GO! Diabetes Program.

GO! Diabetes Program

Goals For Today Review evidence based guidelines and equip you to deliver state of the art care to your diabetic patients Understand tools that support practice performance and improvement Review oral and injectable medicines hypoglycemics Review multifaceted approach to cardiovascular disease protection

Effect of Tighter Glycemic Control on Progression of Retinopathy DCCT

Effect of Intense Glycemic Control on Nephropathy from DCCT

United Kingdom Prospective Diabetes Study
Study summary – 10 years Type 2 diabetics – convention vs. intense control Glycemic control – 7.0 vs. 7.9 Hypertension control – 144/82 vs. 154/87 Glycemic control metformin, sulfonylureas, and insulin Hypertension captopril, atenolol

UKPDS Blood Pressure Study: Tight vs. Less Tight Control
1148 type 2 patients BP lowered to avg. 144/82 (controls-154/87); 9 yr follow-up Endpoint Risk Reduction(%) P Value______ Any diabetes related endpoint Diabetes related deaths Heart failure Stroke Myocardial infarction NS Microvascular disease In the UKPDS, tighter control of blood pressure paid much higher dividends in disease related endpoints compared to glycemic control. UKPDS. BMJ. 317:

Glycemic Control Reduces Complications
DCCT UKPDS HbA1C % % Retinopathy 63% 17% to 21 % Nephropathy 54% 24% to 33% Neuropathy 60% - Cardiovascular Disease 41% 16% Diabetes Control and Complications Trial (DCCT) Research Group. N Engl J Med 1893:329: UK Prospective Diabetes Study (UKPDS) Group. Lancet 1993; 352:

ABCs Of Diabetes Management
Glycemic control A1C <7.0% Preprandial plasma glucose mg/dL Postprandial plasma glucose <180 mg/dL Blood pressure <130/80 mmHg Lipids LDL-cholesterol <100 mm/dL Triglycerides <150 mm/dL HDL >40 mm/dL Antiplatelet therapy Everyone over 40 Smoking cessation Universal 2007 ADA Standards of Care for diabetics Diabetes Care 2009;32:S6-12

Control of CV Risk Factors in Diabetic Hypertensive Patients in Academic Medical Centers
27% LDL <100 36% BP <130/85 mmHg 27% Daily Aspirin (ASA) Use 46% BP, Lipids and A1C 3% BP, Lipids, A1C + ASA A study published in Diabetes Care regarding control of CV risk factors at two urban academic medical centers in Brooklyn and Detroit. Optimal control judged by ADA guidelines was met in a small minority of patients. 2% McFarlane SI. Diabetes Care 2002;25:718

Type 1 Vs Type 2: How To Tell Them Apart
Treatment Always insulin; 4+ shots Pills  Insulin Age at Onset 10% of adults w/ new dx 50% of children w/ new dx Weight ~20% obese ~10% thin Family History 10% w/ a close relative >50% w/ a close relative DKA Can happen Blood Glucose More variable; big hypo’s More stable; milder hypo’s Thyroid Disease Often Sometimes Antibodies Usually (Anti-GAD) Not usually C-peptide Early: low nl; Late: ~0 Early: high nl; Late: low nl

Diabetes: Early Detection and Lifestyle Monitoring

Metabolic Syndrome Requires 3 or more:
Triglycerides > 150 HDL < 40 Waist size >40” men, >35” women BP > 130/85 Fasting glucose > 100 Caveat: Treatment counts for requirements… (Grundy, Circulation, 2005)

Pre-Diabetes Definition
If FBG >100 there is a 10-15% risk of DM within 7 years… or Fasting GTT 13

Who and When to Screen? Starting at age 45, a fasting blood glucose every three years More frequent screening if: Family history Overweight (BMI 25) Dyslipidemia HTN High risk ethnicity Vascular disease Prior glucose elevation Hx or exam findings

Role of Obesity in Diabetes
Obesity (specifically abdominal) has one of the highest associations with insulin resistance and glucose intolerance Numerous studies have tied weight loss to diabetes prevention A 5-10% weight loss yields a 58% reduction in the incidence of diabetes! At the end of four years Diet and exercise regimens average a 4kg loss after two years Advice alone results in a 1kg gain (Franz, Journal Amer. Diabetes Assoc, 2007)

