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Management of Type 2 Diabetes
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General approach to therapyNonpharmacologic
therapy Pharmacologic therapy
Treatment of concomitant diseases Treatment of acute complications Treatment of
chronic complications Outcome evaluation
Glycemic targets
●HbA1c < 7.0% (mean PG 150-160 mg/dl
●Pre-prandial PG <130 mg/dl●Post-prandial PG <180 mg/dl
●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
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Nonpharmacologic Therapy●Medical nutrition therapy
●recommended for all DM patients●provides optimal metabolic and physiologic outcomes
(glucose, lipids, BP, proteinuria, weight)
●prevents/treats chronic DM complications●Regulates insulin administration with a
balanced diet to achieve/maintain a healthy weight
●carbohydrate counting or exchanges
●Promotes weight loss to overweight patients●caloric restriction
●Moderate weight loss has been shown to reduce CV risk as well as delay or prevent the onset of DM in those with pre-diabetes (follow TLC)
●General rule for weight loss diet is that it should supply 1000-1200 kcal/day for women and 1200-1600 kcal/day for men.
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Nonpharmacologic Therapy●Exercise
●improves insulin resistance, glycemic control
●reduces CV risk (HTN and elevated serum lipids)
●helps with weight loss or maintenance
●improves well-being
●Patients without contraindications
● >150 min/week moderate-intensity aerobic exercise (50- 70% of maximum heart rate)
●resistance training for 30 min 3 times/week
●Start exercise slowly in previously sedentary patients.
Nonpharmacologic Therapy●Psychological assessment and care
●Determining the patient’s attitude regarding DM, expectations of medical management and outcomes, mood and affect, general and diabetes quality of life and financial, social and emotional resources.
●Immunization•Provide influenza vaccine annually to all diabetic patients
≥6 months of age•Administer pneumococcal polysaccharide vaccine to
all diabetic patients ≥2 years–One-time revaccination recommended for those >64 years previously
immunized at <65 yearsif administered >5 years ago
–Other indications for repeat vaccination: nephrotic syndrome, chronic renal disease, immunocompromised states
•Administer hepatitis B vaccination to unvaccinated adults with diabetes who are aged 19 through 59 years
•Consider administering hepatitis B vaccination to unvaccinated adults with diabetes who are aged ≥60 years
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Therapeutic options:●Oral agents & non-insulin injectables
●Metformin●Sulfonylureas
●Thiazolidinediones●DPP-4 inhibitors
●GLP-1 receptor agonists●a-glucosidase inhibitors
●Amylin mimetics
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Biguanide (Metformin)
GenericName
Dose (mg) Recommended StartingDosage (mg/day)
MaximumDose
(mg/day)
Duration ofAction
Metabolism or Therapeutic Notes
Nonelderly Elderly
Metformin 500, 850, 500 mg Assess renal 2,550 Up to 24 hours No metabolism; renally secreted and1,000 twice a day function excreted
Metformin 500, 750, 500–1,000 Assess renal 2,550 Up to 24 hours Take with evening meal or may splitextended- 1,000 mg with function dose; can consider trial if intolerant torelease evening immediate-release
meal133
●Enhance hepatic & peripheral (muscle) tissue insulin sensitivity
●increases uptake of glucose in tissues
●No direct effect on β cells●Decrease hepatic glucose production
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Biguanide: Effects●Average HbA1c reduction: 1.5 to 2.0%
●FBG reduction: 60 to 80 mg/dL●Reduce FBG levels when > 300 mg/dL
●Decrease plasma triglycerides & LDL-C by ~8 to 15%
●Increases HDL-C: 2%●Weight loss: 2 to 3 kg
●Use in all type 2 DM patients●if tolerated & not contraindicated
●only oral antidiabetic agent proven to reduce mortality risk
●UKPDS shows metformin is best suited for obese type 2 DM patients; reduces mortality
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Biguanide: Side effects & contraindications
●GI: abdominal discomfort, stomach upset, diarrhea
●minimize with slow dose titration
●may improve with time●administer with food to
lessen adverse effects●switch to extended-release
may improve tolerability●Weight loss can occur
●anorexia●stomach fullness
●Long term use – reduction in vitamin B12 levels
●Most common adverse●Contraindications: effects:
●High risk patients for lactic acidosis (due to decrease conversion of lactate to glucose (decreased gluconeogenesis) and increase lactate production in the gut and liver)
●CHF, hypoxic states, shock, septicemia, severe liver disease, alcohol use
●Renal insufficiency●SCr ≥ 1.4 mg/dL in
women●SCr ≥ 1.5 mg/dL in
men●Intravenous dye
procedures●risk of acute renal failure
●withhold the day of procedure
●may restart 2 to 3 days post- procedure
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Sulfonylureas●Enhance insulin secretion
●bind SUR receptors on pancreatic β cells●Elevated secretion of insulin from the
pancreas travels via the portal vein and subsequently suppresses hepatic glucose production.
