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Obesity and Hyperinsulinemia in HIV Positive Children: 

Obesity and Hyperinsulinemia in HIV Positive Children Robert M. Lawrence, MD 16th Annual HIV Conference Florida/Caribbean AETC

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Disclosure of Financial Relationships: 

Disclosure of Financial Relationships This speaker has no significant financial relationships with commercial entities to disclose. This slide set has been peer-reviewed to ensure that there are no conflicts of interest represented in the presentation. The Florida/Caribbean AETC is supported in large part by the Health Resources and Services Administration (HRSA), HIV/AIDS Bureau (HAB). DHHS-HAB Grant No. 2 H4A HA 00049-04-00.

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Definition: 

Definition To determine childhood obesity we need to calculate the Body Mass Index (BMI) BMI = Weight (kg) Height x Height (m2) or Weight (pounds) x 703 Height x Height (inches2)

DEFINITIONS: 

DEFINITIONS Based on Body Mass Index (BMI): Children: At risk for overweight (previously 'overweight'): BMI  85th percentile and andlt; 95th percentile for age and sex. Overweight (previously 'obese'): BMI  95th percentile for age and sex.

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Insulin Resistance: 

Insulin Resistance No consensus on definition of insulin resistance. Normal range for assays vary between different institutions, therefore it is difficult to arrive at a consensus for a cutoff. Gold standard: euglycemic hyperinsulinemic clamp More practical measures: - Elevated fasting insulin (andgt;20 μIU/ml) - Indices that combine fasting insulin and glucose have been shown to correlate well with gold standard: Fasting glucose to insulin ratio andgt;4. QUICKI (1/[log fasting insulin + log fasting glucose]) andlt;0.312 Keep in mind that a normal fasting insulin does not rule out insulin resistance and in a high-risk child it may indicate -cell failure.

ADA Diagnostic Criteriafor Pre-Diabetes and Type 2 Diabetes: 

ADA Diagnostic Criteria for Pre-Diabetes and Type 2 Diabetes Pre-diabetes -Impaired Fasting Glucose (IFG): ≥100 and andlt;126 mg/dl -Impaired Glucose Tolerance (IGT): 2-hour blood glucose during OGTT ≥140 and andlt;200 mg/dl Diabetes -Fasting blood glucose ≥126 mg/dl -2-hour blood glucose during OGTT ≥200 mg/dl -Random blood glucose ≥200 mg/dl associated with symptoms of polydypsia, polyuria and/or weight loss. Note: HgbA1C is not a diagnostic criteria for diabetes

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INSULIN RESISTANCE -cell failure TYPE 2 DIABETES Hyperinsulinemia Normal Glucose Tolerance (Compensated Insulin Resistance) Impaired Fasting Glucose/ Impaired Glucose Tolerance (PRE-DIABETES) Genetics Obesity Glucotoxicity Lipotoxicity M. Huerta, MD

Atherosclerosis Begins in Childhood: 

Atherosclerosis Begins in Childhood The Pathological Determinants of Atherosclerosis in Youth Study was the first one to show that fatty streaks were present in the intima of large arteries in adolescents. Using high resolution vascular ultrasound techniques, changes in carotid intima-media thickness have been shown in children with type 1 diabetes and hypercholesterolemia compared with controls.

Cardiovascular Risk in Childhood Obesity: 

Cardiovascular Risk in Childhood Obesity The Bogalusa Heart Study showed that 60% of overweight children (BMI ≥ 95th percentile for age and sex) have at least one cardiovascular risk factor such as: - hyperinsulinemia - hypertension - hyperlipidemia Berenson GS, et. al. Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults. New England Journal of Medicine 1998; 338: 1650-1656.

