin SU Metformin STEP 3: COMBINE 3 DRUGS Metformin + SU + Acarbose Metformin + SU + Incretin Metformin + SU + Basal Insulin (or Metformin + Pre-mix)

40 Alternative therapies for special circumstances Preferred therapies Glycaemic control: SEMDSA 2012 algorithm STEP 1: INITIATE AT LEAST ONE ORAL DRUG AT DIAGNOSIS SU DPP-4i Acarbose Metformin Lifestyle measures plus Incretin Acarbose STEP 2: COMBINE ANY 2 DRUGS d Basal Insulin SU Metformin STEP 3: COMBINE 3 DRUGS Metformin + SU + Acarbose Metformin + SU + Incretin Metformin + SU + Basal Insulin (or Metformin + Pre-mix) STEP 4: MORE ADVANCED THERAPIES Metformin + Pre-mix insulin (if not used yet) Refer to specialist for Basal + mealtime insulin ± Metformin ± Acarbose ± Incretin Refer to specialist for Basal + mealtime insulin ± Metformin ± Acarbose ± Incretin

41 Non-insulin therapies Metformin A1c ↓Therapeutic considerationsDisadvantages ↓↓ Negligible hypoglycaemia risk as monotherapy Weight neutral (promotes less weight gain when combined with other agents). Proven reduction in CV events and mortality in obese subjects (primary endpoint in UKPDS). Metformin-XR has better GI tolerability (is preferred to switching to another class). Frequent GI side effects; 5-10% discontinuation. Lactic acidosis (rare). Vitamin B 12 deficiency. Renal impairment: reduce dose to 1000mg/d if eGFR <45 and discontinue if eGFR < 30ml/min/1.73m 2 Contraindications: Cardiac failure, PAD, Liver disease, COPD, IV Contrast media

42 Metformin in the 2012 SEMDSA algorithm Step 1: Monotherapy – Initial therapy of choice – Start at time of diagnosis in all patients (overweight and normal weight) unless specifically contra-indicated. Step 2: Dual therapy – Can be added as a second-line agent in patients where treatment has been initiated with any other class of anti- diabetic drug. It is recommended that metformin therapy continue even when other classes of anti-diabetic agents (including insulin) are added subsequently.

43 Sulphonylureas HbA1c Therapeutic considerationsDisadvantages ↓↓ Generally well tolerated. Proven reduction in microvascular endpoints. Relatively rapid glucose- lowering response. Consider using another class in patients at high risk of hypoglycaemia. If SU must be used in such individuals, gliclazide-MR < glimepiride / glipizide < glibenclamide. Can cause severe hypo, (especially glib. in renal impairment). Weight gain; 2 to 5kg; worst with glibenclamide May blunt myocardial ischemic preconditioning (especially glibenclamide). Glibenclamide contra- indicated if eGFR<60ml/min/1.73m 2 ; glimepiride and glipizide dose may need to be reduced.

44 SU in the 2012 SEMDSA algorithm Step 1: Monotherapy – at diagnosis in persons intolerant of metformin, or in normal weight individuals or those with marked symptoms of hyperglycaemia. Step 2: Dual therapy – Add as 2 nd drug to metformin, or any other drug used at Step 1 Step 3: Triple therapy – with metformin and basal insulin, or metformin and incretin. In gestational diabetes, glibenclamide is the sulphonylurea of choice (for specialist use only)

45 Non-insulin therapies Meglitinides HbA1c Therapeutic considerationsDisadvantages ↓ to ↓↓ Nateglinide is the least effective secretagogue. Targets postprandial glycemia; use if fasting glucose is at target but HbA1c remains high. Associated with less hypoglycemia compared to SU in the context of missed meals; useful for patients with unpredictable meals. Causes hypoglycemia. Causes weight gain. May blunt myocardial ischemic preconditioning. Frequent dosing (mealtime).

46 Meglitinides in the 2012 SEMDSA algorithm Instead of SU – If FPG is at target but HbA 1C and PPG levels are elevated

47 Non-insulin therapies Acarbose HbA1c ↓Therapeutic considerationsDisadvantages ↓ Negligible hypoglycaemia risk as monotherapy. Non-systemic effect. Weight neutral. Targets post-prandial hyperglycaemia 49% reduction in CV risk (pre- planned 2 o analysis in STOP- NIDDM Trial) GI effects (gas, flatulence, diarrhea). Frequent dosing (mealtime).

48 Non-insulin therapies DPP-4 Inhibitors HbA1c Therapeutic considerationsDisadvantages ↓ Negligible hypoglycaemia risk as monotherapy Weight neutral. Improves post-prandial control. Drug-specific recommendations for hepatic and renal disease. Occasional reports of urticaria/angioedema Cases of pancreatitis observed Newer agent with unknown long-term safety.