●Classification: 1st & 2nd generation●differences in potency, adverse effects,
serum protein binding●no therapeutic superiority among agents
●Glipizide preferred over glyburide (Glibenclamide)
●glyburide requires adjustment for renal dysfunction; higher risk of hypoglycemia
SulfonylureasGeneric Name Dose
(mg)
Recommended Starting Dosage (mg/day)
Equivalent Therapeutic Dose (mg)
Maximum Dose
(mg/day)
Duration of Action
Metabolism or Therapeutic Notes
None Elderly
Elderly
1st Generation
Acetohexamide 250,500
250 125–250 500 1,500 Up to 16 hours
Metabolized in liver; metabolite potency equal to parent compound; renally eliminated
Chlorpropamide 100,250
250 100 250 500 Up to 72 hours
Metabolized in liver; also excreted unchanged renally
Tolazamide 100,250,500
100–250 100 250 1,000 Up to 24 hours
Metabolized in liver; metabolite less active than parent compound; renally eliminated
Tolbutamide 250,500
1,000–2,000 500–1,000
1,000 3,000 Up to 12 hours
Metabolized in liver to inactive metabolites that are renally excreted
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SulfonylureasGeneric Name Dose
(mg)
Recommended Starting Dosage (mg/day)
Equivalent Therapeutic Dose (mg)
Maximum Dose
(mg/day)
Duration of Action
Metabolism or Therapeutic Notes
None Elderly
Elderly
2nd Generation
Glipizide 5, 10 5 2.5–5 5 40 Up to 20 hours
Metabolized in liver to inactive metabolites
Glipizide 2.5, 5,10, 20
5 2.5–5 5 20 24 hours Slow-release form; do not cut tablet
Glyburide 1.25,2.5, 5
5 1.25–2.5 5 20 Up to 24 hours
Metabolized in liver; elimination ½ renal, ½ feces
Glyburide, micronized
1.5, 3, 6 3 1.5–3 3 12 Up to 24 hours
Equal control, but better absorption from micronized preparation
Glimepiride 1, 2, 4 1–2 0.5–1 2 8 24 hours Metabolized in liver to inactive metabolites
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Sulfonylureas●Most common side effect: hypoglycemia
●higher with chlorpropamide & glyburide; longer t½
●high risk patients require lower doses●elderly
●renal/hepatic disease●patients that skip meals
●vigorous exercise●substantial weight loss
●Weight gain also common●Less common adverse effects: rash,
hemolytic anemia, GI upset, cholestasis
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Sulfonylureas●Tolbutamide, chlorpropamide
●hyponatremia may result from increased antidiuretic hormone
●disulfram-type reactions can result when alcohol is consumed
●Titrate sulfonylureas doses every 1 to 2 weeks
●Maximal effective dose ~60 to 75% stated max dose
●At equipotent doses, all sulfonylureas equally effective at lowering blood glucose
Sulfonylureas●All sulfonylureas are metabolized in
the liver●CYP2C9 involved in sulfonylurea
metabolism
aMany drug interactions metabolism-based
bInducer
Drug Interactions with Sulfonylureas
Interaction Drugs
Displacement from protein binding sitesa
warfarin, salicylates, phenylbutazone, sulfonamides
Alters sulfonylurea hepatic metabolism (cytochrome P450)
chloramphenicol, monoamine oxidase inhibitors, cimetidine, rifampinb
Altered renal excretion allopurinol, probenecid
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Sulfonylureas●Average HbA1c reduction: 1.5 to 2%
●FBG reduction: 60 to 70 mg/dL●Most patients do not reach glycemic
goal with monotherapy●1 ˚failure: < 30 mg/dL drop in FBG
●low C-peptide●high (> 250 mg/dL) FBG
●2˚failure: good initial response, but insufficient to reach or maintain glycemic goal
●5 to 7% per year failure rate
