Hyperlipoproteinemia: Difference between revisions
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== | == Overview == | ||
== | == Synopsis == | ||
{| class="sortable" border="1" cellpadding="5" cellspacing="0" align="center" | |||
|- | |||
!Hyperlipoproteinemia | |||
!Synonyms | |||
!Problems | |||
!Labs description | |||
!Treatment | |||
|- | |||
!Type I | |||
|Buerger-Gruetz syndrome, primary hyperlipoproteinaemia, or [[familial hyperchylomicronemia]] | |||
|Decreased [[lipoprotein lipase]] (LPL) or altered [[Apolipoprotein C2|ApoC2]] | |||
|Elevated [[chylomicrons]] | |||
|Diet control | |||
|- | |||
!Type IIa | |||
|Polygenic hypercholesterolaemia or familial hypercholesterolemia | |||
|[[LDL receptor]] deficiency | |||
|Elevated [[LDL]] only | |||
[[ | |Bile acid sequestrants, [[statin]]s, [[niacin]] | ||
|- | |||
!Type IIb | |||
[[ | |[[Combined hyperlipidemia]] | ||
|Decreased [[LDL receptor]] and increased [[Apolipoprotein B|ApoB]] | |||
|Elevated [[LDL]], [[VLDL]] and triglycerides | |||
|[[Statin]]s, [[niacin]], [[gemfibrozil]] | |||
|- | |||
[[ | !Type III | ||
|Familial Dysbetalipoproteinemia | |||
|Defect in [[Apolipoprotein E|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]] | |||
|} | |||
== Classification == | |||
{{Lipopedia}} | {{Lipopedia}} | ||
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{{WH}} | {{WH}} | ||
{{WS}} | {{WS}} | ||
== References == |
Revision as of 19:46, 8 November 2016
Hyperlipoproteinemia Microchapters |
ACC/AHA Guideline Recommendations |
Intensity of statin therapy in primary and secondary prevention |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Synopsis
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 |