| Effects of apolipoprotein and low density lipoprotein receptor gene polymorphisms on lipid metabolism, and the lipid risk factors of coronary artery disease | ||
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CETP activity was higher in females (201 (53) nmol/h/l) than in males (162 (45) nmol/h/l) with p=0.03, but no differences were detected between the sexes during colestipol or lovastatin treatment. The CETP activities or changes during the drug treatment were similar in non-FH and FH patients and in patients with type II a and II b hypercholesterolemia.
The CETP activity was 183 (59) nmol/h/ml in the apo E 2/3 and 3/3 patients and 179 (43) nmol/h/ml in the patients with the E4 allele. Colestipol reduced plasma CETP activity by 19.5% in the patients with apo E 2/3 or 3/3, and by 13.3% (p=0.41) in the patients with apo E 3/4 or 4/4, the corresponding reductions for lovastatin being 19.4% and 20.0 % (p=0.99). The best correlations between the CETP basal activity and the lipids were observed with LDL and total cholesterol after lovastatin treatment in the patients with apo E 2/3 or 3/3 (Table 5-6). The CETP change correlated well with the HDL cholesterol change during colestipol, but not lovastatin treatment in both the patients with the apo E 4 allele and those without it (Figure 5-3).
Table 5-6. Pearson correlation of lipids and their changes with the cholesteryl ester transfer protein basal activity according to apo E phenotype
| Apo E 2/3 and 3/3 | Apo E 4/3 and 4/4 | |
|---|---|---|
| Total cholesterol | 0.52 p=0.01 | 0.13 p=0.65 |
| colestipol | 0.51 p=0.02 | 0.04 p=0.90 |
| lovastatin | 0.65 p=0.001 | 0.57 p=0.03 |
| LDL cholesterol | 0.49 p=0.02 | 0.07 p=0.81 |
| colestipol | 0.42 p=0.06 | -0.09 p=0.77 |
| lovastatin | 0.65 p=0.0009 | 0.23 p=0.42 |
| HDL cholesterol | 0.26 p=0.24 | 0.17 p=0.56 |
| colestipol | 0.16 p=0.48 | 0.45 p=0.11 |
| lovastatin | 0.36 p=0.10 | 0.32 p=0.27 |
| Triglycerides | -0.27 p=0.22 | 0.13 p=0.65 |
| colestipol | 0.21 p=0.36 | 0.16 p=0.59 |
| lovastatin | -0.001 p=0.99 | 0.44 p=0.11 |