TZDs: Thiazolidinediones●May be used in type 2 DM therapy
●Enhance insulin sensitivity at muscle, liver, fat tissues
●Decrease hepatic glucose production●Requires presence of insulin
GenericName
Dose (mg) Recommended StartingDosage (mg/day)
MaximumDose
(mg/day)
Durationof Action
Metabolism or TherapeuticNotes
Nonelderly Elderly
Pioglitazone 15, 30, 45 15 15 45 24 hours Metabolized by CYP2C8 andCYP3A4; two metabolites have longer half-lives than parent compound
Rosiglitazone 2, 4, 8 2–4 2 8 mg/day or4 mg twice a
day
24 hours Metabolized by CYP2C8 andCYP2C9 to inactive metabolites that are renally excreted
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TZD Adverse Effects●May increase ALT
●CI if ALT > 2.5 times upper limit of normal (ULN)
●discontinue if ALT > 3 times ULN●troglitazone (1st approved TZD) removed from
market in 2000 due to deaths from liver failure
●Fluid retention●edema, dilutional anemia, pulmonary edema,
HF●CI in NYHA Class III & IV
●black box warning for chronic heart failure
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TZD Adverse Effects●Weight Gain
●1.5 to 4 kg●fluid retention & fat accumulation
●Increased fracture risk●upper & lower limbs of postmenopausal women
●Ovulation●anovulatory patients can resume ovulation
●pregnancy & contraception precautions required●pregnancy category C
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TZDs●Average HbA1c reduction ~1.5%
●FBG reduction: 60 to 70 mg/dL at max doses●Maximal glycemic-lowering effects after 3 to 4
months●Triglycerides:
●pioglitazone: 10 to 20% decrease●rosiglitazone: neutral effect
●LDL:●pioglitazone: no significant increase
●rosiglitazone: 5 to 15% increase
●HDL: both increase 3 to 9 mg/dL
α-Glucosidase Inhibitors●Competitively inhibit enzymes in the small intestine
●delay sucrose & complex carbohydrate breakdown
●Reduce postprandial hyperglycemia●Used in both type 1 & type 2 DM
GenericName
Dose (mg) Recommended Starting Dosage(mg/day)
Maximum Dose(mg/day)
Duration ofAction
Metabolism orTherapeutic Notes
Nonelderly Elderly
Acarbose 25, 50, 100 25 mg one to threetimes a day
25 mg one tothree times a day
25–100 mg threetimes a day
1–3 hours Eliminated inbile
Miglitol 25, 50, 100 25 mg one to threetimes a day
25 mg one tothree times a day
25–100 mg threetimes a day
1–3 hours Eliminatedrenally
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α-Glucosidase Inhibitors●Adverse effect:
●GI side effects most common●flatulence, bloating, abdominal discomfort, diarrhea
●may elevate serum aminotransferase
●Contraindications:●IBD
●colonic ulceration●intestinal obstruction
●cirrhosis
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α-Glucosidase Inhibitors●Efficacy
●reduce postprandial glucose 40 to 50 mg/dL●FBG relatively unchanged (~10% reduction)
●average HbA1c reduction: 0.3 to 1%●beneficial in patients close to target HbA1c
with near- normal FBG but high postprandial levels
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α-Glucosidase Inhibitor●May be monotherapy or used with
metformin, sulfonylureas, insulin●Initiate with very low dose
●25 mg with one meal a day
●Increase gradually to maximum dose●50 mg TID patients ≤ 60 kg
●100 mg TID patients > 60 kg
●Take with 1st bite of a meal●must be present to inhibit enzyme
activity
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Incretin-Based Therapies●The most recent advances in therapy for type 2 diabetes
have revolved around the discovery and exploration of the effects of incretins.
