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Review highlights factors determining lipoprotein(a) levels across health and disease, indicating primarily genetic regulation alongside modifiable metabolic influences.
Lipoprotein(a) (Lp(a)) is an established risk marker of cardiovascular diseases which is independent from other risk markers. The main difference of Lp(a) compared to low density lipoprotein (LDL) is the apo(a) residue which is covalently bound to apoB. Apo(a) is a glycoprotein which underlies a large genetic polymorphism. The latter is caused by a variation of the kringle-IV-type-2 repeats of the protein which is characterized by a large structural homology to plasminogen. The Lp(a) plasma concentration in the population is highly skewed and determined to more than 90 % by genetic factors. In healthy subjects the Lp(a)-concentration is correlated to its synthesis and not to its metabolism. However, plasma concentrations of Lp(a) are also affected by different diseases (e.g. diseases of liver and kidney), hormonal factors (e.g. sexual steroids, glucocorticoids, thyroid hormones), individual and environmental factors (e.g. age, cigarette smoking) as well as pharmaceuticals (e.g. derivatives of nicotinic acid) and therapeutic procedures (lipid apheresis). Aim of this review was to describe the physiological regulation of Lp(a) as well as factors influencing its plasma concentration.
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R. Siekmeier (2010) studied this question.
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