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    K13 - Metabolic Syndrome

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    Reiza Primayana Vig
    This document discusses the history and definitions of metabolic syndrome and insulin resistance syndrome. It traces the evolution of definitions from Eskil Kylin in 1923 through the WHO in 1998, NCEP-ATP III in 2001, and IDF in 2006. Key components of metabolic syndrome are defined as abdominal obesity, elevated triglycerides, low HDL, hypertension, and elevated fasting glucose. The relationship between insulin resistance, obesity, and metabolic syndrome is explored. Treatment involves lifestyle changes like diet and exercise as well as medications targeting components of metabolic syndrome.

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    K13 - Metabolic Syndrome

    Uploaded by

    Reiza Primayana Vig
    101 views32 pages
    This document discusses the history and definitions of metabolic syndrome and insulin resistance syndrome. It traces the evolution of definitions from Eskil Kylin in 1923 through the WHO in 1998, NCEP-ATP III in 2001, and IDF in 2006. Key components of metabolic syndrome are defined as abdominal obesity, elevated triglycerides, low HDL, hypertension, and elevated fasting glucose. The relationship between insulin resistance, obesity, and metabolic syndrome is explored. Treatment involves lifestyle changes like diet and exercise as well as medications targeting components of metabolic syndrome.

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    This document discusses the history and definitions of metabolic syndrome and insulin resistance syndrome. It traces the evolution of definitions from Eskil Kylin in 1923 through the WHO in 1998, NCEP-ATP III in 2001, and IDF in 2006. Key components of metabolic syndrome are defined as abdominal obesity, elevated triglycerides, low HDL, hypertension, and elevated fasting glucose. The relationship between insulin resistance, obesity, and metabolic syndrome is explored. Treatment involves lifestyle changes like diet and exercise as well as medications targeting components of metabolic syndrome.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    101 views32 pages

    K13 - Metabolic Syndrome

    Uploaded by

    Reiza Primayana Vig
    This document discusses the history and definitions of metabolic syndrome and insulin resistance syndrome. It traces the evolution of definitions from Eskil Kylin in 1923 through the WHO in 1998, NCEP-ATP III in 2001, and IDF in 2006. Key components of metabolic syndrome are defined as abdominal obesity, elevated triglycerides, low HDL, hypertension, and elevated fasting glucose. The relationship between insulin resistance, obesity, and metabolic syndrome is explored. Treatment involves lifestyle changes like diet and exercise as well as medications targeting components of metabolic syndrome.

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    Pugud Samodro

    Eskil Kylin 1923 HT, Glucose, UA


    Reaven 1988 named Syndrome X (IR)
    WHO definition-1998 Metabolic syndrome
    NCEP-ATP III 2001 MS strong CV Risk
    First World Congress on IRS Nov 2003
    Second World Congress on IRS 2004
    2005 Quarrel about the word syndrome

    New IDF definition 2006 - consensus

    Metabolic Syndrome (MS)


    Insulin Resistance Syndrome (IRS)
    Syndrome X (Metabolic), Deadly Quartet
    Dysmetabolic Syndrome, Beer belly syndrome

    Cardiometabolic Syndrome
    Pleuri Metabolic Syndrome
    ICD Code # 277.7

    Clustering of CV Risk Factors

    Central

    Obesity
    Insulin
    Resistance

    IR

    Smoke

    BB

    MS

    CVD

    DM

    Insulin Resistance

    Obesity

    Metabolic Syndrome

    Diabetes

    2x

    4x

    Cardio Vascular Disease (CVD)

    Reilly MP et al
    Circulation 2003; 108: 1546-1551

    Insulin
    Resistance
    Inadequate
    Insulin prod
    Type 2 DM

    CKD,DPN

    Hyper
    Insulinemia

    CAD

    Metabolic
    Syndrome
    HT, Stroke,
    PCOS, NASH
    ACE Position Statement on IRS
    Endocr Pract. 2003;9(3)

    Etiology not fully elucidated


    Insulin Resistance
    Acquired causes
    Overweight and central obesity
    Physical inactivity, aging, ethnicity
    High CHO diets (>60%)

    Proinflammatory state, hormones


    Poly Genic causes

    IR, Insulin

    Dyslipidemia

    IGT, IFG

    ED, Vessel

    Increased
    CV Risk

    Pro Thrombotic

    Hypertension

    Visceral obesity

    Pro Inflammatory

    Insulin resistance Hyperinsulinemia


    Abd. Obesity ( WC, WC / ht ratio), BMI
    Hyperglycemia IFG, IGT, T2DM
    Hypertension, Endothelial Dysfunction (ED)
    Dyslipidemia ( TG, sLDL, HDL)
    Pro-inflammatory state ( CRP, TNF-, IL-6)
    Pro-coagulant state ( PAI-1, Fibrinogen)
    Premature atherosclerosis, CAD

    Central
    Obesity

    TG

    HDL

    Hypertension
    FPG

    Subcutaneous fat
    Abdominal muscle
    layer
    Intra-abdominal fat

    Is this correct?
    M. Davidson, MD.