●Incretins are insulinotropic hormones secreted from specialized neuroendocrine cells in the small intestinal mucosa in response to carbohydrate ingestion and absorption.
●The two hormones accounting for most incretin effects are:
●glucose-dependent insulinotropic polypeptide (GIP)
●glucagonlike peptide-1 (GLP-1)●GIP and GLP-1 stimulate pancreatic β-cells in a glucose-
dependent manner, contributing to the early phase insulin response.
●GLP-1 also inhibits pancreatic α-cells, thus reducing glucagon secretion and hepatic glucose production.
●Incretin action is efficient, but short lived. As they enter the blood vessels, incretins undergo rapid metabolism via proteolytic cleavage by dipeptidyl peptidase-4 (DPP-4) to inactive metabolites. Thus, only small amounts are needed to exert their effects on glucose metabolism.
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GLP-1 Mimetics/Analogs: Exenatide●Synthetic analog of amino acid peptide
exendin-4●isolated from Gila monster saliva
●Mechanism similar to human GLP-1●enhances insulin secretion
●suppresses postprandial glucagon when blood glucose elevated; reduces hepatic glucose production
●Slows gastric emptying, reduces food intake, promotes weight loss
●Unlike GLP-1, exenatide does not increase gastric secretions
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Exenatide●Indication: adjunctive therapy for
type 2 DM●Not recommended in end-stage renal
disease or dialysis patients●prolongs t½
●increases incidence of GI side effects
●Adverse effects:●nausea, vomiting, diarrhea
●may improve over time●dose-related, slowly titrate dose
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Exenatide●Postmarketing cases of acute pancreatitis
●May delay absorption of other medications: slow gastric emptying
●not recommended for patients with gastroparesis
●Dose●start with 5 mcg BID
●may titrate to 10 mcg BID when tolerated●inject subcutaneously within 60 min of
morning & evening meals
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Exenatide●Average HbA1c reduction ~0.9%
●Significantly decreases postprandial glucose excursions
●Modest effects on FBG●Average weight loss in studies: 1 to 2
kg over 30 weeks●long-term, open-labeled trials show
continued weight loss for at least 2.5 years with 10 mcg BID dose
●Improvements in triglycerides & HDL seen with exenatide 10 mcg BID
16
DPP-IV Inhibitors●Inhibit DPP-IV which degrades GLP-1
●prolongs GLP-1 t½●GLP-1 deficient in type 2 DM
●Partially reduces elevated postprandial glucagon●Stimulates glucose-dependent insulin secretion
Generic Name Dose (mg) Recommended StartingDosage (mg/day)
MaximumDose
(mg/day)
Durationof Action
Metabolism or TherapeuticNotes
Nonelderly Elderly
Sitagliptin 25, 50, 100 100 mg daily 25 to 100 mgdaily based on renal function
100 mg daily 24 hours 50 mg daily if: creatinineclearance > 30 to < 50 mL/minute25 mg if: creatinine clearance < 30 mL/min
Saxagliptin (N) 2.5, 5 5 mg daily 2.5–5 mg daily based on renal function
5 mg daily 24 hours 2.5 mg daily if creatinine clearance <50 mL/min or if on strong inhibitors of CYP3A4/5 2
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DPP-IV Inhibitors●May be used as monotherapy or in
combination therapy●Average HbA1c reduction 0.7 to 1.0%
●Mild hypoglycemia may occur●Postmarking reports of serious
hypersensitivity reactions●anaphylaxis●angioedema
●exfoliative skin conditions (Stevens-Johnson syndrome)
164
Amylin Receptor Agonists (Amylinomimetics)
●Amylin, or islet amyloid polypeptide, is a hormone found in the β-cells where it is co-manufactured, stored, and released with insulin in response to food intake.