Effect of Childhood Cardiovascular Risk Markers in Adulthood: 

Effect of Childhood Cardiovascular Risk Markers in Adulthood Cardiovascular risk factors present during childhood, such as elevated LDL-C, elevated systolic blood pressure and higher BMI are associated with: - increased carotid intima media thickness - increased risk for CVD - increased risk for all-cause and CVD-related mortality in adulthood. Gunnell D. Am J Clin Nutr 1998; 67: 1111-1118

Prevalence of Overweight Children in US: 

Prevalence of Overweight Children in US Hedley et al, NHANES JAMA 291:2847, 2004

Association between BMI in Childhood and Adulthood: 

Association between BMI in Childhood and Adulthood Bogalusa Heart Study 2617 subjects (2-17 years old) re-examined at 18-37 years old with a mean follow-up of 17 years Of 186 overweight children (BMI andgt; 95th%) 77% (144) were obese as adults. Only 7% of 1317 normal weight children became obese adults. Freedman DS et al, Pediatrics 2001, 108:712-718.

Why our Children Obese?: 

Why our Children Obese? Their parents are obese. Fast Food consumption has increased. Increased consumption of junk food and soft drinks in schools. Less physical activity. Increased TV viewing and computer time. Food advertising directed at children.

Pediatric Type 2 Diabetes: 

Pediatric Type 2 Diabetes Florida: Among 682 patients with newly diagnosed diabetes seen at 3 university diabetes centers the proportion of type 2 diabetes increased from 8.7% in 1994 to 19% in 1998. Cincinnati, OH: from 1000 children 0-19 years of age with new onset diabetes: - 1982-1992: 2-4% had type 2 diabetes - 1994: 16% had type 2 diabetes (33% of those between 10-19 years of age) Macaluso CJ et al, Pub Health Rep. 2002;117:373-9. Pinhas-Hamiel et al, J Pediatr 128:608-15.

Pediatric Type 2 Diabetes: 

Pediatric Type 2 Diabetes More prevalent in minority children including African-Americans, Hispanic-Americans and Native-Americans. It represents up to 46% of all new cases of pediatric diabetes in communities with large minority populations.

Prevalence of Pre-Diabetes in Children and Adolescents: 

Prevalence of Pre-Diabetes in Children and Adolescents In children and adolescents with BMI ≥ 95th percentile: Impaired Glucose Tolerance (pre-diabetes) was found in: - 25% of obese children age 4-10y - 21% of obese adolescents age 11-18y Asymptomatic type 2 diabetes was found in 4% of obese adolescents Fasting glucose failed to identify those children with impaired glucose tolerance. Sinha R, et al. New England Journal of Medicine 2002; 346: 802-810.

Prevalence of Pre-Diabetes in Children and Adolescents: 

Prevalence of Pre-Diabetes in Children and Adolescents In obese Hispanic adolescents with BMI ≥ 85th percentile and a family history of type 2 diabetes, 28 % have IGT based on 2-hour glucose by OGTT. (Goran M, JCEM 2003; 88: 1417-1427)

Prevalence of Impaired Fasting Glucose (IFG) : 

Prevalence of Impaired Fasting Glucose (IFG) 1999-2000 NHANES data 915 adolescents 12 to 19 years of age: Overall prevalence of IFG: 7% - Trend for IFG to be more prevalent in boys (10%) than in girls (4%). In those with BMI ≥ 95th percentile: prevalence of IFG was 17.8% - Racial differences: Mexican Americans 13% Non-Hispanic whites 7% Non-Hispanic blacks 4.2% Williams DE. Pediatrics 2005; 116: 1122-1126.

Prevalence of Impaired Fasting Glucose: 

Prevalence of Impaired Fasting Glucose In a cohort of 8th Grade Students (50% Hispanic, 23% AA): IFG was found in 40.5% (n=1643) IGT was found in 2.3% (n=1128) STOPP-T2D Study Group. Diabetes Care 2006; 29: 212-217 Study in the Princeton School District (n=2500): IFG was found in 7.5% of students 9-20 years of age. 0.08% had type 2 diabetes. Dolan LM. J Pediatrics 2005; 146: 751-758.

Why is it important to identify Impaired Glucose Tolerance (IGT)?: 

Why is it important to identify Impaired Glucose Tolerance (IGT)? Data from adults studies has shown that: IGT is associated with the development of microvascular diabetic complications. IGT is associated with 2- to 5-fold increased risk for cardiovascular disease and increased all-cause and cardiovascular disease-related mortality.