    Previous Criteria Proposed for Clinical Diagnosis of


    Metabolic Syndrome
    Clinical
    Measure

    WHO
    (1998)

    EGIR
    (1999)

    ATP III
    (2001)

    AACE
    (2003)

    Insulin
    Resistance

    IGT,IFG,T2DM or
    Lower insulin sensitivity
    Plus any 2 of the following

    Plasma Insulin
    > 75th percentile
    Plus any 2 of the
    following

    None, But any 3 of


    the following 5
    Features

    IGT or IFG plus any


    of following based on
    clinical judgement

    Body
    Weight

    Men : WHR > 0.90


    Women : WHR > 0.85
    And/or BMI > 30 kg/m2

    WC >94 cm in men
    Or
    >80 cm in women

    WC > 102 cm in men


    Or
    > 88 cm in women

    BMI > 25 kg/m2

    Lipid

    TG> 150 mg/.dl or


    HDL-C<35 mg/dl in men
    Or < 39 mg/dl in women

    TG >150 mg/dl &


    or
    HDL-C < 39 mg/dl
    In men or women

    TG> 150 mg/.dl or


    HDL-C<40 mg/dl in men
    Or < 50 mg/dl in women

    TG> 150 mg/.dl or


    HDL-C<40 mg/dl in
    men
    Or < 50 mg/dl in
    women

    Blood
    Pressure

    > 140/90 mmHg

    > 140/90 mmHg


    or non hypertension

    > 130/85 mmHg

    130/85 mmHg

    Glucose

    IGT, IFG or T2DM

    IGT or IFG
    (but not diabetes)

    IGT or IFG
    (but not diabetes)

    Other

    Microalbuminuria

    > 110 mg/dl


    (Include diabetes)
    FPG >110 mg/dl (2001)
    FPG > 100 mg/dl (2004)

    IDF
    (2005)
    None

    Increase WC
    (population specific)
    Plus any 2 of the
    following

    TG> 150 mg/.dl or


    HDL-C<40 mg/dl in men
    Or < 50 mg/dl in women

    > 130 mmHg systolic or


    > 85 mmHg diastolic or
    Non hypertention Rx
    > 100 mg/dl
    (include diabetes)

    Other features of
    Insulin resistance
    (PCOS,T2DM etc)

    (Grundy et al, 2005)

    90 (M), 80 (F)

    Waist Circum

    2 of 5

    Triglycerides

    >150 mg

    HDL

    <40 (M) < 50 (F)

    Dysglycemia FPG >100 or DM


    Hypertension

    >130 or 85

    Rx. for any of the above conditions

    Features

    Insulin Resistance

    Hyperglycemia

    PPBG, Usually FBG is N

    Obesity, WC, ACN

    BMI > 23, WC > 90, ACN+

    TG, HDL, sLDL

    Dyslipidemia Present

    Cluster of metabolic factors

    Metabolic Syndrome

    Hypertension (>130/80)

    Usually is a feature

    Recent weight change

    Increase

    Fasting C peptide / Insulin

    Increased (HOMA)

    Treatment

    Exercise, Sensitizers

    Can we measure insulin resistance ? Yes !

    It will be of use to confirm IR


    Fasting C-Peptide levels, FBG
    CISI Composite Insulin Sensitivity Index
    QUICKI Quantitative Insulin Sensitivity Index
    HOMA IR Homeostasis Model Assessment

    HOMA calculator is available

    Normal

    Visceral Adiposity

    Courtesy of Wilfred Y. Fujimoto, MD.

    ADIPONECTIN
    Adipose
    Tissue

    Adiponectin

    FFA
    Oxidation
    TG

    Insulin
    Sensitivity

    FFA
    Influx

    FFA
    Oxidation

    Glucose TG
    Insulin
    Sensitivity

    (Ouchi N, et al, Curr Opin in Lipidol 2003)

    Vascular
    Inflammation

    Increased visceral fat


    Thiazolidinediones

    Increased lipolysis

    Increased TNF
    Increased FFA levels

    IR

    Shear stress

    Decreased adiponectin

    Endothelium

    NO production
    Vasoconstriction

    Adapted from Steinberg H et al. Diabetes. 2000;49:1231.

    Fat Cells

    Liver
    FFA

    IR X

    CE

    TG
    Apo B
    VLDL

    VLDL

    (CETP) HDL

    (hepatic
    lipase)

    TG

    Apo A-1

    CE (CETP) TG

    Kidney
    Insulin
    LDL

    sLDL

    (lipoprotein or hepatic lipase)

    Atherogenic Dyslipidemia
    Elevated Triglycerides > 150 mg
    Low HDL <40 (M), <50 (F)

    Increase in dense LDL type


    Small Dense LDL (sLDL)
    Increased Apolipoprotein
    B
    Lipoprotein a - Lp(a)

    Abdominal
    Obesity

    Insulin
    Resistance

    Lipids and
    BP control

    Primary

    Secondary

    Drug Rx

    PPAR -Fibrates

    Total Lifestyle

    TG, sLDL

    Calorie restriction

    LDL & Apo B

    Statins full dose

    Physical Activity

    HDL

    Niacin, Aspirin

    Change in Diet

    Attain goal BP

    ACE/ARB, other

    Statins, Fibrate
    ACE/ARB

    Exercise
    Calorie
    Glitazones

    Metformin

    Metabolic syndrome is a hidden volcano

    Evaluate every one >25 years of age for MS


    One manifestation screen for all the rest
    WC must be measured routinely like taking BP
    Remember MS is the PRE for T2DM and CVD
    We should not wait till these killers develop
    There are effective Rx strategies

    DEMI LOVATO NEON LIGHTS

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