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Abstract
Although the genetic background is the most important determinant of lipoprotein (a) (Lp(a)) concentration other factors, such as coexistent dyslipidaemia, could modify its levels. We undertook the present study to examine the serum Lp(a) concentration in various dyslipidaemias and to reveal any correlation of serum Lp(a) concentration with the other lipid parameters in a large group of dyslipidaemic Greek patients. A total of 242 patients followed as outpatients in our lipid clinic were studied. The patients were stratified into four main groups. Patients with cholesterol levels greater than 5.17 mmol/ L but normal triglycerides were regarded as hypercholesterolaemic (n = 85), patients with triglycerides greater than 2.25 mmol/L but normal cholesterol levels as hypertriglyceridaemic (n = 51), patients with both increased cholesterol and triglyceride levels as having mixed hyperlipidaemia (n = 62), and finally patients with decreased (<0.90 mmol/L) high-density lipoprotein (HDL) cholesterol but normal cholesterol and triglyceride levels as having primary hypoalphalipoproteinaemia (n = 44). Hypercholesterolaemic patients exhibited the highest serum Lp(a) levels, while hypertriglyceri-daemic patients exhibited the lowest. Patients with mixed hyperlipidaemia had intermediate serum Lp(a) concentration, which was significantly higher than that of hypertriglyceridaemic patients but significantly lower than that of hypercholesterolaemic patients. Interestingly, patients with low serum HDL-cholesterol levels presented with low serum Lp(a) concentration similar to that of hypertriglyceridaemic patients. In hypercholesterolaemic patients no correlation was found between serum total and low-density lipoprotein (LDL) cholesterol nor apolipoprotein B (apoB) levels and Lp(a) concentration. On the contrary, in hypertriglyceridaemic patients an inverse correlation was observed between serum triglycerides and Lp(a) concentration. After dividing the hypertriglyceridaemic patients into one group with elevated (>1.3 g/L) serum apoB levels (n = 32) and another group with normal apoB levels (n = 19), we found that the median serum Lp(a) concentration was three times higher in hyperapoB patients compared to patients with normal apoB levels. We conclude that serum Lp(a) levels are different in various types of primary hyperlipidaemia and are modulated according to the type of lipid elevation.