Pre-diabetes and CV risk factors: 

Pre-diabetes and CV risk factors Adolescents with IFG also had: higher total and LDL-cholesterol higher triglycerides lower HDL-cholesterol higher systolic blood pressure Than those with normal fasting glucose. Williams DE. Pediatrics 2005; 116: 1122-1126.

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Can we do anything to break the link? Childhood Obesity Type 2 Diabetes Atherosclerosis

What about Obesity in HIV Positive Children?: 

What about Obesity in HIV Positive Children? Fat Maldistribution and Body Habitus Changes Lipodystrophy Lipohypertrophy Lipoatrophy Hyperlipidemia Guidelines for the Use of Antiretroviral Agents in Pediatric HIV Infection Supplement III - Pediatric Adverse Drug Effects, October 26, 2006

Lipodystrophy in HIV + Children: 

Lipodystrophy in HIV + Children Changes in body fat distribution This has been reported in 1%, 10%, 18%, 29% and 33% of HIV-infected children treated with ARVs!! This is either loss of subcutaneous fat (peripheral fat wasting/lipoatrophy) or deposition of fat tissue subcutaneously or in visceral stores or a mixture of the two.

Lipohypertrophy (central fat accumulation): 

Lipohypertrophy (central fat accumulation) Dorsocervical fat accumulation 'buffalo hump' Increased visceral adipose tissue (VAT) Increased abdominal girth Increased waist-to-hip ratio Breast enlargement

Definition / Measurementof Lipohypertrophy: 

Definition / Measurement of Lipohypertrophy Trunk/arm skinfold ratio andgt; 2 standard deviations from the mean. DEXA scan identified increase in trunk/total fat or trunk/limb fat ratio. Clinical findings alone. MRI or CT measured increase in intra-abdominal adipose tissue (IAT) single-slice measurements for calculation of total, visceral, or subcutaneoustissue (TAT, VAT, or SAT) Bioelectric Impedance Analysis (BIA)

Proposed Causes of Fat Maldistribution in HIV: 

Proposed Causes of Fat Maldistribution in HIV Lipoatrophy –PI use and NRTIs (d4T, ddI) Very low plasma leptin concentrations Low plasma adiponectin levels Alterations in mitochrondial function - due to NRTIs – d4t, ddI, ddC Lipohypertrophy – insulin resistance, PI use, elevated cholesterol or triglycerides Adverse Drug Events from Guidelines for Pediatric HIV; October 26, 2006

Assessment and Monitoringof Lipodystrophy: 

Assessment and Monitoring of Lipodystrophy No current recommended routine Anthropometric measurements – waist circumference, waist-to-hip ratio, triceps skin fold thickness Single-slice MRI or CT scan for TAT, VAT and SAT Bioelectric Impedance Analysis DEXA Scanning Adverse Drug Events from Guidelines for Pediatric HIV; October 26, 2006

Treatment ofFat Maldistribution Syndrome: 

Treatment of Fat Maldistribution Syndrome Multiple potential causes - ? Multiplepotential treatments ? Lack of standard definitions of the differentabnormalities Switching antiretrovirals may help in prevention or treatment – no studies in children. Diet, exercise, insulin-sensitizing medications or lipid-lowering agents - there are no studies in children Adverse Drug Events from Guidelines for Pediatric HIV; October 26, 2006

Insulin Resistance andHyperglycemia: 

Insulin Resistance and Hyperglycemia Insulin resistance without fasting hyperglycemia Asymptomatic fasting hyperglycemia New-onset diabetes mellitus Exacerbation of pre-existing DM All of these have been reported in patients treated with ARV therapy. Adverse Drug Events from Guidelines for Pediatric HIV; October 26, 2006

HIV Positive Children: 

HIV Positive Children Insulin resistance and increased free fatty acids often occur with fat maldistribution syndromes related to PI or d4T containing regimens. New onset clinical diabetes rarely occurs in children or adolescents treated with PIs. Adverse Drug Events from Guidelines for Pediatric HIV; October 26, 2006 Arpadi et al, J Acquir Immune Defic Syndr 2001. 27:30-34. Jaquet et al. AIDS 2000. 14:2123-28.