●Its actions seem to be centrally mediated and include slowing gastric emptying, suppressing glucagon secretion, and modulating the regulation of appetite.
●Amylin is absent in patients with type 1 diabetes. In patients with type 2 diabetes, its concentrations are altered to mirror those of insulin at different points in the progression of the disease.
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Amylinomimetics: Pramlintide●Adjunctive therapy for patients using
insulin●Synthetic analog of amylin
●neurohormone co-secreted from β-cells with insulin
●Suppresses postprandial glucagon secretion
●Reduces food intake●Slows gastric emptying
166
Pramlintide●Subcutaneous injection in abdomen
or thigh●variable absorption with arm injection
●Adverse effects:●GI most common
●nausea, vomiting, anorexia●may decrease over time
●dose-related, slowly titrate dose upwards
●May delay absorption of other medications; slow gastric emptying
167
Pramlintide●Reduce preprandial insulin dose 30 to
50% at pramlintide initiation●Basal insulin dose may be reduced if
FBG close to goal●Dosing
●type 2: 60 to 120 mcg prior to meals●type 1: 15 to 60 mcg prior to meals
●2.5 units on 100 units/ml insulin syringe = 15 mcg of pramlinitide
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Pramlintide●Average HbA1c reduction 0.4 to 0.6%
●Decreases prandial glucose excursions●Little effect of FBG concentrations
●Main advantage in type 1 DM is that it stabilizes wide postprandial glycemic swings
●Average weight loss in controlled trials: 1 to 2 kg
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Management strategies for Type 2 DM●Implementation strategies:
●Initial therapy●Advancing to dual combination therapy
●Advancing to triple combination therapy●Transitions to & titrations of insulin
Treatment of acute complications
205
hypoglycemiahyperosmolar
hyperglycemic state
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1- Hypoglycemia●low blood sugar,
●defined clinically as a blood glucose level of less than 50 mg/dL.●Individuals with DM can experience symptoms of hypoglycemia at
varying blood glucose levels.●Patients who have regular blood glucose levels as high as 300 to 400
mg/dL may experience symptoms of hypoglycemia once blood glucose levels are lowered to the middle to upper 100 mg/dL range.
●Most people whose blood glucose levels are controlled adequately may experience symptoms when levels fall below 70 mg/dL.
●Symptoms include: shakiness, sweating, fatigue, hunger, headaches, and confusion.
●Common causes include:●delayed or inadequate amounts of food intake, especially
carbohydrates,●excessive doses of medications (e.g., sulfonylureas and
insulin),●exercising when insulin doses are reaching peak effect,
●inadequately adjusted drug therapy in renally or hepatically impaired patients.
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Hypoglycemia – management●The key to successful management of hypoglycemia is
recognition and prevention.●Patients experiencing symptoms of hypoglycemia
should:●check their blood glucose level,
●consume 15 g of carbohydrate, and wait 10 to 15 minutes for symptom resolution (15 – 15 – 15)
●Examples of acceptable treatments may include a small box of raisins, approximately 120 mL of orange juice, approximately 240 mL of skim milk, or three to six glucose tablets.
●In patients receiving an α-glucosidase inhibitor in combination with a sulfonylurea or insulin, hypoglycemia should be treated with glucose tablets or skim milk owing to the mechanism of action of the α- glucosidase inhibitors.
