metabolic syndrome dr hemi sinorita

8/12/2019 Metabolic Syndrome Dr Hemi Sinorita

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METABOLIC SYNDROME

Hemi Sinorita

Sub Department of Endocrinology and MetabolismDepartment of Internal Medicine

Medical Faculty, Gadjah Mada UniversityDr. Sardjito Hospital, Yogyakarta


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Prevalence of Patients with Major CardiovascularEvents in Stable CHD Patients Stratified byMetabolic Syndrome and Diabetes Status

Balady, et al, Circulation 2007;115:2675


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Pathogenesis of Metabolic Syndrome

3 potential etiological categories:1. Obesity and disorders of adipose tissue2. Insulin resistance3. Independent factors that mediate

specific components of themetabolic syndrome.Other factors : aging, proinflammatory state,

hormonal changes - have been implicated ascontributors as well.


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Where Is the Fat?


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IR a reduced response of targettissues to circulating insulin

GlucoseExcessivefatty acid

release

Reducedglucoseuptake

Excessiveglucoseproduction

Carb ohydrate

Resistance to the action of insulin

Insulin


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Criteria for Clinical Diagnosis

of Metabolic Syndrome


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WHO Clinical Criteria for Metabolic Syndrome.

Insulin resistance, identified by 1 of the following:Type 2 diabetesImpaired fasting glucoseImpaired glucose tolerance

or for those with normal fasting glucose levels (


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D I A B E T E S M E L L I T U S TGT GDPT NORMAL

Keluhan Klinis Diabetes

Keluhan Klasik (+) Keluhan Klasik (-)

GDPatau

GD2J

126

200


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ATP III Clinical Identification ofthe Metabolic Syndrome

Risk Factor Defining LevelNone, but any 3 of the following 5 features

Abdominal obesity, given as WC* Men >102 cm (> 40 in)

Women >88 cm (>35 in)Triglycerides 150 mg/dLHDL cholesterol

Men


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AACE Clinical Criteria for Diagnosis ofthe Metabolic Syndrome

Risk Factor Components Cutpoints for Abnormality _______________________________________________________IGT or IFG plus any of the following based on clinical judgment

Overweight/obesity BMI 25 kg/m2Elevated triglycerides 150 mg/dL (1.69 mmol/L)Low HDL cholesterol

Men


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IDF Clinical Identification ofthe Metabolic Syndrome

Risk Factor Defining Level _________________________________________________

Increased WC (population specific)Plus any 2 of the following :

Triglycerides 150 mg/dLor on Triglycerides treatment

HDL cholesterolMen


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Management of the Metabolic Syndrome

Appropiate and aggressive therapy

for reducing patient risk ofcardiovascular disease

Lifestyle measure should be the firstactionTreatment should address all off thecomponents


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Inflammatory State CRP, TNF , IL-6

Oxidative Stress F 2Isoprostane, OX-LDL

Endothelial Dysfunction

Impaired Na-Metabolism

Hyperuricemia

Leptin Resistance Hyperleptinemia

Prothrombotic State PAI-1, Factor VII, Fbg

Atherogenic Dyslipidemia TG,

HDL, SD

Insulin Resistance Hyperinsulinemia

MetabolicRisk Factors Complications

Central Obesity

LIFESTYLE

MODIFICATION


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Abdominal Obesity

The primary target7% to 10% from baseline total body weight

during 6 to 12 months

Decreasing caloric intake :500 to 1000 calories/dayGreater physical activity

helps to enhancecaloric deficit.


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Physical Inactivity

a

30 minutes of moderate-intensity exercise (briskwalking), days of the week60 minutes or more of continuous or intermittent

aerobic activity , preferably done every day , willpromote weight loss or weight-loss maintenance


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Physical Inactivity

For high-risk patients (those with recent

acute coronary syndromes or recentrevascularization), physical activity shouldbe carried out under medical supervision .

AHA Guidelines further recommendexercise testing before vigorous exercisein selected patients with cardiovasculardisease and other patients with symptomsor those at high risk .


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Atherogenic and Diabetogenic Diets

Low in saturated fats, trans fats ,cholesterol,sodium, simple sugars.Solid at room temperature (animal meatsand skin, whole milk dairy products:butter, ice cream), lard, cooking oils suchas coconut and palm,eggs and chocolate.

A


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Recommendations :

saturated fat 7% of total caloriesreduce trans fat

dietary cholesterol 200 mg/dL

total fat 25% to 35% of total calories.Most dietary fat should be unsaturated (olive and

sunflower oil) simple sugars should be limited.


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Excess Adipose TissueCan Cause Increased Expression of Some Hormones

Atherogenic Dyslipidemia

FFA

Angiotensinogen

Leptin

Adipsin

TNF-

FFAFat

Stores

LipoproteinLipase

ResistinAdiponectin

Insulin

IL-6

Hypertension

Prothrombotic

state

Inflammation

IFG, IGT

DM = diabetes mellitus; FFA = free fatty acid; PAI-1 = plasminogen activator

inhibitor 1; MCP-1 = monocyte chemo attractant protein-1; TNF- = tumornecrosis factor alpha; IL-6 = interleukin 6.Aronne L (after Bray).

Weightreduction

Aspirin

ACE I, ARB

Statin, Fibrate

Metformin,

ThiazolidinedionesAcarbose

PlasminogenActivator Inhibitor 1

(PAI-1)


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Atherogenic Dyslipidemia

LDL-C is the primary target

Patients with atherogenic dyslipidemia inwhom serum triglyceride levels are 200mg/dL , non-HDL-C becomes the next

target of treatment after the LDL-C goal isreached.When triglycerides are 500 mg/dL ,

triglyceride-lowering drugs should beconsidered to prevent the development ofacute pancreatitis.


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Elevated Blood Pressure

Reduce BP to at least achieve BP of140/90 mm Hg ( 130/80 mm Hg ifdiabetes present).For BP 120/80 mm Hg: Initiate ormaintain lifestyle modification in allpatients with metabolic syndrome: weightcontrol, increased physical activity, alcoholmoderation, sodium reduction, andemphasis on increased consumption offresh fruits, vegetables, and low-fat dairyproducts


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Role of AII in the generation of ROS, impaired insulin signaling, NO

related mechanisms, GLUT4 expression-translocation


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Elevated Fasting Glucose

IFG (or IGT if assessed), weight reduction,increased physical activity , or both willdelay (or prevent) the onset of type 2diabetes mellitus.In addition, metformin, thiazolidinediones,

and acarbose will lower risk for type 2diabetes mellitus in people with IFG orIGT.

Glycemic control to a HbA1C


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Glucose (G)

Adipose tissue

Gut

Stomach

Liver

Thiazolidinediones

Biguanides

Muscle

PancreasInsulin

Adapted from Kobayashi M. Diabetes Obes Metab 1999; 1 (Suppl. 1):S32S40.Nattrass M & Bailey CJ. Baillieres Best Pract Res Clin Endocr inol Metab 1999; 13:309329.

-glucosidase inhibitors

Primary sites of action of OAD agents

Insulin resistance


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