HIV Positive Children: 

HIV Positive Children HIV-infected children, even without ARVs, have demonstrated growth delay and been shown to have resistance to IGF-1, GH and insulin. Geffner ME et al. Pediatr Res, 1993. 34:66-72.

Recommendations for Monitoring Glucose Metabolism: 

Recommendations for Monitoring Glucose Metabolism Educate children and families about symptoms of diabetes and risk factors for cardiovascular disease. For children with fat maldistribution or with risk factors for type 2 diabetes: fasting blood glucose measurments oral glucose tolerance testing may identify children with fasting hyperglycemia or insulin resistance Adverse Drug Events from Guidelines for Pediatric HIV; October 26, 2006

AAP/ADA Recommendations for Screening for Type 2 Diabetes: 

AAP/ADA Recommendations for Screening for Type 2 Diabetes Use fasting glucose to screen children with BMI ≥ 85th percentile and who have at least 2 of the following risk factors: Family history of type 2 diabetes in first or second degree relatives. High risk ethnicity (American Indian, African American, Hispanic, Asian/Pacific Islander) Clinical signs of insulin resistance: acanthosis, hypertension, dyslipidemia or polycystic ovary syndrome. Start at age 10 years or at onset of puberty , whichever occurs first. Repeat test every 2 years.

Screening for Type 2 Diabetes: 

Screening for Type 2 Diabetes All children and adolescents with BMI ≥ 85th percentile should be screened with a fasting insulin and glucose. Recommend OGTT in: - children with fasting glucose ≥ 100 mg/dL but less than 200 mg/dL - children with HgbA1C between 5.5 and 7%.

How does this relate to HIV?: 

How does this relate to HIV? Infection Inflammation – mediators and markers Lipid metabolism Insulin resistance

Role of Adipose Tissue in the Development of Type 2 Diabetes: 

Role of Adipose Tissue in the Development of Type 2 Diabetes Adipose tissue is an endocrine organ. ADIPOKINES are proteins derived from adipocyte and stromal cells of adipose tissue that have local, paracrine and endocrine functions. Adiponectin: protective effect against insulin resistance and atherogenesis. Adiponectin levels are reduced in obesity.

Role of Adipose Tissue in the Development of Type 2 Diabetes: 

Role of Adipose Tissue in the Development of Type 2 Diabetes Leptin: acts in the hypothalamus to suppress appetite and increase energy expenditure. Also decreases fat content in liver and skeletal muscle, therefore improving insulin sensitivity. Leptin levels are elevated in obesity, obesity considered a state of 'leptin resistance'. Resistin: elevated in obesity. Proposed as the link between obesity and insulin resistance.

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Hepatic Synthesis of Acute Phase Response Proteins: C Reactive Protein, PAI-1, fibrinogen, etc. ROLE OF INFLAMMATION IN THE DEVELOPMENT OF TYPE 2 DIABETES AND ATHEROSCLEROSIS ADIPOCYTES Insulin Resistance Type 2 Diabetes Atherosclerosis

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EARLY EVENTS IN ATHEROGENESIS monocyte Endothelial cell in vessel wall Rolling Adhesion Migration Blood flow

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Activation of Pro-Inflammatory Cascade Adipokines Modulate the Inflammatory Cascade Leading to Insulin Resistance and Atherosclerosis ADIPOCYTES Endothelial Activation Monocyte Activation Insulin Resistance

Diabetes Prevention Program: 

Diabetes Prevention Program The Diabetes Prevention Program demonstrated the feasibility of preventing type 2 diabetes in adults with impaired glucose tolerance. Intensive lifestyle intervention resulted in 58% decrease in incidence of type 2 diabetes vs. 31% with metformin. Only 7% weight loss was required to achieve this goal.