Quantifying Obesity Easiest is by waist circumferences.
40” males, 35” females Some variation by ethnicity (35” and 31” for Asians) Measured across iliac crest in the back and the umbilicus in the front

Healthcare Maintenance
Latest ADA guidelines (2009) Lab surveillance Diabetic education Vaccinations/routine healthcare Smoking cessation Foot exams Eye exams

Reasons to Look at Feet Up to 70% of diabetics eventually develop a neuropathy Up to 25% develop foot ulcers Diabetes doubles your risk of LE disease (vascular, neuro, skin) More than half of the foot ulcers become infected at some point

Foot Surveillance Examine the feet at every visit
Annual comprehensive evaluation Sensation Pulses Skin condition (ulcers, hair, nails) Anatomic deformities Shoe evaluation

Sensory Exam 10-gram monofilament Patient should not watch
Five sites per foot Apply filament perpendicular to skin Allow slight buckle of filament in one motion Each site should take 1-2 sec Do not apply to ulcers or calluses

Eye Care Diabetic retinopathy is the leading preventable cause of blindness Prevalence of DR increases with duration of diabetes (100% Type 1, 60% Type 2 after 20 years) Of all recommendations, eye screening is the least likely to get done

Pathogenesis Increased circulating glucose leads to weakness of capillary walls Microaneurysms and leakage occurs causing eventual infarction of the nerve fiber layers (cotton wool spots) The localized hypoxia then leads to vasoproliferation Extension into the vitrea (+/- hemorrhage) leads to fibrosis and vision loss

Refer patients for ophthalmologist evaluation
Diabetic Retinopathy Normal Retina (left) contrasted with Proliferative Diabetic Retinopathy (right) Refer patients for ophthalmologist evaluation

Glycemic Control – Oral Agents

General Rules Hypoglycemic Therapy
Normalize fasting glucose levels first ( mg/dl) Many patients will achieve A1C < 7% When to target postprandial glucose levels? Fasting and preprandial values are at goal A1C levels are not met Measure 1-2 hours after beginning of the meal Glucose are generally at their peak Many type 2 diabetics will meet their target A1C with normalization of their fasting glucose. Later in the course of the disease post prandial hyperglycemia becomes more problematic and their A1C targets won’t be met unless they improve their postprandial glucose levels. This can be accomplished by sulfonylureas, glinides, mealtime insulin.

Glycemic Goals of Therapy
Verbal Target ~100 <<200 As low as possible w/o unacceptable adverse effects Goal Premeal plasma glucose (mg/dL) 2-h postprandial plasma glucose A1C ADA 90-130 <180* <7%** * Evaluation and treatment of postprandial glucose may be useful in the setting of suspected postprandial hyperglycemia, with the use of agents targeting postprandial hyperglycemia and for suspected hypoglycemia ** More stringent glycemic goals (i.e. a normal A1C, <6%) may further reduce complications at the cost of increased risk of hypoglycemia Diabetes Care 2009;32:S6-12

Biguanides: Metformin
Mechanism of action Reduces hepatic glucose production Depends upon presence of insulin Safety and efficacy Decreases A1C 1-2% Adverse effects: diarrhea and nausea; main risk: lactic acidosis Discontinuation rate 5% Contraindications: renal, cardiac, hepatic insufficiency; IV contrast No direct effect on kidney Dosing Initial dose: 500 mg once a day; dosing: usually BID Maximum effective dose: 2,000 mg per day Titration frequency: week(s) to months Alternate formulations: “XR” and combinations

Metformin Outperformed Other Meds in Obese Patients (UKPDS)
Lancet 1998 Sep 12;352(9131):

Insulin Secretagogues: Sulfonylureas (SFU) and “Glinides”
Mechanism of action Stimulate basal and postprandial insulin secretion Require functioning beta cells (no effect on beta cell dysfunction) Work quickly Safety and efficacy Decrease A1C approximately 1-2% Lower fasting glucose 20% Adverse events: weight gain, allergy (rare); main risk, hypoglycemia Dosing Initial dose: 1/8 to 1/4 maximum dose; dosing: 1-2 times/day (SFU), 3 times/day (glinides) Maximum effective dose: 1/2 maximum (full dose with nateglinide) Titration frequency: day(s) to weeks

