Lipoprotein (a) is a relatively new independent risk factor of early atherosclerosis with atherogenic and thrombogenic properties. From the structural aspect it resembles LDL-lipoprotein and differs from the latter by the presence of another glycoprotein-apolipoprotein (a). Due to the great similarity of apolipoprotein (a) and plasminogen, lipoprotein (a) is bound to plasminogen receptors on the fibrin surface (fibrinogen) and thus prevents the cumulation and activation of local fibrinolysis. Its levels are under strict genetic control and are very little influenced by external factors and available hypolipidaemic treatment. There is a great interindividual variability of lipoprotein(a) concentrations which is due above all to the structural variability of apolipoprotein (a). At present at least 34 isoforms of apolipoprotein(a) were described which differ as to the size of the molecule. This great structural variability has an impact not only on the function and pathogenicity of lipoprotein (a) but also on methods of its assessment. High lipoprotein(a) concentrations are found in subjects with early clinical manifestations of atherosclerosis, in nephrotic syndrome, in chronic renal insufficiency, in haemodialyzed patients and other diseases. They rise in women after the menopause and are favourably influenced by hormonal substitution therapy. There is a number of immunochemical methods used for its estimation which are very well reproducible within the same laboratory. The high interlaboratory coefficients of variation indicate, however, that unification of lipoprotein(a) analyses is urgent.

Keywords: Arteriosclerosis /physiopathology/; Humans; Lipoprotein(a) /chemistry/; Risk Factors; Thrombosis /physiopathology/