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E6 Endocrinology
Rosuvastatin to Prevent Vascular Events in Men and Women with Elevated C-Reactive Protein (Jupiter Study)
NEJM 2008;359(21):2195-207
Study: Randomized Control Trial
Intervention: Statin Therapy
Results: Rosuvastatin reduced LDL cholesterol levels by 50% and high-sensitivity C-reactive protein levels by 37%. The rates of the primary end point were 0.77 and 1.36 per 100 person-years
of follow-up in the rosuvastatin and placebo groups, respectively (hazard ratio for rosuvastatin, 0.56; 95% confidence interval [CI], 0.46-0.69; P<0.00001), with corresponding rates of 0.17
and 0.37 for myocardial infarction (hazard ratio, 0.46; 95% CI, 0.30-0.70; P=0.0002), 0.18 and 0.34 for stroke (hazard ratio, 0.52; 95% CI, 0.34-0.79; P=0.002), 0.41 and 0.77 for revascularization or unstable angina (hazard ratio, 0.53; 95% CI, 0.40- 0.70; P<0.00001), 0.45 and 0.85 for the combined end point of myocardial infarction, stroke, or death from cardiovascular causes (hazard ratio, 0.53; 95% CI, 0.40-0.69; P<0.00001), and 1.00 and 1.25 for death from any cause (hazard ratio, 0.80; 95% CI, 0.67-0.97; P=0.02)
Conclusion: Statins reduce the incidence of major cardiovascular events even in healthy people without hyperlipidemia but with elevated c-reactive protein.
Three Year Efficacy of Complex Insulin Regimens in Type 2 DM: 4T Trial
NEJM 2009;361:1736-1747
Study: Randomized unblinded trial with 3 yr of follow-up.
Population: 708 patients with Type 2 DM, not on insulin or thiazolidinedione therapy on maximal metformin and sulfonylurea therapy.
Intervention: Thrice-daily prandial insulin aspart, versus twice-daily biphasic insulin aspart, versus once-daily basal insulin detemir. Sulfonylurea therapy was replaced with a secondary insulin regime specific to each arm if there was persistent hyperglycemia.
Primary Outcome: Three yr hemoglobin HbA1c. Results: Significant difference in rates of patient withdrawal from the study: 5.1% biphasic, 11.7% prandial, 8.5% basal regimens (p=0.04). There were no significant differences in median HbA1c levels between all three arms from yr 1-3. A smaller proportion of patients reached HbA1c <6.5% or <7.0% in the biphasic arm. The basal arm had least weight gain and least weight circumference increase, but highest rate of secondary insulin requirement. The basal arm had fewest severe hypoglycemic events per patient year, while the biphasic had the most serious adverse effects. Conclusion: Basal insulin regime provides the best glycemic control over a 3 yr study, with better HbA1c control, fewer hypoglycemic events, and less weight gain.
Disorders of Glucose Metabolism Toronto Notes 2019 Approach to Treatment
For clinical guidelines see Can J Cardiol 2016;32:1263-1282
• considertreatmentforpatientswithstatin-indicatedconditions;riskassessmentisnotrequired • forprimaryprevention:
■ estimate 10 yr risk of CAD using Framingham Risk Score (FRS) model ■ establish treatment targets
■ low FRS does not require statin treatment
Table 5. Treatment of Hypercholesterolemia and Hypertriglyceridemia
Treatment of Hypercholesterolemia
Conservative: 4-6 mo trial unless high risk group, in which case medical treatment should start immediately
Diet: Mediterranean, DASH or Portfolio diet Decrease fat: <30% calories
Decrease saturated fat: <10% calories Decrease cholesterol: <200 mg/d Increase fibre: >30 g/d
Decrease alcohol intake to ≤1-2 drinks/d
Smoking cessation
Aerobic exercise: ≥150 min/wk in bouts of ≥10 min Weight loss: target BMI <25
Medical: HMG-CoA reductase inhibitors, ezetimibe, bile acid sequestrants, PCSK9 inhibitors) (see Common Medications, E50)
Treatment of Hypertriglyceridemia
Conservative: 4-6 mo trial Diet:
Decrease fat and simple carbohydrates
Increase omega-3 polyunsaturated fatty acid
Control blood sugars
Stop alcohol for severe hyperTG, otherwise, intake to ≤1-2 drinks/d
Smoking cessation
Aerobic exercise: ≥150 min/wk in bouts of ≥10 min Weight loss: target BMI <25
Medical: fibrates, fish oil 1-12 g/d, rarely niacin (see Common Medications, E50)
Indications:
Failed conservative measures
TG >10 mmol/L (885 mg/dL) to prevent pancreatitis Combined hyperlipidemia
Disorders of Glucose Metabolism
Overview of Glucose Regulation
β cells of the pancreas stimulated to release insulin into the blood stream
Increase in blood glucose levels
Liver breaks down glycogen stores and releases glucose into the blood
Figure 4. Blood glucose regulation
Insulin
Body cells take up more glucose
Blood Glucose Level
Glucagon
Decrease in blood glucose levels
α cells of the pancreas stimulated to release glucagon into the blood
Liver takes up excess glucose and stores it as glycogen
α cells
Pre-Diabetes (Impaired Glucose Tolerance/
Impaired Fasting Glucose)
• 1-5%peryrgoontodevelopDM
• 50-80%reverttonormalglucosetolerance
• weightlossmayimproveglucosetolerance
• increasedriskofdevelopingmacrovascularcomplications(IGT>IFG) • lifestylemodificationsdecreaseprogressiontoDMby58%
Diagnostic Criteria (CDA Guidelines)
• impairedfastingglucose(IFG):fastingplasmaglucose(FPG)6.1-6.9mmol/L
• impairedglucosetolerance(IGT):2h75goralglucosetolerancetest(OGTT)7.8-11.0mmol/L • HbA1c: 6.0-6.4%
β cells
© Susan Le 2016