Decades after its first description by Berg 1963 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 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. Plasma concentrations of Lp(a) are 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).
However, even though a large number of studies on Lp(a) were performed up to now many details of its physiological
function and regulation of plasma concentration are not yet understood. In addition, studies showed contradictory results
because there were large differences of the included patients, use of not sufficiently validated tests as well as analysis
of frozen samples. Aim of our review was to describe function and physiological regulation of Lp(a) as well as factors influencing
its plasma concentration.