49 DPP-4 inhibitors in the 2012 SEMDSA algorithm Contraindications to DPP-4 inhibitors  There is a compelling indication for insulin therapy  History of a serious hypersensitivity reaction to DPP-4 inhibitors.  Patients with a history of acute pancreatitis, chronic or recurring pancreatitis and those with pancreatic cancer.

50 DPP-4i and Acarbose in the 2012 SEMDSA algorithm At Step 3: Add-on therapy as part of an oral 3-drug regimen  Inadequate glycemic control on combination therapy with metformin and sulphonylurea, and  Patient is a poor candidate for insulin therapy, and  Required reduction in HbA 1C is < 1% Discontinue after 3-6 months if HbA 1C reduction is < 0.5%

51 DPP-4i and Acarbose in the 2012 SEMDSA algorithm At Step 2: Add-on therapy as part of an oral 2 drug regimen  Inadequate glycemic control on monotherapy with metformin or sulphonylurea, and  Unable to tolerate or has contraindications to addition of the 2 nd as yet unused agent from the above mentioned (metformin or sulphonylurea), and  Required reduction in HbA 1C is < 1% Discontinue after 3-6 months if HbA 1C reduction is < 0.5%

52 DPP-4i and Acarbose in the 2012 SEMDSA algorithm At Step 1: Use as monotherapy  Candidate for oral therapy and is intolerant of or has contraindications to use of both metformin and sulphonylureas, and  Required reduction in HbA 1C is < 1% Discontinue after 3-6 months if HbA 1C reduction is < 0.5%

53 GLP-1 Agonists HbA1c Therapeutic considerationsDisadvantages ↓↓ Negligible hypoglycaemia risk as monotherapy. Enhances satiety and causes weight loss. Possible potential for improved beta cell mass and function. Avoid initiating therapy in individuals whom the potential for dehydration poses a considerable risk (e.g., frail elderly, multiple co-morbid conditions, etc.) Injectable Initial GI side effects (nausea, vomiting, diarrhea) Cases of acute pancreatitis observed Causes C-cell hyperplasia / medullary thyroid tumors in animals (liraglutide) Newer agent with unknown long-term safety.

54 GLP-1 agonists in the 2012 SEMDSA algorithm Contraindications to GLP-1 use  There is a compelling indication for insulin therapy  History of hypersensitivity to GLP-1 agonist  Renal failure (consult product label to assess suitability)  Personal or family history of medullary thyroid carcinoma or Multiple Endocrine Neoplasia syndrome type 2 (liraglutide).  Patient has severe gastrointestinal disease, including gastroparesis.  Patient has a history of pancreatitis Relative exclusions to use include triglyceride level > 10mmol/L, gallstones with intact gallbladder, and alcohol abuse.  Planned treatment regimen includes a DPP-4 inhbitor, meglitinide or acarbose (unstudied)

55 GLP-1 agonists in the 2012 SEMDSA algorithm At Step 3: Add on therapy as part of a 3 drug regimen: Inadequate glycemic control on combination therapy with maximally tolerated doses of metformin and sulphonylurea, and  Patient is not a candidate for a 3 rd oral agent from step 3, and  Patient is a poor candidate for insulin therapy, and  Required reduction in HbA 1C is < 1.5% in order to reach patient specific goal Only continue therapy beyond 6 months if there has been a good clinical response to therapy: HbA 1C reduction >0.5% AND weight loss >3%, OR HbA 1C reduction >1%, OR Weight loss >5%

56 GLP-1 agonists in the 2012 SEMDSA algorithm At Step 2: Add on therapy as part of a 2 drug regimen:  Patient has not achieved desired HbA1c and with optimum doses of one oral agent and is not a candidate for any other agent (oral or insulin) available at Step 2; and  Required reduction in HbA 1C is < 1.5% in order to reach patient specific goal Only continue therapy beyond 6 months if there has been a good clinical response to therapy: HbA 1C reduction >0.5% AND weight loss >3%, OR HbA 1C reduction >1%, OR Weight loss >5%

57 Circumstances where insulin therapy may not be desirable Insulin allergy Failure or inability to master injections or self-titration Frequent or severe hypoglycemia despite multiple dosage adjustments Circumstances exist where the risk of severe hypoglycemia and/or its potential consequences are significant and/or catastrophic Workers with frequent rotating shifts Occupations such as truck or bus drivers / heavy machine operators) Obesity related morbidity which has worsened or is likely to worsen significantly with weight gain from insulin therapy

58 Thiazolidenediones Rosiglitazone – Increased CV outcome events – Voluntarily withdrawn in SA Other problems – Fluid retention, ppt heart failure – Weight gain – Long bone fractures – Bladder cancer Not included in the algorithm

