Hyperlipoproteinemia classification: Difference between revisions
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{{familytree | | | | | | | B01 | | | | | | | | | | | | | | B02 | B01= '''Primary'''<br>(Genetic)| B02= '''Secondary'''}} | {{familytree | | | | | | | B01 | | | | | | | | | | | | | | B02 | B01= '''Primary'''<br>(Genetic)| B02= '''Secondary'''}} | ||
{{familytree | | | | | | | |!| | | | | | | | | | | | | | | |!| }} | {{familytree | | | | | | | |!| | | | | | | | | | | | | | | |!| }} | ||
{{familytree | |,|-|-|-|v|-|^|-|v|-|-|-|.| | | | | | | | | C01 | C01= [[Alcohol]] <br> [[Diabetes]] <br> [[Drug]]s <br> [[Liver disease]] <br> [[Obesity]] <br> [[Renal disease]] <br> [[Smoking]] <br> [[Thyroid]]}} | |||
{{familytree | |,|-|-|-|v|-|^|-|v|-|-|-|.| | | | | }} | {{familytree | D01 | | D02 | | D03 | | D04 | | | | D01= '''LDL'''| D02= '''Chylomicron Remnants'''| D03= '''Lipoproteins Rich in Triglyceride'''<br> '''(Chylomicrons, VLDL, IDL)'''| D04= '''HDL'''}} | ||
{{familytree | D01 | | D02 | | D03 | | D04 | | | }} | |||
{{familytree | |!| | | |!| | | |!| | | |!| | | | }} | {{familytree | |!| | | |!| | | |!| | | |!| | | | }} | ||
{{familytree | E01 | | E02 | | E03 | | E04 | | | }} | {{familytree | E01 | | E02 | | E03 | | E04 | | | |E01= -Familial hypercholesterolemia <br> -Familial defective apo B 100 <br> -Autosomal dominant hypercholesterolemia (PCSK9) <br> -Autosomal recessive hypercholesterolemia <br> -Familial sistosterolemia <br> -Familial lipoprotein a lipoproteinemia| E02= -Deficiency in hepatic lipase<br> -Type III dysbetalipoproteinemia| E03= -Deficiency in lipoprotein lipase<br> -Deficiency in Apo C-II <br> -Deficiency in Apo A-V <br> -Familial combined hyperlipidemia<br> -Familial hypertriglyceridemia| E04= -Cholesteryl ester transferase protein deficiency }} | ||
{{familytree/end}} | {{familytree/end}} | ||
Latest revision as of 19:10, 17 September 2013
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
Hyperlipoproteinemia can be classified into primary and secondary hyperlipoproteinemia depending on the etiology. Primary lipoprotein disorders, caused by genetic mutations, can affect mainly the LDL particle, HDL, or more than one lipoprotein at the same time. In addition, secondary lipoproteinemia include medical conditions that lead to low lipoprotein levels.
Classification
Etiology
Shown below is an algorithm depicting the classification of hyperlipoproteinemia into primary and secondary.
Hyperlipoproteinemia | |||||||||||||||||||||||||||||||||||||||||||||||||||||
Primary (Genetic) | Secondary | ||||||||||||||||||||||||||||||||||||||||||||||||||||
Alcohol Diabetes Drugs Liver disease Obesity Renal disease Smoking Thyroid | |||||||||||||||||||||||||||||||||||||||||||||||||||||
LDL | Chylomicron Remnants | Lipoproteins Rich in Triglyceride (Chylomicrons, VLDL, IDL) | HDL | ||||||||||||||||||||||||||||||||||||||||||||||||||
-Familial hypercholesterolemia -Familial defective apo B 100 -Autosomal dominant hypercholesterolemia (PCSK9) -Autosomal recessive hypercholesterolemia -Familial sistosterolemia -Familial lipoprotein a lipoproteinemia | -Deficiency in hepatic lipase -Type III dysbetalipoproteinemia | -Deficiency in lipoprotein lipase -Deficiency in Apo C-II -Deficiency in Apo A-V -Familial combined hyperlipidemia -Familial hypertriglyceridemia | -Cholesteryl ester transferase protein deficiency | ||||||||||||||||||||||||||||||||||||||||||||||||||
Laboratory Results
Hyperlipoproteinemia can be classified according to which major lipoprotein or major lipid affected as detected in blood laboratory tests: