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Lp Level

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Chromosome 6 human [1]. This section needs additional citations for verification. Please help improve this article by adding citations to reliable sources.

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National Center for Biotechnology Information, U. National Library of Medicine. Heart J. Acta Pathol Microbiol Scand. Inheritance and relation to Lp a -lipoprotein concentrations in plasma".

Molecular Genetics and Metabolism. The Journal of Biological Chemistry. Current Opinion in Lipidology. Pharmacological Research. European Heart Journal.

Thrombosis and Haemostasis. The New England Journal of Medicine. Journal of the American Heart Association.

Curr Vasc Pharmacol. Journal of Orthomolecular Medicine. Kidney Int. Abigon Press. Metabolism: Clinical and Experimental. Reduction is supported by other studies".

Biomark Med. Lipid Res. J Clin Epidemiol. Kloss-Brandstaetter A ed. Beyond cholesterol: 7 life-saving heart disease tests that your doctor may not give you.

New York: St. Martin's Griffin. Contribution of Lp a glycoprotein phenotypes to normal lipid variation". J Med Food.

The American Journal of Cardiology. Lipids : lipoprotein particle metabolism. Hidden categories: CS1: long volume value CS1 maint: uses authors parameter Articles needing additional references from October All articles needing additional references Articles using small message boxes All articles with unsourced statements Articles with unsourced statements from September All articles lacking reliable references Articles lacking reliable references from June Articles with unsourced statements from April Recent research suggests that blood levels of Lipoprotein a or Lp a may be an important marker for the risk developing of heart disease.

However, measurements of Lp a are not widely available and are seldom used in routine clinical practice. Measurements of lipids levels are frequently used to assess the risk of future coronary heart disease or stroke.

These two disease conditions are commonly termed cardiovascular disease CVD. Lp a is a strong risk factor for CVD. However, the lack of clinical trial data has resulted in Lp a being largely ignored by clinical guidelines assessing the prevention of CVD.

Clinicians should consider screening statin-treated patients with recurrent heart disease, in addition to those considered at moderate to high risk of heart disease.

Lipoproteins are composed of proteins apolipoproteins , phospholipids, triglycerides and cholesterol. The lipoproteins vary in the major lipoprotein present and the relative contents of the different lipid components.

Lp a is a lipoprotein rich in cholesterol. It as assumed that Lp a is produced by liver cells. However, the pathways for the clearance of this substance are not clearly understood.

Plasma levels of Lp a rise shortly after birth and the levels appear to become consistent within a few months. In adults, plasma levels of Lp a vary widely, ranging from 0.

The levels are similar in men and women. A meta-analysis of prospective studies provided evidence of a link between Lp a and coronary artery disease.

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Specifically, the larger the isoform, the more apo a precursor protein accumulates intracellularly in the endoplasmic reticulum. Lp a is not fully synthesised until the precursor protein is released from the cell, so the slower rate of production for the larger isoforms limits the plasma concentration.

This range of concentrations is observed in all populations studied by scientists so far. The mean and median concentrations differ among world populations.

Most prominently, there is a two- to threefold higher mean Lp a plasma concentration in populations of African descent compared to Asian, Oceanic, or European populations.

The general inverse correlation between apo a isoform size and Lp a plasma concentration is observed in all populations. In addition to size effects, mutations in the LPA promoter may also lead to a decreased apo a production.

Lp a is assembled at the hepatocyte cell membrane surface, which is similar to typical LDL particles. However, there are other possible locations of assembly.

The particles mainly exist in plasma. Lp a contributes to the process of atherogenesis. The structure of apolipoprotein a is similar 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. Moreover, Lp a carries atherosclerosis -causing cholesterol and binds atherogenic pro-inflammatory oxidised phospholipids as a preferential carrier of oxidised phospholipids in human plasma, [21] which attracts inflammatory cells to vessel walls and leads to smooth muscle cell proliferation.

Nonetheless, individuals without Lp a or with very low Lp a levels seem to be healthy. Thus, plasma Lp a is not vital, at least under normal environmental conditions.

