2008 Clinical Practice Guidelines - Canadian Diabetes Association

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<strong>2008</strong> CLINICAL PRACTICE GUIDELINES S110 Table 2B. Other lipid-modifying medications Drug class* Generic name* (trade name) Bile acid sequestrants • cholestyramine resin (Questran, Questran Light and generic) • colestipol HCl (Colestid) Cholesterol absorption inhibitor • ezetimibe (Ezetrol) Fibrates • bezafibrate (Bezalip and generic) • fenofibrate (micronized/microcoated) (Lipidil Micro/Lipidil Supra, Lipidil EZ and generic) • gemfibrozil (Lopid and generic) Nicotinic acid • Extended-release niacin (Niaspan) • Immediate-release niacin (generic, non-prescription) • Long-acting (e.g. “no-flush”) niacin (generic, nonprescription) Not recommended and mortality associated with prediabetes and metabolic syndrome, an aggressive approach aimed at associated CV risk factors, including dyslipidemia, is warranted. Lifestyle interventions aimed at reducing the risk of developing both type 2 diabetes and coronary disease are essential. TC/HDL-C RATIO, HDL-C,TG The TC/HDL-C ratio is a sensitive and specific index of CV risk (31). This simple lipid ratio is recommended as a secondary goal of therapy. Once the LDL-C goal of ≤2.0 mmol/L has been reached, one can consider lowering the TC/HDL- C ratio to the recommended goal of
mally controlled with a statin), niacin (immediate-release or extended-release formulation) is the adjuvant agent of choice. Combination lipid-lowering therapy with niacin is generally safe (32-35). Niacin can cause deterioration of glycemic control (32) (although there is now evidence that the adverse effects of niacin on glycemia may have been overemphasized [33]). In the placebo-controlled HDL Atherosclerosis Treatment Study (HATS) (34), combined low-dose simvastatin (10 to 20 mg/day) and high-dose niacin (2 to 4 g/day) stabilized coronary atherosclerosis with an associated ≥13% absolute risk reduction (up to 90% relative risk reduction) for CV outcomes, although the number of subjects with diabetes was small. In the Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol (ARBITER) 2 trial, 1 g extended-release niacin added to existing statin therapy significantly improved HDL-C (21%),TG and non- HDL-C, and likely contributed to observed reduction of carotid intima-media thickness in subjects also treated with a statin (35). Specific targets for TG are not provided in these guidelines because there are very few clinical trial data to support recommendations based on specific TG target levels. Nonetheless, aTG level of 10.0 mmol/L who do not respond to other measures such as tight glycemic control, weight loss and restriction of refined carbohydrates and alcohol. For those with moderate hyper-TG (4.5 to 10.0 mmol/L), either a statin or a fibrate can be attempted as first-line therapy, with the addition of a second lipid-lowering agent of a different class if target lipid levels are not achieved after 4 to 6 months on monotherapy.While several studies have shown that CVD prevention is associated with fibrate treatment (38-42), there is much less evidence for CVD risk reduction with fibrates relative to statins in people with diabetes. In some studies, no statistically significant reduction in the primary endpoint was demonstrated with fibrate therapy (43,44). Combination therapy with fenofibrate (45,46) or bezafibrate plus a statin appears to be relatively safe if appropriate precautions are taken (Tables 2A and 2B), but the efficacy of these approaches with regard to outcomes has yet to be established. Because of an increased risk of myopathy and rhabdomyolysis, statins should not be used in combination with gemfibrozil (47). Although monotherapy with niacin or fibrates has been shown to prevent CVD events, there is currently insufficient evidence for statin plus niacin and no evidence for fibrate plus niacin combinations to reduce CV risk in people with diabetes. However, adequately powered, event-reduction, prospective, randomized, controlled clinical trials are currently underway with various classes of agents to examine whether the addition of other therapies in individuals already treated with statins further reduces CV events and/or prolongs survival (Action to Control Cardiovascular Risk in <strong>Diabetes</strong> [ACCORD] for statin plus fibrate; Atherothrombosis Intervention in Metabolic Syndrome with Low HDL-C/High Triglyceride and Impact on Global Health Outcomes [AIM HIGH] for statin plus extended-release niacin). Until the results of these clinical trials become available, for high-risk individuals who have a persistent elevation of TC/HDL-C despite achieving the primary LDL-C target of ≤2.0 mmol/L, niacin or fibrates can be added to statin therapy at the physician’s discretion. ADDITIONAL LIPID MARKERS OF CVD RISK Apo B, Apo B/Apo A1 ratio There is 1 apolipoprotein B molecule (apo B) per LDL, very low-density lipoprotein and intermediate-density lipoprotein particle (all of which are atherogenic).Apo B has repeatedly been shown to be a better risk marker for CVD events than LDL-C; consequently, the measurement of apo B and its monitoring in response to lipid-lowering therapy has been advocated by some (48).The measurement of apo B is most clinically useful in the individual with hyper-TG, since it provides an indication of the total number of atherogenic lipoprotein particles in the circulation. In such cases, knowledge of the apo B level may guide the aggressiveness with which lipid-lowering therapy is pursued (i.e. more aggressive therapy in individuals in whom the apo B level is elevated).An optimal level of apo B in high-risk individuals has not yet been precisely determined, but based on available evidence can be considered to be ~
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2008 Clinical Practice Guidelines - Canadian Diabetes Association

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