Metformin Therapy in Obese Adolescents: 

Metformin Therapy in Obese Adolescents Freemark M. Pharmacologic Approaches to the Prevention of Type 2 Diabetes in High Risk Pediatric Patients. J Clin Endocrinol Metab 2003; 88: 3-13 Effect of Metformin 500 mg po BID for 6 months (n=29) Change in BMI: metformin : -1.3% vs. placebo: +2.3%

Metformin Plus Diet in Obese Adolescents: 

Metformin Plus Diet in Obese Adolescents Kay JP et. al. Beneficial effects of metformin in normoglycemic morbidly obese adolescents. Metabolism 2001; 50: 1457-1461. Data are means (SE). * pandlt;0.25, ** pandlt;0.005 by t-test.

Metformin Therapy for Insulin Resistance: 

Metformin Therapy for Insulin Resistance Randomized crossover clinical trial of metformin 1000 mg po BID vs. placebo for 6 months in 22 adolescents with insulin resistance defined by FGIR andgt;4.5 or presence of acanthosis. Variable Treatment Effect p-value Weight (kg) -4.35 0.02 BMI (kg/m2) -1.26 0.002 BMI z-score -0.12 0.005 Fasting insulin -2.2 0.011 Fasting glucose -0.2 0.048 Insulin sensitivity (Si) +0.17 0.506 Percentage of body fat (DEXA) -0.67% 0.062

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Effect of Metformin on BMI z-score

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Effect of Metformin on Insulin Sensitivity

Metformin Therapy for Pre-Diabetes: 

Metformin Therapy for Pre-Diabetes Not enough efficacy data in children and adolescents. Use only for children with pre-diabetes after a 3- to 6-month trial of lifestyle changes. Do OGTT before using for treatment of insulin resistance or weight loss. Dose: -Metformin 500 mg BID x 2 weeks, then 850 mg BID. -Glucophage XR 500 mg po for 1 week, then 1000 mg po for 1 week, then 1500 mg po. Duration: 6-12 months while implementing lifestyle changes.

Metformin Therapy for Pre-Diabetes: 

Metformin Therapy for Pre-Diabetes Approved for use in children ≥ 10 years of age. Do not use if liver enzymes andgt; 3 times the upper limit of normal or kidney failure. Most common side effects (25-50% of patients): gastrointestinal (nausea or diarrhea), usually transient. Must take metformin after meals to increase absorption and minimize side effects.

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Six-Month Clinical Trial Comparing the effect of Metformin vs. Lifestyle Modification on the risk for Type 2 Diabetes and Atherosclerosis in Obese Children

Criteria for Enrollment: 

Criteria for Enrollment Children 10-18 years of age BMI ≥ 85th percentile Healthy except for mild allergic rhinitis or asthma Not using chronic medications other than non-steroidal medications for allergic rhinitis or asthma.

Prevention of Pediatric Type 2 Diabetes: 

Prevention of Pediatric Type 2 Diabetes Studies to Treat or Prevent Pediatric Type 2 Diabetes (STOPP-T2D) Comparing the effect of: - metformin alone vs. - metformin plus rosiglitazone vs. - metformin plus lifesytle modification on the prevention of type 2 diabetes in overweight children.

Obesity and Hyperinsulinemia inHIV Positive Children and Adolescents: 

Obesity and Hyperinsulinemia in HIV Positive Children and Adolescents Watch out for these problems Establish clear definitions and criteria for the different syndromes or conditions. Develop studies to evaluate and treat these conditions in HIV positive children and adolescents. Involve your pediatric endocrinologists.

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Diagnostic Criteria: 

Diagnostic Criteria Normal Borderline Elevated Total andlt;170 170-199  200 Cholesterol (mg/dL) LDL andlt;110 110-129 130 Cholesterol (mg/dL) HDL- andgt; 40 35-39 andlt; 35 Cholesterol (mg/dL) Triglycerides andlt;150 150-199  200 (mg/dL)

Hypertension: 

Hypertension Measure blood pressure manually with a cuff of appropriate size. Use tables to determine SBP and DBP percentiles according to height, age and gender. Identify those with: Borderline hypertension: SBP or DBP andgt;90th and andlt;95th percentile. Hypertension: SBP or DBP andgt; 95th percentile.

