Lipoprotein disorders causes: Difference between revisions

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Secondary to some underlying "non-lipid" etiology
Secondary to some underlying "non-lipid" etiology


*Type 2 [[diabetes mellitus]]
*Type 2 [[diabetes mellitus]] <ref name="pmid3893447">{{cite journal| author=Zavaroni I, Dall'Aglio E, Alpi O, Bruschi F, Bonora E, Pezzarossa A et al.| title=Evidence for an independent relationship between plasma insulin and concentration of high density lipoprotein cholesterol and triglyceride. | journal=Atherosclerosis | year= 1985 | volume= 55 | issue= 3 | pages= 259-66 | pmid=3893447 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3893447  }} </ref>
*[[Nephrotic syndrome]]
*[[Nephrotic syndrome]]
*[[Chronic renal failure]]
*[[Chronic renal failure]]

Revision as of 13:17, 23 October 2012

Lipoprotein Disorders Microchapters

Patient Information

Overview

Causes

Classification

Hyperlipoproteinemia
Hypolipoproteinemia

Treatment

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Hyperlipidemia can occur as either a primary event or secondary to some underlying disease. The primary hyperlipidemias include chylomicronemia, hypercholesterolemia, dysbetalipoproteinemia, hypertriglyceridemia, mixed hyperlipoproteinemia, and combined hyperlipoproteinemia. Other diseases, such as diabetes mellitus, pancreatitis, renal disease, and hypothyroidism, can cause the secondary form.

Causes

Primary hyperlipidemia

Hyperlipoproteinemia type I

Hyperlipoproteinemia type II

Type IIa
  • Familial hypercholesterolemia
    • Sporadic (due to dietary factors)
    • Polygenic (multiple abnormalities in LDL metabolism)
    • Truly familial (as a result of a mutation in the LDL receptor gene on chromosome 19 (0.2% of the population), the apo B gene (0.2%) or the proprotein convertase subtilisin kexin 9 (PCSK9) gene (very rare))
Type IIb
  • Familial combined hyperlipoproteinemia (FCH)
    • Overproduction of hepatically-derived apo B-100 associated with VLDL
    • Overproduction of substrates, including triglycerides and acetyl-CoA
    • Decreased clearance of LDL

Hyperlipoproteinemia type III

  • Presence of apo E E2/E2 genotype resulting in cholesterol-rich VLDL (β-VLDL)

Hyperlipoproteinemia type IV

  • Genetic defect, which is passed on in an autosomal dominant fashion

Hyperlipoproteinemia type V

  • Very similar to type I, but with high VLDL in addition to chylomicrons
  • Associated with glucose intolerance and hyperuricemia

Secondary hyperlipidemia

Secondary to some underlying "non-lipid" etiology

References

  1. Zavaroni I, Dall'Aglio E, Alpi O, Bruschi F, Bonora E, Pezzarossa A; et al. (1985). "Evidence for an independent relationship between plasma insulin and concentration of high density lipoprotein cholesterol and triglyceride". Atherosclerosis. 55 (3): 259–66. PMID 3893447.


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