59 Lipids

60 Lipid targets Aligned with LASSA and SA Heart Total cholesterol< 4.5mmol/L LDL cholesterol< 1.8mmol/L a HDL cholesterol > 1.0 mmol/L (men) > 1.2 mmol/L (women) Triglycerides< 1.7mmol/L a The LDL-cholesterol goal is < 2.5 mmol/l in patients with type 2 diabetes who meet all of the following criteria: 1.No cardiovascular disease and no chronic kidney disease 2.Less than 40 years old OR duration of diabetes less than 10 years 3.No other cardiovascular risk factor

61 Lipids Measure 10-hr fasting lipid profile at diagnosis Subsequent monitoring targeted only at abnormalities (no need for full profile in every patient) Specialist referral: TG > 5 mmol/l in the controlled diabetic, or > 15 mmol/l before treatment.

62 Initiate statin therapy in all patients with: Existing cardiovascular disease (i.e. ischaemic heart disease, cerebrovascular disease or peripheral vascular disease). Chronic kidney disease (eGFR < 60 ml/minute/1.73m 2 ). Age >40 years or diabetes duration >10 yrs with one or more additional cardiovascular risk factor – hypertension, cigarette smoker, low HDL-cholesterol level, family history of early coronary heart disease, microalbuminuria

63 Statins Consider statin + ezetimibe if patient is unable to tolerate / achieve LDL cholesterol goals on the maximum dose of a highly potent statin Simvastatin should not be co-prescribed with most antiretroviral agents Use low doses of simvastatin with CCB’s. Never initiate therapy with Simvastatin 80 mg/day

64 Referrals Baseline TG >15mmol/L TG > 5mmol/l with low HDL, despite good glycaemic control Combination therapy (statin + fibrate) being considered.

65 Blood pressure

66 Highlights: Blood pressure targets Previous SBP target lacks clinical evidence base Definition of hypertension – SBP ≥ 140mmHg – DBP ≥ 80mmHg Target BP – SBP 120-140mmHg – DBP 70-80mmHg Rhonda M, Cooper-DeHoff, Egelund EF, Pepine C. Blood pressure lowering in patients with diabetes—one level might not fit all. Nature Reviews Cardiology. 2011;8:42-49

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68 In-hospital management: regular meal pattern maintained Well controlled – Continue usual therapy Poorly controlled: Basal bolus therapy – Estimate TDD (conservatively 0.2 to 0.5u/kg) – Basal (50%) + prandial (50%) insulin Correction dose insulin – Correction factor (CF) = 100/TDD or 85/TDD – Correction dose = (Measured BG – target BG) ÷ CF Umpierrez G, Smiley D, Zisman A, et al. Randomized study of basal-bolus insulin therapy in the inpatient management of patients with type 2 diabetes (RABBIT 2 trial). Diabetes Care. 2007;30:2181-2186.

69 Example 45yr old weighing 100kg taking Actraphane 40u/20u BID prior to hospitalisation – Estimated TDD = 60u – Give 30u NPH/long acting analogue at night + – 10u TDS rapid analogue or short acting regular – Target preprandial glucose 7.8mmol/L; <10 at any other time – CF = 100/60 = 1.7 (85/60 for regular human insulin) If post-meal BG is 20mmol/L, correction dose = 20 (current) - 10 (target) x 1.7 =17u Add 80% of daily correction dose to next days basal-bolus insulin

70 In-hospital management: regular meal pattern disrupted NPO – Use only correction dose insulin, or NPH twice daily or long acting analogue once daily Bolus eneteral feeds – Basal bolus therapy + correction doses Continuous enteral feeds – NPH 12-hrly or long acting analogue ± scheduled regular insulin, OR – Premixed insulin 8-hourly TPN – IV insulin infusion (infusion protocol), or – 50% TDD added to TPN as regular insulin, and 50% given as basal – Calculate TDD : 1u/10g carbohydrate

71 In-hospital management: critically ill patients Insulin infusion preferred if facilities and staff training exist; if not use basal-bolus + correction doses Target BG is 7.8 – 10.0 mmol/L; not lower than 6.1mmol/L Mix 50u insulin in 100ml 5% dextrose water Detailed response protocol needed for staff Glucose (mmol/l) 10.0-13.914.0-16.616.7-20.0>20.0 Bolus injection 4 units6 units8 units10 units Infusion rate 2 u/hr3 u/hr4 u/hr5 u/hr Adapted from Gunderson Lutheran Medical Center protocol Am J Health –Syst Pharm 2007; 64: 392

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73 ADA/EASD 2012 Algorithm


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