2008 Clinical Practice Guidelines - Canadian Diabetes Association

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2008 CLINICAL PRACTICE GUIDELINES S16 factors on having undiagnosed type 2 diabetes differs between populations of different ethnic origins, and risk scores developed in Caucasian populations cannot be applied to populations of other ethnic groups (16). RECOMMENDATIONS 1. All individuals should be evaluated annually for type 2 diabetes risk on the basis of demographic and clinical criteria [Grade D, Consensus]. 2. Screening for diabetes using an FPG should be performed every 3 years in individuals ≥40 years of age [Grade D, Consensus]. More frequent and/or earlier testing with either an FPG or a 2hPG in a 75-g OGTT should be considered in people with additional risk factors for diabetes [Grade D, Consensus].These risk factors include: • First-degree relative with type 2 diabetes • Member of high-risk population (e.g. people of Aboriginal, Hispanic,Asian, South Asian or African descent) • History of IGT or IFG • Presence of complications associated with diabetes • Vascular disease (coronary, cerebrovascular or peripheral) • History of gestational diabetes mellitus • History of delivery of a macrosomic infant • Hypertension • Dyslipidemia • Overweight • Abdominal obesity • Polycystic ovary syndrome • Acanthosis nigricans • Schizophrenia • Other risk factors (see Appendix 1) 3.Testing with a 2hPG in a 75-g OGTT should be undertaken in individuals with an FPG of 6.1 to 6.9 mmol/L in order to identify individuals with IGT or diabetes [Grade D, Consensus]. 4.Testing with a 2hPG in a 75-g OGTT may be undertaken in individuals with an FPG of 5.6 to 6.0 mmol/L and ≥1 risk factors in order to identify individuals with IGT or diabetes [Grade D, Consensus]. OTHER RELEVANT GUIDELINES Definition, Classification and Diagnosis of Diabetes and Other Dysglycemic Categories, p. S10 Prevention of Diabetes, p. S17 Type 1 Diabetes in Children and Adolescents, p. S150 Type 2 Diabetes in Children and Adolescents, p. S162 RELEVANT APPENDIX Appendix 1. Etiologic Classification of Diabetes Mellitus REFERENCES 1. Harjutsalo V, Reunanen A,Tuomilehto J. Differential transmission of type 1 diabetes from diabetic fathers and mothers to their offspring. Diabetes. 2006;55:1517-1524. 2. Decochez K, Truyen I, van der Auwera B, et al; Belgian Diabetes Registry. Combined positivity for HLA DQ2/DQ8 and IA-2 antibodies defines population at high risk of developing type 1 diabetes. Diabetologia. 2005;48:687-694. 3. Bingley PJ. Interactions of age, islet cell antibodies, insulin autoantibodies, and first-phase insulin response in predicting risk of progression to IDDM in ICA+ relatives: the ICARUS data set. Islet Cell Antibody Register Users Study Diabetes. 1996; 45:1720-1728. 4. Cowie CC, Rust KF, Byrd-Holt DD, et al. Prevalence of diabetes and impaired fasting glucose in adults in the U.S. population: National Health And Nutrition Examination Survey 1999-2002. Diabetes Care. 2006;29:1263-1268. 5. Rolka DB, Narayan KM, Thompson TJ, et al. Performance of recommended screening tests for undiagnosed diabetes and dysglycemia. Diabetes Care. 2001;24:1899-1903. 6. Rathmann W, Haastert B, Icks A, et al. High prevalence of undiagnosed diabetes mellitus in Southern Germany: target populations for efficient screening. The KORA survey 2000. Diabetologia. 2003;46:182-189. 7. Raikou M, McGuire A.The economics of screening and treatment in type 2 diabetes mellitus. Pharmacoeconomics. 2003;21: 543-564. 8. The cost-effectiveness of screening for type 2 diabetes. CDC Diabetes Cost-Effectiveness Study Group, Centers for Disease Control and Prevention. JAMA. 1998;280:1757-1763. 9. Knowler WC. Screening for NIDDM. Opportunities for detection, treatment, and prevention. Diabetes Care. 1994;17: 445-450. 10. Leiter LA, Barr A, Bélanger A, et al; Diabetes Screening in Canada (DIASCAN) Study. Diabetes Screening in Canada (DIASCAN) Study: prevalence of undiagnosed diabetes and glucose intolerance in family physician offices. Diabetes Care. 2001;24:1038-1043. 11. Saydah SH, Byrd-Holt D, Harris MI. Projected impact of implementing the results of the Diabetes Prevention Program in the U.S. population. Diabetes Care. 2002;25:1940-1945. 12. McKee HA, D’Arcy PF,Wilson PJ. Diabetes and schizophrenia — a preliminary study. J Clin Hosp Pharm. 1986;11:297-299. 13. Mukherjee S, Decina P, Bocola V, et al. Diabetes mellitus in schizophrenic patients. Compr Psychiatry. 1996;37:68-73. 14. Dixon L, Weiden P, Delahanty J, et al. Prevalence and correlates of diabetes in national schizophrenia samples. Schizophr Bull. 2000;26:903-912. 15. Hu G, Qiao Q, Tuomilehto J, et al; DECODE Study Group. Prevalence of the metabolic syndrome and its relation to allcause and cardiovascular mortality in nondiabetic European men and women. Arch Intern Med. 2004;164:1066-1076. 16. Glumer C,Vistisen D, Borch-Johnsen K, et al for the Detect 2 Collaboration. Risk scores for type 2 diabetes can be applied in some populations but not all. Diabetes Care. 2006;29:410-414.