Metabolic Syndrome: 

Metabolic Syndrome NHANES definition 3 or more of the following criteria: Fasting triglycerides andgt; 100 mg/dL HDL andlt; 50 mg/dL (boys 15-19y andlt;45 mg/dL) Fasting glucose ≥ 110 mg/dL Waist circumference andgt; 75th percentile for age and gender SBP andgt; 90th percentile for age, gender and height De Ferranti SD, et al. Circulation 2004; 110:2494-2497.

Metabolic Syndrome- NHANES III: 

Metabolic Syndrome- NHANES III From 1960 adolescents 12 to 19 years old: Two thirds (63%) had at least one metabolic abnormality 1 in 10 had Metabolic Syndrome Among overweight adolescents (BMI ≥ 85th percentile) : One third (31.2%) had metabolic syndrome De Ferranti SD, et al. Circulation 2004; 110:2494-2497.

Childhood Obesity Treatment Programs: 

Childhood Obesity Treatment Programs Dr. Epstein’s program – Buffalo, NY Subjects: Children 6-12 years old - Diet: Traffic Light Diet providing 900-1200 calories per day. - Weekly family treatment sessions with a counselor for 8-16 weeks, followed by monthly meetings for 6-12 months Plus participation in separate child and parent group sessions. Results: Decrease of 10-20% in percent overweight at the end of intervention. Decrease of 8-15% in percent overweight maintained at 5-year-and10-year- follow-up. Epstein LH. Health Pscyhology 1994; 13:373-383.

Effect of Baseline BMI Percentile on Percent change in BMI z-score: 

Effect of Baseline BMI Percentile on Percent change in BMI z-score At 6 months: For all subjects (66/300): - 4.4 ± 5% Subjects with BMIandlt; 99th percentile: - 8.09 ± 6.75 % vs. Subjects with BMI  99th percentile: - 3.07 ± 3.8%. (p=0.0012)

Progression from Pre-Diabetes to Diabetes in Adults: 

Progression from Pre-Diabetes to Diabetes in Adults - Rate of conversion from pre-diabetes to type 2 diabetes is 7% per year. - Transition is a gradual phenomenon that occurs over 5-10 years - An International Diabetes Federation consensus workshop concluded that more than 60% of people who developed diabetes had either IGT or IFG within the 5-year period preceding diagnosis of diabetes. - In Dutch adults, 38% of those with IFG and 32.4% of those with IGT develop diabetes over a 6-year period.

Progression from Pre-Diabetes to Diabetes in Adolescents: 

Progression from Pre-Diabetes to Diabetes in Adolescents 117 obese children and adolescents who had OGTT a baseline and 2 years later At baseline: 84 had NGT and 33 had IGT After 2 years: 8 IGT subjects developed T2D (24.2%) 15 IGT subjects reverted to NGT (45.5%) 10 IGT subjects remained IGT (30.3%) Best predictors of development of T2D: Severe obesity (BMI ≥ 97th percentile) and persistent weight gain African-American race Weiss R. et al. Diabetes Care 2005; 28:902-909

Diagnostic Criteria: 

Diagnostic Criteria Normal Borderline Elevated Total andlt;170 170-199  200 Cholesterol LDL andlt;110 110-129 130 Cholesterol HDL- andgt; 40 35-39 andlt; 35 Cholesterol Triglycerides andlt;150 150-199  200

Bordeline LDL: 

Bordeline LDL LDL between 110 and 129 mg/dL Discuss cardiovascular risk factors Begin Step-One Diet (saturated fat andlt; 10% of total calories, total cholesterol andlt; 300 mg/day). Other dietary changes: - increase soluble fiber consumption (10-25 grs/day or age plus 5 grs/day) - encourage intake of plant sterols and stanols (e.g. Benachol margarine) Weight reduction if overweight Increase physical activity Reevaluate status in 1 year

Elevated LDL: 

Elevated LDL LDL ≥ 130 mg/dL Evaluate secondary causes: hypothyroidism, nephrotic syndrome Evaluate for familial disorders: screen family members Begin Step-Two diet (saturated fat andlt; 7% of total calories, total cholesterol andlt; 200 mg/day). This should be done in consultation with a registered dietitian. Effect of diet on LDL-C: variable, may decrease from 8 to 24%.

