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14-September-2008 10:43:22 - Hyperlipidemia Redirected from Fredrickson classification Jump to: navigation, search Hyperlipidemia Classification and external resources ICD-10 E78. ICD-9 272.0-272.4 DiseasesDB 6255 MeSH D006949 Hyperlipidemia, hyperlipoproteinemia or dyslipidemia is the presence of raised or abnormal levels of lipids and/or lipoproteins in the blood. Lipids fatty molecules are transported in a protein capsule, and the density of the lipids and type of protein determines the fate of the particle and its influence on metabolism. Lipid and lipoprotein abnormalities are extremely common in the general population, and are regarded as a highly modifiable risk factor for cardiovascular disease due to the influence of cholesterol, one of the most clinically relevant lipid substances, on atherosclerosis. In addition, some forms may predispose to acute pancreatitis. Contents 1 Classification 1.1 Hyperlipoproteinemia type I 1.2 Hyperlipoproteinemia type II 1.2.1 Type IIa 1.2.2 Type IIb 1.2.3 Treatment 1.3 Hyperlipoproteinemia type III 1.4 Hyperlipoproteinemia type IV 1.5 Hyperlipoproteinemia type V 2 Unclassified forms 3 References 4 External links Classification Hyperlipidemias are classified according to the Fredrickson classification which is based on the pattern of lipoproteins on electrophoresis or ultracentrifugation.1 It was later adopted by the World Health Organization WHO. It does not directly account for HDL, and it does not distinguish among the different genes that may be partially responsible for some of these conditions. It remains a popular system of classification, but is considered dated by many. Fredrickson classification of Hyperlipidemias Hyperlipoproteinemia Synonyms Problems Labs description Treatment Type I Buerger-Gruetz syndrome, Primary hyperlipoproteinaemia, or Familial hyperchylomicronemia Decreased lipoprotein lipase LPL or altered ApoC2 Elevated Chylomicrons Diet Control Type IIa Polygenic hypercholesterolaemia or Familial hypercholesterolemia LDL receptor deficiency Elevated LDL only Bile Acid Sequestrants, Statins, Niacin Type IIb Combined hyperlipidemia Decreased LDL receptor and Increased ApoB Elevated LDL and VLDL and Triglycerides Statins, Niacin, Fibrate Type III Familial Dysbetalipoproteinemia Defect in ApoE synthesis Increased IDL Drug of choice: Fibrate Type IV Endogenous Hyperlipemia Increased VLDL production and Decreased elimination Increased VLDL Drug of choice: Fibrate, Niacin Type V Familial Hypertriglyceridemia Increased VLDL production and Decreased LPL Increased VLDL and Chylomicrons Niacin, Fibrate Hyperlipoproteinemia type I This very rare form also known as Buerger-Gruetz syndrome, primary hyperlipoproteinaemia, or familial hyperchylomicronemia is due to a deficiency of lipoprotein lipase LPL or altered apolipoprotein C2, resulting in elevated chylomicrons, the particles that transfer fatty acids from the digestive tract to the liver. Lipoprotein lipase is also responsible for the initial breakdown of endogenously made triacylglycerides in the form of very low density lipoprotein VLDL. As such, one would expect a defect in LPL to also result in elevated VLDL. Its prevalence is 0.1% of the population. Hyperlipoproteinemia type II Hyperlipoproteinemia type II, by far the most common form, is further classified into type IIa and type IIb, depending mainly on whether there is elevation in the triglyceride level in addition to LDL cholesterol. Type IIa Main article: Familial hypercholesterolemia This may be sporadic due to dietary factors, polygenic, or truly familial as a result of a mutation either in the LDL receptor gene on chromosome 19 0.2% of the population or the ApoB gene 0.2%. The familial form is characterized by tendon xanthoma, xanthelasma and premature cardiovascular disease. Type IIb The high VLDL levels are due to overproduction of substrates, including