Preferred Sulfonylureas
All available as generic agents Glipizide ER 5-20 mg once per day Once daily, flat profile, low plasma levels resulting in a low risk of weight gain and hypoglycemia Glipizide 2.5 to 20 mg twice a day Twice daily. Half-life 2-4 hours, peaks in 2-3 hours. By taking it once a day at low dose it stimulates insulin secretion for 6-12 hours Glimepiride 1-8 mg per day Once daily. Half-life 9 hours, peak action for 4 hours. Special utility like with glipizide but with longer half-life Buse J. Personal Opinion Melander A. Diabetes 2004;53 Suppl 3:S151

Thiazolidinediones (TZD’s or Glitazones): Pioglitazone and Rosiglitazone
Mechanism of action Enhance insulin sensitivity in muscle, adipose tissue Inhibit hepatic gluconeogenesis Reduced rate of beta cell dysfunction Safety and efficacy Decrease A1C 1-2% Adverse events: edema, weight gain, anemia; rare serious risk: liver failure Dosing Initial dose (monotherapy): 1/2 to 2/3 maximum; dosing,1-2 x/day Maximum effective dose: maximum dose Titration frequency: weeks to month(s)

Oral Hypoglycemics TZD Lipid Effects
Rosiglitazone (Avandia) +LDL +HDL +Triglycerides Pioglitazone (Actos) +LDL +HDL -Triglycerides Rosiglitazone – Black box warning for CHF and ischemic heart disease; warnings about increased fracture risk in women Pioglitzaone – Black box warning for CHF and warning about increase fracture risk. No evidence to suggest increased ischemic heart disease.

AHA/ADA Consensus Statement for TZDs
Not recommended for patients with NY Heart Association class III or IV heart failure TZDs alone, or particularly in combination with insulin, may cause fluid retention which can lead to heart failure Incidence of CHF <1% with TZD monotherapy Increased to 2%-3% in combination with insulin Patients should be observed for signs and symptoms of heart failure TZDs should be discontinued if any deterioration in cardiac status occurs Nesto RW et al. Diabetes Care 2004;27:256

Alpha-Glucosidase Inhibitors: Acarbose And Miglitol
Mechanism of action Delay absorption of carbohydrates Depend upon postprandial hyperglycemia Safety and efficacy Decrease A1C % Adverse events: flatulence; main risk: rare liver enzyme elevation Dosing Initial dose: 1/4 maximum once daily; dosing: 3 times daily Maximum effective dose: 1/2 maximum dose Titration frequency: week(s) to months Used infrequently by most clinicians

INCRETINS Role of Glucagon Like Peptide (GLP-1) in Glucose Homeostasis
Deficiency Type 2 DM/+/-type 1 Site of synthesis Small intestine Glucose dependent stimulation of insulin secretion Yes Slow gastric emptying Reduce inappropriate glucagon secretion Weight loss Yes (exenatide) Beta cell proliferation/regeneration Therapies Exenatide (Byetta) Sitagliptin (Januvia) Target population Type 2 on oral agents

Incretin Drugs Exenatide (Byetta) – GLP-1 analog
Injection twice daily 5mcg bid AC x 1 month, then 10mcg bid AC Beneficial effects described previously Expensive Weight loss Reduction in HgBA1C Sitagliptin (Januvia)– DPP4 inhibitor Technically not an incretin but similar effects Oral administration 100mg daily Weight neutral

Key Points to Consider for Therapy
Maximal benefits of metformin are observed at the recommended daily dose of 2000 mg (1 g BID)1 Thiazolidinediones should be started at low doses and slowly increased to minimize side effects2 Glucose-lowering effects of a sulfonylurea plateau at half the maximum recommended dose3 Garber AJ et al. Am J Med 1997;103:491 Nesto RW et al. Diabetes Care 2004;27:256 Stenman S et al. Ann Intern Med 1993;118:169

Glycemic Control - Injected Therapies

63% Of Patients with Diabetes Are Not at ADA A1C Goal <7%
Adults aged years with previously diagnosed diabetes who participated in the interview and examination components of the National Health And Nutrition Examination Survey (NHANES), 37.2% >8% 63% 7% 7.8% 25.8% 37.0% 17.0% 12.4% A1C % of Subjects n=404 Review of data from the Third National Health and Nutrition Examination Survey ( ). Nearly 2/3 of patients in this survey were not reaching recommended A1C Goal of < 7%. NHANES is administered by a CDC agency – the National Center for Health Statistics (NCHS) Saydah SH et al. JAMA 2004;291:335

