Factors affecting plasma lipoprotein(a) levels: role of hormones and other nongenetic factors.

Abstract

Lp(a) appears to be one of the most atherogenic lipoproteins. It consists of an low-density lipoprotein core in addition to a covalently bound glycoprotein, apo(a). Apo(a) exists in numerous polymorphic forms. The size of the polymorphism is mediated by the variable number of kringle-4 Type 2 repeats found in apo(a). Plasma Lp(a) levels are determined to more than 90% by genetic factors. Plasma Lp(a) levels in healthy individuals correlate significantly highly with apo(a) biosynthesis, and not with its catabolism. There are several hormones that are known to have a strong effect on Lp(a) metabolism. In certain diseases, such as kidney disease, the Lp(a) catabolism is impaired, leading to elevations that are up to a fivefold increase. Lp(a) levels rise with age but are otherwise only little influenced by diet and lifestyle. There is no safe and efficient way of treating individuals with elevated plasma Lp(a) concentrations. Most of the lipid-lowering drugs have either no significant influence on Lp(a) or exhibit a variable effect in patients with different forms of primary and secondary hyperlipoproteinemia.