Pharmacologic Intervention: 

Pharmacologic Intervention Consider pharmacologic intervention if after 3 months of dietary intervention, LDL remains elevated: LDL andgt; 190, or LDL andgt; 160 in children with strong family history of premature CAD (males andlt;55y or females andlt;65y) or at least 2 cardiovascular risk factors: - low HDL - smoking - obesity - hypertension - diabetes

Pharmacologic Therapy: 

Pharmacologic Therapy Statins (HMG CoA reductase inhibitors): Mechanism of action: inhibit cholesterol synthesis in the liver. Reduce LDL-C by 21 to 45%. - Several studies have now shown the safety and efficacy of statin therapy in children and adolescents as young as 4 years of age. - use in children  10 years of age; may use at younger age in familial hypercholesterolemia. - monitor liver functions tests at baseline and every 3 months - discontinue if muscle pain occurs - consider oral contraceptive use in sexually active adolescent females

Pharmacologic Therapy: 

Pharmacologic Therapy Ezetimibe (Zetia) Mechanism of Action: Prevents absorption of cholesterol and plant sterols at the brush border of the small intestine. Decreases LDL-C by 18% in adults. Recommended as adjunctive to statin therapy in order to avoid using higher doses of statins which may be associated with higher incidence of side effects.

Low HDL-Cholesterol: 

Low HDL-Cholesterol Diet low in saturated fats Increase consumption of healthy fats (fish, almonds, avocado) Increase physical activity Weight reduction Avoid smoking

Treatment of Elevated Triglycerides: 

Treatment of Elevated Triglycerides Weight reduction Increase physical activity. Dietary interventions: - decrease consumption of fat and simple sugars - increase intake of omega-3 fatty acids (fish oil and flaxseed oil) Maximize glycemic control in patients with diabetes.

Treatment of Elevated Triglycerides: 

Treatment of Elevated Triglycerides Consider pharmacologic therapy if triglycerides ≥ 400 mg/dL after 3 months of dietary intervention. Concern about risk to develop pancreatitis. Usually requires pharmacologic therapy and a very low fat diet (andlt;15% of total calories from fat).

Pharmacologic Treatment: 

Pharmacologic Treatment Fibric Acid derivatives: Gemfibrozil, fenofibrate and clofibrate Niacin High-dose statins

Criteria for Referral to Pediatric Endocrine Lipid/Type 2 Diabetes Clinic: 

Criteria for Referral to Pediatric Endocrine Lipid/Type 2 Diabetes Clinic Pre-diabetes IGT: 2-hour blood sugar in OGTT ≥ 140mg/dL and andlt; 200 mg/dL. IFG: Fasting blood sugar ≥ 100 and andlt; 126 mg/dL (if asymptomatic, please obtain OGTT prior to referral to further evaluate for type 2 diabetes) If HgbA1C andgt; 5.5% and andlt; 7% and patient is asymptomatic, please obtain an OGTT to determine glucose tolerance.

Criteria for Referral to Pediatric Endocrine Lipid/Type 2 Diabetes Clinic: 

Criteria for Referral to Pediatric Endocrine Lipid/Type 2 Diabetes Clinic 2) Lipid disorders that require pharmacologic therapy - Familial hypercholesterolemia - LDL andgt; 160 - Triglycerides andgt; 400 3) Other lipid abnormalities that will benefit from dietary intervention - LDL andgt;130 - Triglycerides andgt; 200 and andlt; 400 - HDL andlt; 40

Criteria for Referral to Pediatric Endocrine Lipid/Type 2 Diabetes Clinic: 

Criteria for Referral to Pediatric Endocrine Lipid/Type 2 Diabetes Clinic Patient with diabetes diagnosed by ADA criteria will be seen in new onset type 2 diabetes clinic: - Symptomatic with blood sugar ≥ 200 mg/dL. - 2-hour blood sugar in OGTT ≥ 200 mg/dL - Fasting blood sugar ≥ 126 mg/dL in at least 2 separate occasions. For those with HgbA1C andgt;7% who do not meet any of the above criteria, please obtain OGTT prior to referral for complete evaluation of glucose tolerance .

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