Serum lipoprotein(a) levels differ in different phenotypes of primary hyperlipoproteinemia.

Previous studies have indicated that serum lipoprotein(a) [Lp(a)] levels are mostly under genetic control. We have attempted to determine whether serum Lp(a) levels differ in different phenotypes of primary hyperlipoproteinemia (HL). A total of 129 subjects with HL (three with type I, 43 with familial hypercholesterolemia [FH], 17 with type IIa [non-FH], 11 with type IIb, six with type Ill [E22], 44 with type IV, and five with type V) and 18 normolipidemic controls were included in the study. Thirty-two FH subjects were being treated with hypolipidemic agents, but none of the other subjects were receiving any medication. Fasting blood samples were collected for determination of both serum lipid and Lp(a) levels. Lp(a) level was measured by enzyme-linked immunosorbent assay. The 18 controls had serum Lp(a) concentrations of 18.0 ± 14.5 mg/dL (mean ± SD), and four of them had high serum Lp(a) levels (≥ 25 mg/dL). Serum Lp(a) concentrations in FH subjects tended to be higher than in the controls (30.5 ± 25.0 mg/dL), and the incidence of high Lp(a) levels in FH subjects was significantly higher than in the controls (51% v 22%, P < .01). There was no difference between serum Lp(a) levels of FH subjects depending on whether they were receiving medication. In contrast, most of the subjects with selective hypertriglyceridemia had very low serum Lp(a) levels (1.5 ± 0.7, 8.1 ± 8.3, and 3.5 ± 5.3 mg/dL in type I, IV, and V, respectively; P < .01 v controls). In eight subjects who were receiving medication for treatment of hypertriglyceridemia, serum Lp(a) levels increased significantly (P < .05), indicating that serum triglyceride has a significant influence on serum Lp(a) levels. In summary, the present study demonstrated that serum Lp(a) levels differ in different phenotypes of primary HL. The precise mechanism underlying the possible association between the two remains to be addressed in future studies.