●If the blood glucose level has dropped below 50 mg/dL, as much as 30 g of carbohydrate may be necessary to raise blood glucose levels adequately.
glucagon injection will vomit.208
●For patients with hypoglycemia experiencing a loss of consciousness,
●a glucagon emergency kit should be administered by intramuscular or subcutaneous route,
●Glucagon dose:●for a child younger than 5 years of age is 0.25 to
0.5 mg;
●for children 5 to 10 years of age, 0.5 to 1 mg;
●for patients older than 10 years, 1 mg)
●If glucagon is unavailable € IV glucose
●emergency medical personnel should be contacted.
●The patient should be rolled onto his or her side to prevent aspiration since manypatients receiving the
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2 -Hyperosmolar Hyperglycemic state (HHS)●Diabetic emergency – arise from inadequate insulin
●Typically older type 2 DM patients●Fluid deficits & blood glucose concentrations generally
greater than DKA●Blood glucose can be of greater than 600 mg/dL
●serum osmolality > 320 mOsm/kg € osmotic diuresis and fluid deficits
●Lacks the lipolysis, ketonemia and acidosis associated with DKA
●Precipitating Factors●infection/illness
●prolonged hyperglycemia●prolonged dehydration
●renal insufficiency
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HHS - treatment●Lower blood glucose levels gradually
●Treatment●Fluid replacement
●hypotonic fluids (0.45% saline) should be used if serum sodium > 150 meq/L
●low-dose insulin infusions (1 to 2 units/hour)
●Avoid rapid correction of glucose levels●no greater than 75 to 100 mg/dL
●may result in cerebral edema
Recommended Monitoringblood pressure each visit
body weight/BMI each visit
hemoglobin A1c not at goal: every 10-12 weeks at goal: every 6 months
fasting lipid profile
not at goal: each visit at goal: annually
foot exam each visit: physical exam; monofilament annually
urine albumin assessment
annually
dilated ophthalmologic exam
annually; more frequently with identified abnormalities
pneumococcal vaccine
At least 1 lifetime vaccination, vaccinate patients > age 64 if last vaccination was > 5 years ago
influenza vaccine annually unless contraindicated
smoking cessation each visit220
PREVENTION AND MANAGEMENT OF
DIABETES COMPLICATIONS
•CVD is the major cause of morbidity, mortality for those with diabetes
•Common conditions coexisting with type 2 diabetes )e.g., hypertension, dyslipidemia) are clear risk
factors for CVD•Diabetes itself confers independent risk•Benefits observed when individual cardiovascular risk
factors are controlled to prevent/slow CVD in people with diabetes
ADA. VI. Prevention, Management of Complications. Diabetes Care 2013;36)suppl 1):S28-29.
Cardiovascular Disease (CVD) in Individuals with Diabetes
Recommendations: Hypertension/Blood Pressure Control
ADA. VI. Prevention, Management of Complications. Diabetes Care 2013;36)suppl 1):S28-S29.
Screening and diagnosis•Blood pressure should be measured at every routine
visit•Patients found to have elevated blood pressure should
have blood pressure confirmed on a separate day )B)
Goals•People with diabetes and hypertension should be
treated to a systolic blood pressure goal of >140 mmHg )B)
•Lower systolic targets, such as >130 mmHg, may be appropriate for certain individuals, such as younger
patients, if it can be achieved without undue treatment burden )C)
•Patients with diabetes should be treated to a diastolic blood pressure >80 mmHg )B)
Recommendations: Hypertension/Blood Pressure Control
ADA. VI. Prevention, Management of Complications. Diabetes Care 2013;36)suppl 1):S29.
