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    Unni Krishnan R G
    This table classifies genetic forms of dyslipidemia into 5 main types based on abnormalities in lipid levels and associated genetic defects. Type I is characterized by severely elevated triglyceride levels over 1000 mg/dL due to defects in lipoprotein lipase or ApoCII genes. Type IIa involves increased LDL cholesterol levels over 190 mg/dL from LDL receptor dysfunction. Type IIb combines elevated triglycerides and cholesterol due to defects in apolipoproteins or lipoprotein lipase. Type III causes increased triglycerides and intermediate density lipoprotein cholesterol from ApoE defects. Type IV and V involve elevated triglycerides and specific lipoprotein abnormalities but have unknown genetic causes. Each type is associated with

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    This table classifies genetic forms of dyslipidemia into 5 main types based on abnormalities in lipid levels and associated genetic defects. Type I is characterized by severely elevated triglyceride levels over 1000 mg/dL due to defects in lipoprotein lipase or ApoCII genes. Type IIa involves increased LDL cholesterol levels over 190 mg/dL from LDL receptor dysfunction. Type IIb combines elevated triglycerides and cholesterol due to defects in apolipoproteins or lipoprotein lipase. Type III causes increased triglycerides and intermediate density lipoprotein cholesterol from ApoE defects. Type IV and V involve elevated triglycerides and specific lipoprotein abnormalities but have unknown genetic causes. Each type is associated with

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    This table classifies genetic forms of dyslipidemia into 5 main types based on abnormalities in lipid levels and associated genetic defects. Type I is characterized by severely elevated triglyceride levels over 1000 mg/dL due to defects in lipoprotein lipase or ApoCII genes. Type IIa involves increased LDL cholesterol levels over 190 mg/dL from LDL receptor dysfunction. Type IIb combines elevated triglycerides and cholesterol due to defects in apolipoproteins or lipoprotein lipase. Type III causes increased triglycerides and intermediate density lipoprotein cholesterol from ApoE defects. Type IV and V involve elevated triglycerides and specific lipoprotein abnormalities but have unknown genetic causes. Each type is associated with

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    81 views2 pages

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    Uploaded by

    Unni Krishnan R G
    This table classifies genetic forms of dyslipidemia into 5 main types based on abnormalities in lipid levels and associated genetic defects. Type I is characterized by severely elevated triglyceride levels over 1000 mg/dL due to defects in lipoprotein lipase or ApoCII genes. Type IIa involves increased LDL cholesterol levels over 190 mg/dL from LDL receptor dysfunction. Type IIb combines elevated triglycerides and cholesterol due to defects in apolipoproteins or lipoprotein lipase. Type III causes increased triglycerides and intermediate density lipoprotein cholesterol from ApoE defects. Type IV and V involve elevated triglycerides and specific lipoprotein abnormalities but have unknown genetic causes. Each type is associated with

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    Table 1. Genetic classification of dyslipidemia.

    Classification Examples of Genetic Diseases* Genetic Defect Common Lipid Clinical Findings
    (Frequency) Abnormalities**
    Genetic defect of LPL TG levels in the 1000’s, Eruptive
    Type I Lipoprotein lipase deficiency gene – autosomal with as high as over xanthomas
    ‘Chylomicronemia recessive 10,000 mg/dl Pancreatitis
    syndrome’ (increased
    triglyceride levels and ApoCII deficiency (1:1,000,000 for Genetic defect Partial genetic
    chylomicron particles) either of the above) of ApoCII gene – defects may have TG
    autosomal recessive levels > 500 mg/dL
    Multiple genetic
    defects – inheritance
    Polygenic hypercholesterolemia LDL-C levels > 130 Increased risk of
    likely dependent upon
    (1:20) mg/dL ASCVD
    underlying genetic
    abnormality
    Type IIa (increased Increased risk of
    Heterozygous familial
    LDL cholesterol levels premature ASCVD
    hypercholesterolemia LDL-C levels > 190
    and/or particles) Dysfunction or
    (1:500) mg/dL
    absence of LDL Tendon xanthoma
    receptor – autosomal LDL-C levels Increased risk of
    Homozygous familial dominant sometimes > 350 mg/ premature ASCVD
    hypercholesterolemia
    dL, but most often 500
    (1:1,000,000)
    - 1000 mg/dL Tendon xanthoma
    Type IIb (increased LDL-C levels > 160 Increased risk of
    Multiple genetic
    triglyceride levels, mg/dL ASCVD
    defects of various apo-
    and increased LDL Familial combined hyperlipidemia
    lipoproteins and/or LPL TG levels> 300 mg/dL
    and VLDL cholesterol (1:50-1:200)
    genes - ? autosomal
    levels and/or
    dominant
    particles)
    LDL-C > 220 mg/dL Palmar
    xanthomata
    Type III (increased TG levels > 300 mg/dL (orange
    triglyceride levels Genetic defect of apoE discoloration of
    and increased gene – autosomal skin creases,
    Familial dysbetalipoproteinemia
    intermediate-density recessive, or more tuberoeruptive
    (1:1000-1:5000)
    lipoprotein cholesterol rarely, autosomal xantomata of
    levels and/or dominant elbows and knees
    particles)
    Increased risk of
    premature ASCVD
    Type IV (increased TG levels > 150 mg/dL Unclear if
    triglyceride levels Unknown genetic increased risk of
    Familial hypertriglyceridemia
    and increased VLDL defect – autosomal ASCVD
    (1:50-1:100)
    cholesterol levels and/ dominant
    or particles)
    Eruptive
    Type V (increased xanthomas
    triglyceride levels Unknown genetic TG levels > 500 mg/dL
    and increased Hyperprebetalipoproteinemia (un- defect – possibly due Pancreatitis
    chylomicron and VLDL known frequency, very rare) to an LPL inhibitor –
    cholesterol levels and/ unknown inheritance LDL-C levels > 130
    mg/dL Increased risk of
    or particles) ASCVD

    LDL = low-density lipoprotein; VLDL = very low-density lipoprotein; Apo = apolipoprotein; LPL = lipoprotein lipase.
    *In addition to genetic causes, many of these hyperlipoproteinemias may be acquired or secondary to high carbohydrate diets,
    medications, and/or underlying diseases. Hence, the frequencies listed above only refer to the number of patients with the genetic
    abnormality specified and do not reflect the total frequency by which the types of lipid phenotypes are observed in clinical practice.

    ** The listed lipid values for genetic abnormalities should be considered common lipid values, intended to provide general values that
    might be encountered in clinical practice. These lipid values are not intended to be diagnostic. Lipid values can vary widely among
    individual patients with genetic abnormalities, especially when combined with secondary causes of dyslipidemia and other genetic
    abnormalities.

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