Difficulties In Achieving Target A1C Values
Challenges Late diagnosis and initiation of therapy Therapeutic inertia Lack of effective lifestyle intervention Secondary failure Adverse events associated with antihyperglycemic therapies Complexity of care Role of postprandial glucose in failure

Common Concerns When Transitioning To Insulin
Fear of needles or pain from injections Fear of hypoglycemia Weight gain Fear of needles or pain from injections Describe/show very fine needles Offer insulin pens or other devices that hide the needle from view or may be less painful Point out that injections are less painful the SMBG tests Psychological counseling when needed Fear of hypoglycemia Discuss insulin action times and minimal minimal potential for hypoglycemia Describe difference in risks for hypoglycemia between multiple and once a day injections Describe prevention and treatment of hypoglycemia Weight gain Educate about strategies to minimize weight gain Funnel M. Self-management Support for Insulin Therapy in Type 2 Diabetes. The Diabetes Educator 2004;30:274

Common Concerns When Transitioning To Insulin
Adverse impact on lifestyle; inconvenient; loss of personal freedom and independence Belief that insulin means diabetes is worse or more serious disease Insulin as a personal failure Insulin causes complications Treated differently by family members Adverse impact on lifestyle; inconvenient; loss of personal freedom and independence Discuss intensifying as a way to increase flexibility Use once daily insulin Offer available resources and support Belief that insulin means diabetes is worse or more serious disease. Review all treatment options as a progression from the inception of education's. Explain how insulin is a logical step in the progression as it related to insulin resistance and beta cell failure. Insulin as a personal failure Teach initially and review that beta-cell failure is progressive. Avoid statements such as “You failed oral agents”. Reframe as “oral agents have failed you”. Avoid using insulin as a threat to encourage weight loss and activity. Funnel M. Self-management support for insulin therapy in type 2 diabetes. The Diabetes Educator 2004;30:274

Potential Insulin Regimens
Insulin pump Physiologic/COMPLEX/Flexible Multiple daily injections Free mixing - twice daily Pre-mixed - twice daily Basal only SIMPLE/Inflexible Presenter reviews options for insulin initiation. How do we balance simplicity and flexibility to achieve glycemic control?

Indications for Insulin
Not contraindicated at anytime Consider as initial therapy HgbA1C > 10% Fasting glucose > 250mg/dl Random glucose > 300 Recommended as initial therapy Polyuria, polydipsia, weight loss, ketones

Insulin Initiation Answers to Provider Concerns
Normalize the fasting glucose Fasting FSBS Once Daily Options Start 10 units or 0.2 u/kg Basal Insulin (glargine or detemir) NPH (bedtime) Premixed before dinner Increase 2-3 units every 3 days prn to reach target of fasting Decrease 3 units for fasting < 70

Once Daily Insulin Options Basals vs. NPH vs. Premixed
INSULIN TYPE ADVANTAGES DISADVANTAGES Glargine Peakless, less hypoglycemia, less wt gain; simple Cost; can’t mix; no meal time coverage Detemir Less wt gain, less hypoglycemia; simple Cost, shorter duration than glargine; can’t mix, basal only Pre Mixed 70/30 or 75/25 Covers meal time and basal; easy transition to bid More hypoglycemia and weight gain than basals NPH Less expensive More hypoglycemia than basals

Insulin Action Effect Of Various Formulations
140 Rapid (Glulisine, Lispro, Aspart,) 120 100 Short (Regular) Insulin Level (U/ml) 80 Intermediate (NPH) 60 Long (Glargine) 40 Detimir 20 2 4 6 8 10 12 14 16 Hours

Fasting Glucose at Target HgbA1C Not at Goal
Must Normalize Post Prandial Glucose Options Change HS NPH to BID NPH Change Pre-mixed Insulin from QD to BID Add Mealtime Insulin to Basal Insulins

Monomeric Insulin Analogs
How to switch or start Insulin immediately before the meal (or after) Review signs, symptoms and management of hypoglycemia Safety Arguably, glulisine, aspart, lispro and are safer than regular human insulin Patient preference Significant patient preference for monomeric analog versus regular human insulin Duration of action Covers postprandial glucose surge well In type 1 diabetes, will need an additional injection of basal or NPH

