Apolipoprotein(a)

Alternative Names

  • LPA
  • Lipoprotein(a)
  • Lp(a)
  • Lipoprotein Types--Lp System Lp(a) Hyperlipoproteinemia
  • Sinking Pre-Beta-Lipoprotein
  • SPB
  • Lipoprotein(a) Deficiency, Congenital
  • Lp(a) Deficiency, Congenital
  • Coronary Artery Disease, Susceptibility to
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WHO-ICD-10 version:2010

Endocrine, nutritional and metabolic diseases

Metabolic disorders

OMIM Number

152200

Mode of Inheritance

Autosomal dominant

Gene Map Locus

6q25-q26

Description

Lipoprotein(a), denoted as Lp(a), is a subclass of lipoproteins, consisting of a low-density lipoprotein (LDL)-like particle, formed by the association of glycosylated apolipoprotein(a) with apolipoprotein B100. Hyperlipoproteinemia, or raised levels of plasma lipoproteins have been found to be associated with an increased incidence of a variety of cardiovascular diseases, including silent coronary artery disease, acute myocardial infarction, asymptomatic carotid atherosclerosis, stroke, and peripheral artery occlusive disease.

Hyperlipoproteinemia can be managed with cholesterol lowering drugs, like statins. As supportive therapy, weight reduction and diet control is necessary.

The physiological function of Lp(a)/apo(a) is still unknown. Considering the high level of homology between apo(a) and plasminogen, researchers have postulated a role for this protein within the coagulation system.

The apo(a) gene is located in a gene cluster within 400 kb of genomic DNA on the telomeric region of chromosome 6q. Apart from the sequence encoding apo(a), this region also includes sequences for plasminogen and other two pseudogenes with highly homologous untranslated 5? flanking regions. Three additional homologues genes, designated as plasminogen?related genes, unlinked to the apo(a) gene cluster have also been identified on chromosomes 2 and 4. Lp(a) is assembled by attaching apo(a) to apo B100 through a single disulfide bond.

Most variability in Lp(a) levels is of genetic origin. Over 40% of this variability arises from polymorphisms in the apo(a) gene. Another 15% is due to polymorphisms in the promoter of this gene. Metabolic abnormalities, such as the acute?phase response, hormonal homeostasis, diabetes, liver, and renal failure, also contribute to variations in Lp(a) levels.

Epidemiology in the Arab World

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Other Reports

Kuwait

In order to establish reference values for Lp(a) values in newborns, Alsaeid et al. (1999) measured cord blood serum Lp(a) concentrations in 107 Arab neonates (65 males, 42 females) born in Kuwait. Of these, 62 were Kuwaitis, while 45 were non-Kuwaiti Arabs. The mean and median Lp(a) concentrations among this group were found to be 54,75 and 33 mg/L, respectively. Mean Lp(a) levels were significantly higher in the females (77.3), compared to the males (40.2). Lp(a) levels did not show any correlation with maternal or infant characteristics, or mode of delivery, confirming its predominant genetic control.

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