triglycerides, acetyl CoA, and an increase in B-100 synthesis. They may also be caused by the decreased clearance of LDL. Prevalence in the population is 10%. Familial combined hyperlipoproteinemia FCH Secondary combined hyperlipoproteinemia usually in the context of metabolic syndrome, for which it is a diagnostic criterion Treatment While dietary modification is the initial approach, many patients require treatment with statins HMG-CoA reductase inhibitors to reduce cardiovascular risk. If the triglyceride level is markedly raised, fibrates may be preferable due to their beneficial effects. Combination treatment of statins and fibrates, while highly effective, causes a markedly increased risk of myopathy and rhabdomyolysis and is therefore only done under close supervision. Other agents commonly added to statins are ezetimibe, niacin and bile acid sequestrants. There is some evidence for benefit of plant sterol-containing products and ω3-fatty acids2 Hyperlipoproteinemia type III This form is due to high chylomicrons and IDL intermediate density lipoprotein. Also known as broad beta disease or dysbetalipoproteinemia, the most common cause for this form is the presence of ApoE E2/E2 genotype. It is due to cholesterol-rich VLDL β-VLDL. Prevalence is 0.02% of the population. Hyperlipoproteinemia type IV This form is due to high triglycerides. It is also known as hypertriglyceridemia or pure hypertriglyceridemia. According to the NCEP-ATPIII definition of high triglycerides 200 mg/dl, prevalence is about 16% of adult population.3 Hyperlipoproteinemia type V This type is very similar to type I, but with high VLDL in addition to chylomicrons. It is also associated with glucose intolerance and hyperuricemia Unclassified forms Non-classified forms are extremely rare: Hypo-alpha lipoproteinemia Hypo-beta lipoproteinemia prevalence 0.01-0.1% References ^ Frederickson DS, Lee RS. A system for phenotyping hyperlipidemia. Circulation 1965;31:321-7. PMID 14262568. ^ Thompson GR. Management of dyslipidaemia. Heart 2004;90:949-55. PMID 15253984. ^ Third Report of the National Cholesterol Education Program NCEP Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults Adult Treatment Panel III Final Report. Circulation 2002; 106; page 3240 External links The Fredrickson papers with photos from early lipoprotein research Hyperlipoproteinemia OMIM GPnotebook WebMD Others Type I Online 'Mendelian Inheritance in Man' OMIM 238600 . MeritCare Type IIa Online 'Mendelian Inheritance in Man' OMIM 144400 . Merck Type IIb . Type III . WebMD Yahoo Type IV Online 'Mendelian Inheritance in Man' OMIM 144600 WebMD Yahoo Type V Online 'Mendelian Inheritance in Man' OMIM 144600 . . v d e Lipid metabolism disorders / Inborn error of lipid metabolism - dyslipidemia E78 and E71.3, 272 Hyperlipidemia Hypercholesterolemia/Hypertriglyceridemia Familial hypercholesterolemia, Combined hyperlipidemia - Xanthoma Hypolipoproteinemia Hypoalphalipoproteinemia/HDL Lecithin cholesterol acyltransferase deficiency, Tangier disease Hypobetalipoproteinemia/LDL Abetalipoproteinemia, Apolipoprotein B deficiency Lipodystrophy Barraquer-Simons syndrome Fatty acid metabolism deficiency transport: Carnitine Primary, I, II, -acylcarnitine - Adrenoleukodystrophy beta oxidation: Acyl CoA dehydrogenase Short-chain, Medium-chain, Long-chain 3-hydroxy, Very long-chain - Mitochondrial trifunctional protein deficiency to acetyl-CoA: Malonic aciduria Cholesterol synthesis Smith-Lemli-Opitz syndrome Other Sjögren-Larsson syndrome - Lipomatosis - Adiposis dolorosa - Lipoid proteinosis see also lipid metabolism enzymes, lipoprotein metabolism Retrieved from http://en..org/wiki/Hyperlipidemia Categories: Metabolic disorders | Cardiology | Lipid disorders Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Deutsch עברית РуÑ?Ñ?кий Svenska This page was last modified on 8 August 2008, at 18:55
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