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Lipoprotein(a) (also called Lipoprotein LP(a) and Lp-a) is a lipoprotein subclass. Lp-a is a risk factor for coronary heart disease and other vascular diseases.
Lipoprotein(a) is assembled in the blood from low density lipoprotein (LDL) molecules and glycoprotein molecules called apolipoprotein-a (apo-a). Plasma apo-a is secreted by the liver. The mechanism and sites of Lp(a) catabolism are unknown.
Lp-a is genetically linked with concentrations varying over one thousandfold, from < 0.2 to > 200 mg/dL. African populations have Lp-a concentrations severalfold higher than Caucasians and Asian populations. Plasma Lp-a levels are inversely related to the size of the Apo-a molecule. Individuals with larger Apo-a particles have lower Lp-a levels, and those with smaller particles have higher Lp-a levels.
Lipoprotein(a) recruits inflammatory cells through interaction with Mac-1 integrin.
Lipoprotein's structure is simillar to plasminogen and tPA (tissue plasminogen activator) and it competes with plasminogen for its binding site, leading to reduced fibrinolysis. Also because Lp(a) stimulates secretion of PAI-1 it leads to thrombogenesis. In addition, because of LDL cholestrol content, Lp-a contributes to atherosclerosis.
Lipoprotein(a) and Disease
High Lp(a) in blood is a risk factor for coronary heart disease (CHD), cerebrovascular disease (CVD), atherosclerosis, thrombosis, and stroke. Lp-a concentrations may be affected by disease states, but are only slightly affected by diet, exercise, and other environmental factors. Commonly prescribed lipid-reducing drugs have little or no effect on Lp(a) concentration. Niacin (nicotinic acid) and aspirin are two relatively safe, easily available and inexpensive drugs known to significantly reduce the levels of Lp(a) in some individuals with high Lp(a); they should be used under the supervision of a qualified physician. A search of the medical literature has revealed some interesting observations:
Vegetarians have higher levels of Lp-a than fish eaters in one homogeneous tribal population of Tanzania raising the possibility that pharmacologic amounts of fish oil supplements may be helpful to lower the levels of Lp-a.
Low fat-high carbohydrate diet raises Lp-a.
Fibrates such as bezafibrate or gemfibrozil have significantly lowered Lp-a in some individuals.
Prolonged and daily intake of large amounts of milk protein (casein) or alcohol extracted soy protein in the diet leads to a very significant decline in the levels of plasma Lp-a. However, consumption of regular soy protein does not lower the levels of Lp-a.
Regular and daily consumption of moderate to large amounts of alcohol leads to significant decline in plasma levels of Lp-a.
High levels of Apo AI HDL cholesterol are protective against atherogenic potential of Lp-a.
Dr. Linus Pauling and his associates recommend a combination of very large amounts of Vitamin C, Lysine and Proline as the only definitive treatmentt to lower Lp-a.
High Lp(a) predicts risk of early atherosclerosis similar to high LDL, but in advanced atherosclerosis, Lp(a) is an independent risk factor not dependent on LDL. Lp(a) then indicates a coagulant risk of plaque thrombosis. Apo(a) contains domains that are very similar to plasminogen (PLG). Lp(a) accumulates in the vessel wall and inhibits binding of PLG to the cell surface, reducing plasmin generation which increases clotting. This inhibition of PLG by Lp(a) also promotes proliferation of smooth muscle cells. These unique features of Lp(a) suggest Lp(a) causes generation of clots and atherosclerosis.
Cardiology diagnostic tests
Lipoprotein(a) - Lp(a)
|This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Lipoprotein(a)". A list of authors is available in Wikipedia.|