Carbohydrate Counting
Technique based on the concept that most meal-related glucose increase is due to the carbohydrate content Patients count either Carbohydrate choices (milk, fruit, breads, sweets, starchy vegetables) Grams of “total carbohydrates” on food label Providers prescribe insulin-to-carbohydrate ratio Start with 1 unit per choice or 1 unit per 15 grams Typical dose is 2-4 units per choice in type 2 diabetes Titrate based on postprandial glucose monitoring Generally, start with glulisine/lispro/aspart administered just after meals

Mixed-Analog Insulin BID
Starting dose in most Pre-breakfast 10 units Pre-supper 10 units Titration, once or twice a week (self-adjusted or with supervision) Alternatively, could just increase at both breakfast and supper in parallel If most values over the last 3 days fall in the range Adjust dose by ≤80 mg/dL -2 units mg/dL no change mg/dL +2 units mg/dL +4 units ≥180 mg/dL +6 units Buse JB et al. Clinical Diabetes 2005;23:78

Pre-Mixed Insulin BID Compared to Basal Alone – INITIATE Study
Aspart 70/30 bid Glargine qhs Minor hypoglycemia % % Median rate per pt per mo Severe hypoglycemia None episode Weight gain (Kg) 5.4  4.5 Total daily insulin (u/Kg) 0.82  0.27 Raskin P et al. Diabetes Care 2005;28:260

Oral Meds – What to Do When Insulin Started (General Rules)
Metformin Continue unless contraindicated Sulfonylureas Continue with basals generally Stop if using large doses of insulin Stop if using premixed insulin TZDs Proceed with caution Exacerbates weight gain and edema

Non Insulin Injectables

General Prescribing Considerations Dosing
Stable Dose 10 mcg BID Stable Dose 5 mcg BID Required DISCUSSION POINTS: Flowchart shows typical treatment initiation and dose escalation schedule. When BYETTA treatment initiation is being considered, the prescriber should evaluate any current dose of sulfonylurea and decide if the dose should be reduced to help reduce the risk of hypoglycemia when BYETTA is added to the current treatment regimen. BYETTA treatment is initiated with the pre-filled pen that delivers fixed 5 mcg doses, and BYETTA should be administered SC BID within 60 minutes before the morning and evening meals. After the first month of treatment with 5 mcg doses of BYETTA, prescriber should assess how well the patient has tolerated BYETTA treatment. If the patient has tolerated BYETTA treatment well, the BYETTA dose can be increased by prescribing the pre-filled pen that delivers fixed 10 mcg doses, and BYETTA should continue to be administered SC BID within 60 minutes before the morning and evening meals. If, after the first month of treatment with 5 mcg doses of BYETTA, prescriber determines patient is not yet able to effectively manage any nausea associated with BYETTA, the 5 mcg dosing BID can be continued until the prescriber and patient determine that BYETTA is being tolerated well enough that the dose can be increased to 10 mcg SC BID. Initiation 1 Mo Indicated for use in patients failing metformin or sulfonylurea Generally reduce SFU dose to smallest tablet to minimize risk of hypoglycemia No dosage adjustments based on meal size or physical activity No additional glucose monitoring required Exenatide Prescribing Information. 2005 Pramlintide Clinical Use A

Glargine Vs Exenatide in Patients Failing Oral Therapies
 Body Weight (lbs) *  A1C (%) This was a study comparing exenatide to insulin glargine for type 2 diabetic patients who were failing oral hypoglycemics. The study showed similar reductions in A1C. The exenatide group lost weight but more GI side effects (nausea/vomiting). The exenatide had lower post-prandial glycemia and the glargine had lower fasting glycemia. ITT patient sample Mean ± SE shown * p<0.0001, exenatide vs insulin glargine at same time point Heine RJ et al. Ann Intern Med 2005;143(8):559

Treatment Algorithm - Glucose
Diagnosis by screening or with symptoms Lifestyle intervention MNT, physical activity, education Yes Quarterly to semi-annual follow-up Are A1C/FPG targets achieved? Monthly to quarterly follow-up Target Insulin Resistance No * * Keep adding agents until target reached. Self-titration at home when possible Target PPG Target Insulin Deficiency FPG >200 mg/dL FPG <130 mg/dL Metformin, glitazone Exenatide, nateglinide, α-glucosidase inhibitors, rapid-acting insulin, pramlintide SFUs/glinide, insulin, exenatide

