|
Objective: To investigate pitavastatin treatment in patients with primary hypercholesterolemia lowering efficacy; analysis SLC0181 521T gt; C gene polymorphism and acquired factors on lipid-lowering efficacy of pitavastatin effects. METHODS: Screening Changsha and 150 patients with primary hypercholesterolemia who collect gender, age, body mass index, complications such as access factors. The patients were randomly divided into two groups according to 1:1, were given pitavastatin 2mg / day or lovastatin 20mg / day, orally at bedtime. 150 patients were using allele-specific PCR (ARMS-PCR) and polymerase chain reaction - restriction fragment length polymorphism (PCR-RFLP) method for detecting SLC0181 the 521T gt; C and 388G gt; A locus gene polymorphism. Pitavastatin groups according to genotype and acquired factors grouped for analysis. Were followed for eight weeks. In taking the medication before and after 8 weeks of the determination of total cholesterol (TC), triglyceride (TG), high density lipoprotein (HDL-C) and low density lipoprotein (LDL-C), and observation of vital signs, urine routine, liver and kidney function, and adverse reactions and other indicators. Results: 1. Pitavastatin and lipid-lowering efficacy of lovastatin comparison: both before treatment generally no significant difference (P gt; 0.05). Pitavastatin group intervention eight weeks after the total effective rate was 83.3%, in patients with TC, TG, HDL-C and LDL-C change rate were -21.0 ± 5.0%, -25.3 ± 6. 8%, 2.4 ± 1.9% and -21.1 ± 6.7%. Lovastatin group, the total effective rate was 81.7%, the patient TC, TG, HDL-C and LDL-C change rate were -20.4 ± 4.7%, -24.8 ± 6.2%, 2 .0 ± 1.5% and -20.6 ± 7.8%. Pitavastatin group and the magnitude of lipid changes between the lovastatin group and the total effective rate was no significant difference was statistically significant (P gt; 0.05). 2 gene polymorphisms: hypercholesterolemia patients, SLC01B1 the 521T gt; C and 388G gt; A mutant allele frequency was 11.1% and 71.1%. For 521T gt; C locus, 521T wild-type homozygotes the total number of 79.3%, 521TC and 521CC 19.3%, respectively, of the total number and 1.4%; 388A homozygous wild-type total number of eight .6%, 388G gt; A mutation heterozygous and homozygous, respectively, 40.7% of the total number and 50.7%. Allele and genotype distributions are in line with Hardy-Weiberg equilibrium. 3. SLC0181 521T gt; C gene polymorphism on pitavastatin lipid-lowering efficacy effects: plasma TC levels in patients with the TT group change rate of -24.3 ± 4.2%, while in TC / CC group of patients the rate of change was -11.1 ± 3.4%, pitavastatin total cholesterol-lowering effect in the TT group was significantly stronger than the TC / CC patients (P lt; 0.05). The TG, LDL-C and HDL-C change value in the two groups was not statistically significant (P gt; 0.05). 4. Efficacy of pitavastatin multivariate analysis: Plasma TC levels in patients with normal weight change rate of -24.8 ± 4.7%, in obese patients in the rate of change of -12.7 ± 3.1%, two groups were significantly different (P lt; 0.05). Plasma TC levels in patients with diabetes mellitus not by the rate of change -22.2 ± 3.7%, in patients with diabetes mellitus in the rate of change of -12.6 ± 2.9%, both groups were significantly different (P lt; 0.05). The logistic regression analysis: Y = 2.704-0.246 × X 1 -0.222 × X 4 -0.541 × X 5 , X 2 = 12.112, P lt; 0.05. Conclusion: In patients with primary hypercholesterolemia orally every day for 8 weeks 2mg pitavastatin significant effect, the total effective rate was 83.3%. 2 SLC0181 521T gt; C and 388G gt; A mutation in both primary hypercholesterolemia populations of common mutations. 3 SLC0181 521T gt; C gene mutation may be in patients with primary hypercholesterolemia pitavastatin total cholesterol lowering efficacy influential; acquired factors, BMI, diabetes may be lipid-lowering efficacy of pitavastatin presence affected.
|