Lipoprotein disorders classification: Difference between revisions
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! Type I | ! Type I | ||
| Buerger-Gruetz syndrome, | | Buerger-Gruetz syndrome, primary hyperlipoproteinaemia, or [[familial hyperchylomicronemia]] | ||
| Decreased [[lipoprotein lipase]] (LPL) or altered [[apolipoprotein C2|ApoC2]] | | Decreased [[lipoprotein lipase]] (LPL) or altered [[apolipoprotein C2|ApoC2]] | ||
| Elevated [[Chylomicrons]] | | Elevated [[Chylomicrons|chylomicrons]] | ||
| Diet | | Diet control | ||
|- | |- | ||
! Type IIa | ! Type IIa | ||
| Polygenic hypercholesterolaemia or | | Polygenic hypercholesterolaemia or familial hypercholesterolemia | ||
| [[LDL receptor]] deficiency | | [[LDL receptor]] deficiency | ||
| Elevated [[LDL]] only | | Elevated [[LDL]] only | ||
| Bile | | Bile acid sequestrants, [[statin]]s, [[niacin]] | ||
|- | |- | ||
! Type IIb | ! Type IIb | ||
| [[Combined hyperlipidemia]] | | [[Combined hyperlipidemia]] | ||
| Decreased [[LDL receptor]] and | | Decreased [[LDL receptor]] and increased [[apolipoprotein B|ApoB]] | ||
| Elevated [[LDL]], [[VLDL]] and | | Elevated [[LDL]], [[VLDL]] and triglycerides | ||
| [[Statin]]s, [[Niacin]], [[Gemfibrozil]] | | [[Statin]]s, [[Niacin]], [[Gemfibrozil]] | ||
|- | |- | ||
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! Type IV | ! Type IV | ||
| Endogenous Hyperlipemia | | Endogenous Hyperlipemia | ||
| Increased [[VLDL]] production and | | Increased [[VLDL]] production and decreased elimination | ||
| Increased [[VLDL]] | | Increased [[VLDL]] | ||
| Drug of choice: [[Niacin]] | | Drug of choice: [[Niacin]] | ||
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! Type V | ! Type V | ||
| Familial Hypertriglyceridemia | | Familial Hypertriglyceridemia | ||
| Increased [[VLDL]] production and | | Increased [[VLDL]] production and decreased [[LPL]] | ||
| Increased [[VLDL]] and [[Chylomicrons]] | | Increased [[VLDL]] and [[Chylomicrons]] | ||
| [[Niacin]], [[Gemfibrozil]] | | [[Niacin]], [[Gemfibrozil]] | ||
Revision as of 13:18, 11 June 2013
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
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Lipoprotein Disorders Microchapters |
Overview
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.
Classification
| 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, VLDL and triglycerides | Statins, Niacin, Gemfibrozil |
| Type III | Familial Dysbetalipoproteinemia | Defect in ApoE synthesis | Increased IDL | Drug of choice: Gemfibrozil |
| Type IV | Endogenous Hyperlipemia | Increased VLDL production and decreased elimination | Increased VLDL | Drug of choice: Niacin |
| Type V | Familial Hypertriglyceridemia | Increased VLDL production and decreased LPL | Increased VLDL and Chylomicrons | Niacin, Gemfibrozil |
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.