Causes of Hypoglycemia
Incorrect amount of insulin/oral agents Skipped or delayed meal/snack Carbohydrate intake less than normal Alcohol intake without food Exercise without insulin/food adjustment Not re-testing 1 to 2 hours after hypoglycemia treatment if meal or snack is not eaten

Treatment of Hypoglycemia
Definition of hypoglycemia: Plasma glucose <70 mg/dL Symptoms may or may not be present Sweaty, cold, unable to concentrate, dizzy Treatment Treat with 15 g carbohydrate; wait 15 minutes; test BG, if BG not >70 mg/dL, treat again All carbohydrates raise blood glucose On average, 15 g of glucose can increase BG from 60 to ~110 mg/dL (50mg/dL) over ~40 minutes BG starts to fall at 60 minutes and reaches previous treatment level at 2 hours Cryer et al. Diabetes Care 2003;26:1902

Treatment of Severe Hypoglycemia
Definition: Requires assistance to treat Inject glucagon with loss of consciousness or seizure Administered by another person May be given intramuscular or subcutaneous Standard dose 1.0 mg for adults; 0.5 mg for children under 5 yrs Prescription is required Precautions May cause nausea/vomiting/headache Call 911

Cardiovascular Disease Prevention Blood Pressure, Dyslipidemia, Antiplatelet Therapy

Diabetes and Hypertension Key Questions
Why should we pay so much attention? What parameters? Non Drug Recommendations Which drugs and how many? What do others besides the ADA say? What about resistant cases?

Diabetes and Hypertension Why?
Volume Expansion Increased insulin levels Higher sympathetic activity Increased glucose level Increased sodium resorption with hyperglycemia Decreased arterial compliance Obesity

UKPDS Blood Pressure Study: Tight vs. Less Tight Control
1148 type 2 patients BP lowered to avg. 144/82 (controls-154/87); 9 yr follow-up Endpoint Risk Reduction(%) P Value Any diabetes related endpoint Diabetes related deaths Heart failure Stroke Myocardial infarction NS Microvascular disease UKPDS. BMJ. 317:

Diabetes Treatment Goals for Blood Pressure
Control blood pressure 130/80 mmHg for most patients 125/75 mmHg for patients who have proteinuria >1 g/day and renal insufficiency Reduce the risk of end-organ failure Reduce the risk of cardiovascular events Myocardial infarction Cardiovascular death Delay or prevent the progression to heart failure JNC 7 Report. JAMA 2003;289:2560; Bakris GL et al. Am J Kidney Dis 2000;36:646 ADA. Diabetes Care 2007;30(suppl 1):S15

Number of Medications to Achieve Goal BP In 5 Trials of DM and/or Renal Disease
UKPDS (<150/85 mmHg) 2.7 ABCD (<75 mmHg DBP) 2.8 MDRD (<92 mmHg MAP) 3.6 HOT (<80 mmHg DBP) 3.3 AASK (<92 mmHg MAP) 3.8 1 2 3 4 Number Of BP Meds Bakris. J Clin Hypertens 1999;1:141

NKF Recommendations On Treatment Of Hypertension And Diabetes
Blood pressure goal: ≤130/80 mmHg BP-lowering medications should reduce both BP + proteinuria Lower goal has been recommended to reduce renal disease progression and incidence of ischemic heart disease Antihypertensive drug classes shown to reduce proteinuria and cardiovascular events ACE inhibitors --blocker (carvedilol) -blockers CCBs Diuretics The NKF and the ADA have similar recommendations for managing hypertension in diabetics. Bakris GL et al. Am J Kidney Dis 2000;36:646

