[Association of endothelial nitric oxide synthase gene polymorphism with level of uric acid in serum for acute coronary syndrome].

OBJECTIVE: To evaluate the association of elevation in serum uric acid with the development of coronary artery disease, and to determine the relationship between uric acid and Glu(298) Asp polymorphism of the endothelial nitric oxide synthase (eNOS) gene in acute coronary syndrome (ACS) in the Chinese Han Nationality. METHODS: The Glu(298) Asp variant of the eNOS gene was detected by polymerase chain reaction/restriction fragment length polymorphism analysis in 58 patients with ACS and 43 healthy controls. The severity of ACS was expressed by the number of affected vessels and by the Duke scoring system. RESULTS: The frequencies of the eNOS Glu/Glu, Glu/Asp, and Asp/Asp genotypes in the ACS group were not significantly different from those of controls (43.1%, 36.2%, 20.7% vs. 48.8%, 34.9%, 16.3%, respectively; chi (2) = 0.446, P = 0.800). In comparison with subjects who had Glu(298) allele in the eNOS gene, the risk of ACS was not increased among Asp/Asp carriers (odds ratio 1.34, 95% confidence interval 0.479 to 3.755, P = 0.575). There was no significant association between the eNOS Glu(298) Asp variant and the Duke score [(46.73+/-19.90) score for Asp/Asp vs. (48.33+/-19.61) score and (38.19+/-15.12) score for Glu/Glu and Glu/Asp, respectively, P=0.248], but there was a significant association between the eNOS Glu(298) Asp variant and the serum uric acid level in ACS group [(298.92+/-87.27) micromol/L for Glu/Glu vs.(380.80+/-95.80) micromol/L and (346.16+/-93.71) micromol/L for Glu/Asp and Asp/Asp, respectively, P = 0.017]. CONCLUSION: Glu(298) Asp polymorphism of the eNOS gene appears to have no association with ACS in the Chinese Han Nationality, but a significant association between the eNOS Glu(298) Asp variant and the serum uric acid level is found in patients with ACS.

[The effect of atorvastatin on the expression of CD55, CD59 in patients with hyperlipidemia].

OBJECTIVE: To study the expressions of CD55 and CD59 in patients with hyperlipidemia and the effects of atorvastatin on it, and to identify the possible influential factors. METHODS: We selected 67 patients with hyperlipidemia, and 24 healthy people matched in terms of age, sex and body weight as control. The expressions of CD55 and CD59 on white blood cells were detected by flow cytometry, and their relationships to blood lipids, complement activation indexes (C(5a), sC(5b-9)), inflammatory factors (high sensitivity C-reactive protein (hsCRP), TNF-alpha, IL-6 were analyzed. 24 patients with hyperlipidemia were treated with atorvastatin for 8-12 weeks and the expressions of CD55 and CD59 were measured before and after atorvastatin therapy. RESULTS: The mean fluorescence intensity (MFI) of CD55 lymphocytes and monocytes were decreased in patients with hyperlipidemia compared with control (2.07 +/- 0.28 vs 2.29 +/- 0.44 and 3.45 +/- 1.02 vs 4.33 +/- 2.32, P < 0.01 and P < 0.05, respectively). CD55 positive lymphocyte MFI was negatively correlated with waist circumference, waist-hip ratio, hsCRP and C(5a). C(5a) was negatively correlated with the MFIs of CD55 positive lymphocytes, monocytes, granulocytes, and positively with TG and diastolic blood pressure. After atorvastatin therapy, the MFIs of CD59 positive lymphocytes, monocytes and granulocytes increased (4.34 +/- 1.16 vs 3.69 +/- 0.76, 4.52 +/- 1.36 vs 3.91 +/- 0.89, 5.67 +/- 1.72 vs 4.56 +/- 1.03, P < 0.05, < 0.05 and < 0.01 respectively), which were not correlated with changes of blood lipids. CONCLUSIONS: The expression of CD55 is down-regulated in hyperlipidemia, which might be influenced by obesity, abdominal distribution of adipose tissue and inflammatory status of hyperlipidemia, but not by blood lipids. The expression of CD55 is related with complement activation; The expression of CD59 is up-regulated after atorvastatin treatment independently of blood lipids.