Another possibility, suggested by Linus Pauling , is that Lp a is a primate adaptation to L-gulonolactone oxidase GULO deficiency, found only in certain lines of mammals.

GULO is required for converting glucose to ascorbic acid vitamin C , which is needed to repair arteries; following the loss of GULO, those primates who adopted diets less abundant in vitamin C may have used Lp a as an ascorbic-acid surrogate to repair arterial walls.

The half-life of Lp a in circulation is approximately three to four days. Uptake via the LDL receptor is not a major pathway of Lp a metabolism.

High Lp a in blood correlates with coronary heart disease CHD , cardiovascular disease CVD , atherosclerosis , thrombosis , and stroke.

Most commonly prescribed lipid-reducing drugs have little or no effect on Lp a concentration. Results using statin medications have been mixed in most trials, although a meta-analysis published in suggests that atorvastatin may be of benefit.

Niacin Vitamin B 3 has been shown to reduce the levels of Lp a in individuals with high levels of low-molecular weight Lp a. High Lp a correlates with early atherosclerosis independently of other cardiac risk factors, including LDL.

In patients with advanced cardiovascular disease, Lp a 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 the binding of PLG to the cell surface, reducing plasmin generation, which increases clotting.

This inhibition of PLG by Lp a also promotes the proliferation of smooth muscle cells. These unique features of Lp a suggest that Lp a causes generation of clots and atherosclerosis.

In one homogeneous tribal population of Tanzania, vegetarians have higher levels of Lp a than fish eaters, raising the possibility that pharmacologic amounts of fish oil supplements may help lower the levels of Lp a.

Numerous studies confirming a strong correlation between elevated Lp a and heart disease have led to the consensus that Lp a is an important independent predictor of cardiovascular disease.

The European Atherosclerosis Society currently recommends that patients with a moderate or high risk of cardiovascular disease should have their Lp a levels checked.

Any patient with one of the following risk factors should be screened:. In addition, the patient's other cardiovascular risk factors including LDL levels should be managed optimally.

Prior studies of the relationship between Lp a and ethnicity have shown inconsistent results. Lp a levels seem to differ in different populations.

One recent study showed that in different ethnic groups, different genetic alterations were associated with increased Lp a levels.

More recent data suggest that prior studies were underpowered. The researchers found that an elevated Lp a conferred the same risk in each group.

African Americans had roughly three times the level of Lp a , however, and Lp a also predicted an increased risk of stroke.

Approximate levels of risk are indicated by the results below, although at present there are a variety of different methods by which to measure Lp a.

Although further standardization is still needed, development of a reference material is an importance step toward standardizing results.

Lipoprotein a - Lp a [50]. Lighter Lp a are also associated with disease. Thus, a test with simple quantitative results may not provide a complete assessment of risk.

The current simplest treatment for elevated Lp a is to take 1—3 grams of niacin daily, typically in an extended-release form. This protocol can reduce Lp a two- to fivefold over a few months.

L-carnitine may also reduce Lp a levels. TRT testosterone replacement therapy also causes Lp a levels to drop. Gingko biloba may be a beneficial treatment, but clinical verification does not exist.

Testosterone is known to reduce Lp a levels. Risks and benefits may need to be considered for each individual. At present, estrogen is not indicated for treatment of elevated Lp a.

The blood will be collected in a tube and sent to a lab for analysis. The lab reports will be sent to your doctor, who can give you more information about the results and what they mean.

You may experience some discomfort when the blood sample is drawn, as with any blood test. Needle sticks may be painful during the test.

Following the test, you may experience pain or throbbing at the injection site. Bruising may also occur. The results of the Lp a test will vary depending on the laboratory where the sample was analyzed.

In many instances, people will have no detectable levels of Lp a in their bloodstream. Talk with your doctor about your results.

This may involve aggressively modifying your diet, starting a consistent exercise program, and taking medications to lower cholesterol and lipoproteins.

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New treatments over the past few years mean that Hep C today is much more manageable than it was in the past. Learn about new treatments and costs. About Lp a.

How to prepare for the test. How the test is administered. Understanding your results.

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