UKPDS: ACE Inhibitor Vs -Blocker Aggregate Clinical Endpoints
Relative Risk & 95% CI RR P 0.5 1 2 Any diabetes-related endpoint 1.10 0.43 Diabetes-related deaths 1.27 0.28 All-cause mortality 1.14 0.44 Myocardial infarction 1.20 0.35 Microvascular disease 1.29 0.30 UKPDS: ACE Inhibitor vs. Beta-blocker for HTN: Aggregate Clinical Endpoints Patients in the UKPDS randomized to tight blood pressure control were also randomized to primary therapy with the angiotensin-converting enzyme (ACE) inhibitor captopril or the beta-blocker atenolol. There was no difference in benefit with regard to reduction of either diabetes-related endpoints or macrovascular events with either ACE inhibitor or beta-blocker treatment. This study indicates that blood pressure lowering, regardless of the type of agent used, will result in a reduction of microvascular disease, heart failure, and stroke. Reference: UK Prospective Diabetes Study Group. Efficacy of atenolol and captopril in reducing risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 39. BMJ 1998;317: Stroke 1.12 0.74 Favors ACE Inhibitor Favors -Blocker UKPDS Group. BMJ 1998;317:713

Which Class Of Agents Should Be Added Second-Line?
Thiazide diuretics Complementary mechanism to ACEs or ARBs ALLHAT showed benefit Particularly effective in African American patients BUT slightly higher deterioration of glucose metabolism Beta blockers Good evidence of benefit particularly for those with coronary heart disease or congestive heart failure BUT mechanism of action may not complement ACEs or ARBs

Additional BP Recommendations
Lower blood pressure gradually in the elderly If unable to achieve goal, don’t hesitate to discuss with peers Check for orthostasis in some patients when clinically indicated If angiotensin modifying drugs or diuretics are used, monitor renal function and potassium Use as many medicines as necessary to achieve blood pressure target 130/80 mmHg 125/75 mmHg if proteinuria is found Begin with an angiotensin modifying drug Add a thiazide in African American patients Add a Beta blocker in patients with heart disease These guidelines are from the 2007 Standards of Care from the ADA. ADA. Diabetes Care 2007;30(Suppl1):16

Causes Of Resistant Hypertension
Improper blood pressure measurement Excess sodium intake Inadequate diuretic therapy Medication Inadequate doses Drug actions and interactions (e.g. nonsteroidal anti-inflammatory drugs (NSAIDs), illicit drugs, sympathomimetics, oral contraceptives) Over-the-counter (OTC) drugs and herbal supplements Excess alcohol intake Identifiable causes of hypertension

Statins: Primary And Secondary Prevention
CARE 4S LIPID HPS (estimated) TNT 25 20 % With CVD Event 15 PROVE-IT 10 WOSCOPS AFCAPS HPS (estimated) CARDS 5 Results of HPS, together with the results from the WOSCOPS and AFCAPS/ TexCAPS trials, show that the benefits of LDL-C lowering with statin therapy in primary prevention of CAD are seen across the broad range of baseline plasma LDL-C concentrations. Together with the results from the 4S, CARE, and LIPID trials, HPS has also established the benefits of LDL-C reduction with statin therapy in secondary prevention of CAD in patients with a wide range of baseline plasma LDL-C concentrations. 50 70 90 110 130 150 170 190 210 LDL-C (mg/dL) Adapted from Illingworth. Med Clin North Am 2000;84:23 and LaRosa. N Engl J Med 2005;352 (e-pub) and Colhoun. Lancet 2004;364:685

ADA Standards 2009 Dyslipidemia
Fasting lipid profile annually Without overt CVD LDL<100 At age 40 start on statin regardless of LDL to reduce LDL 30-40% With overt CVD Start statin to reduce LDL 30-40% LDL<70 is an option Normalizing triglycerides and raising HDL with fibrates reduces CV events

ADA Standards 2009 Dyslipidemia
High LDL, High triglycerides, Low HDL Consider statin + fibric acid Remember the increased risk of rhabdomyolysis Consider statin + niacin Remember niacin can increase glucose levels moderate doses = mild changes in glycemia

Anti-platelet Therapy ADA Standards
Recommendations for Aspirin ASA mg/day for 2o prevention ASA mg/day for 1o prevention Age > 40 Any age with CV risk factors (htn, hyperlipidemia, renal disease, family history, smoking) Not recommended ages < 21 (Reye’s syndrome) Clopidogrel Very high risk diabetics; intolerance to ASA

Practice Performance and Improvement

METRIC Metric stands for Measuring, Evaluating, and Translating Research Into Care. It is an innovative online practice improvement program where you will input records of 10 diabetic patients prior to today and again within 90 days.

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