Treatment•Patients with a blood pressure )BP) >120/80 mmHg should be advised on lifestyle changes to
reduce BP )B)•Patients with confirmed BP ≥140/80 mmHg should, in addition to lifestyle therapy, have prompt
initiation and timely subsequent titration of pharmacological therapy to achieve BP goals )B)•Lifestyle therapy for elevated BP )B)
–Weight loss if overweight–DASH-style dietary pattern including reducing sodium, increasing potassium intake–Moderation of alcohol intake–Increased physical activity
•Pharmacological therapy for patients with diabetes and hypertension )C)–A regimen that includes either an ACE inhibitor or angiotensin II receptor blocker; if one class is not tolerated,
substitute the other
•Multiple drug therapy )two or more agents at maximal doses) generally required to achieve BP targets )B)
•Administer one or more antihypertensive medications at bedtime )A)•If ACE inhibitors, ARBs, or diuretics are used, kidney function, serum potassium levels should be
monitored )E)•In pregnant patients with diabetes and chronic hypertension, blood pressure target goals of 110–
129/65–79 mmHg are suggested in interest of long-term maternal health and minimizing impaired fetal growth; ACE inhibitors, ARBs, contraindicated during pregnancy )E)
Recommendations: Dyslipidemia/Lipid Management
ADA. VI. Prevention, Management of Complications. Diabetes Care 2013;36)suppl 1):S31.
Screening•In most adult patients, measure fasting lipid profile at least annually )B)•In adults with low-risk lipid values
)LDL cholesterol >100 mg/dL, HDL cholesterol >50 mg/dL, and triglycerides >150 mg/dL ,)lipid assessments may be repeated every 2 years )E)
Treatment recommendations and goals )1)•To improve lipid profile in patients with diabetes, recommend lifestyle modification
)A), focusing on–Reduction of saturated fat, trans fat, cholesterol intake–Increased n-3 fatty acids, viscous fiber,
plant stanols/sterols–Weight loss )if indicated)–Increased physical activity
•Statin therapy should be added to lifestyle therapy, regardless of
baseline lipid levels–with overt CVD )A)–without CVD >40 years of age who
have one or more other CVD risk factors )A)
•For patients at lower risk )e.g., without overt CVD, >40 years of age) )C)
–Consider statin therapy in addition to lifestyle therapy if LDL cholesterol
remains >100 mg/dL–In those with multiple CVD risk factors
Recommendations: Dyslipidemia/Lipid Management
ADA. VI. Prevention, Management of Complications. Diabetes Care 2013;36)suppl 1):S31.
Treatment recommendations and goals )cont’d)•In individuals without overt CVD
–Primary goal is an LDL cholesterol>100 mg/dL )2.6 mmol/L) )B)
•In individuals with overt CVD–Lower LDL cholesterol goal of >70 mg/dL
)1.8 mmol/L), using a high dose of a statin, is an option )B)
•If targets not reached on maximal tolerated statin therapy
–Alternative therapeutic goal: reduce LDL cholesterol ~30–40% from baseline )B)
•Triglyceride levels >150 mg/dL )1.7 mmol/L), HDL cholesterol >40 mg/dL )1.0 mmol/L) in men and >50 mg/dL )1.3 mmol/L) in women, are desirable )C)
–However, LDL cholesterol–targeted statin therapy remains the preferred strategy )A)
•Combination therapy has been shown not to provide additional cardiovascularbenefit above statin therapy alone and is not generally recommended )A)
•Statin therapy is contraindicated in pregnancy )B)
Recommendations: Smoking Cessation
ADA. VI. Prevention, Management of Complications. Diabetes Care 2013;36)suppl 1):S34.
•Advise all patients not to smoke or use tobacco products )A)
•Include smoking cessation counseling and other forms of treatment as a routine
component of diabetes care )B)
Recommendations: Coronary Heart Disease Screening
ADA. VI. Prevention, Management of Complications. Diabetes Care 2013;36)suppl 1):S34.
Screening•In asymptomatic patients, routine screening for CAD is not
recommended, as it does not improve outcomes as long as CVD risk factors are treated )A)
Treatment•To reduce risk of cardiovascular events in patients with
known CVD, consider–ACE inhibitor )C)–Aspirin* )A)–Statin therapy* )A)
•In patients with a prior MI–β-blockers should be continued for at least 2 years after the event
)B)•Avoid thiazolidinedione treatment in patients with
symptomatic heart failure )C)•Metformin use in patients with stable CHF
–Indicated if renal function is normal )C)–Should be avoided in unstable or hospitalized patients with CHF
)C)