Prevention of Diabetes Canadian Diabetes Association Clinical Practice Guidelines Expert Committee The initial draft of this chapter was prepared by Ehud Ur MB FRCP, Jean-Louis Chiasson MD, Tom Ransom MD MSc FRCPC and Richard Rowe MBBS MAEd FRCPC KEY MESSAGES • As safe and effective preventive therapies for type 1 diabetes have not yet been identified, any attempts to prevent type 1 diabetes should be undertaken only within the confines of formal research protocols. • Intensive and structured lifestyle modification that results in loss of approximately 5% of initial body weight can reduce the risk of progression from impaired glucose tolerance to type 2 diabetes by almost 60%. • Progression from prediabetes to type 2 diabetes can also be reduced by pharmacologic therapy with metformin (~30% reduction), acarbose (~30% reduction) and thiazolidinedione (~60% reduction). PREVENTION OF TYPE 1 DIABETES Two major trials of interventions to prevent or delay the onset of type 1 diabetes have recently been completed. The European Nicotinamide Diabetes Intervention Trial (ENDIT), a randomized, double-blind, placebo-controlled trial of high-dose nicotinamide therapy, recruited firstdegree relatives of people who were >20 years old when diagnosed with type 1 diabetes, islet cell antibody-positive, >40 years of age and had a normal oral glucose tolerance test (OGTT) result. Although nicotinamide had proved protective in animal studies, no effect was observed in the ENDIT study during the 5-year trial period (1). The Diabetes Prevention Trial–Type 1 (DPT-1) studied the efficacy of low-dose insulin injections in high-risk (>50%) first-degree relatives of subjects with type 1 diabetes. Overall, the insulin treatments had no effect (2), but in a subset of participants with high levels of insulin autoantibodies, a delay, and perhaps a reduction, in the incidence of type 1 diabetes was observed (3). As safe and effective preventive therapies for type 1 diabetes have not yet been identified, any attempts to prevent type 1 diabetes should be undertaken only within the confines of formal research protocols. PREVENTION OF TYPE 2 DIABETES Preventing type 2 diabetes would result in significant public health benefits, including lower rates of cardiovascular disease (CVD), renal failure, blindness and premature mortality. An epidemiologic analysis projected that if all diabetes could be avoided in white American males through effective primary prevention, the risk of all-cause and cardiovascular mortality in the entire population could be reduced by up to 6.2 and 9.0%, respectively (4). Recent data from the US indicate that 28% of cardiovascular expenditures are attributable to diabetes (5). Primary approaches to preventing diabetes in a population include the following: 1) programs targeting high-risk individuals in the community (such as those with impaired glucose tolerance [IGT] or obesity); 2) programs targeting high-risk subgroups of the population, such as high-risk ethnic groups; and 3) programs for the general population, such as those designed to promote physical activity and healthy eating in adults or children (6-8). Prospective cohort studies have identified historical, physical and biochemical variables associated with the subsequent development of type 2 diabetes. These include older age, certain ethnic backgrounds, obesity (especially abdominal obesity), physical inactivity, history of gestational diabetes mellitus, overt coronary artery disease, high fasting insulin levels and IGT (9-11). Results of large, well-designed studies assessing lifestyle and pharmacologic interventions in adults to prevent the progression from IGT to diabetes have been published. Changes in lifestyle were assessed in the Finnish Diabetes Prevention Study (DPS) (12) and the Diabetes Prevention Program (DPP) (13). Dietary modification that targeted a low-calorie, low-fat, low-saturated fat, high-fibre diet and moderate-intensity physical activity of at least 150 minutes per week resulted in loss of approximately 5% of initial body weight. In both studies, the risk reduction for diabetes was 58% at 4 years. These studies included comprehensive, sustained programs to achieve these outcomes. In another lifestyle intervention trial (14), 458 Japanese males with IGT were randomly assigned in a 4:1 ratio to a standard intervention (n=356) or an intensive intervention (n=102) and followed for 4 years. Intensive treatment was associated with a 67.4% reduction in risk of diabetes (p
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