| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1968341 | Clinica Chimica Acta | 2006 | 5 Pages |
BackgroundHomocysteine thiolactone adducts have been proposed as the culprit of homocysteine related cardiovascular diseases. We studied the association of these adducts in plasma, and the gene polymorphism of paraoxonase-2 with coronary heart disease.Methods254 patients and 308 controls were recruited for the study. Homocysteine thiolactone adducts were determined with ELISA. The codon 311 polymorphism of paraoxonase-2 gene was genotyped by using polymerase chain reaction and restrictive digestion.ResultsThe plasma level of homocysteine thiolactone adducts were significantly higher in patients than in controls (40.65 ± 10.87 u/ml vs. 30.58 ± 10.20 u/ml, P < 0.01), with odds ratio of 7.34 (95% confidence interval 4.020∼13.406, P < 0.01), and increased according to the number of atherosclerotic coronary arteries: 35.59 ± 10.34 units/ml (n = 76); 41.88 ± 8.83 (n = 70) and 43.13 ± 11.47 (n = 108) in subjects with 1, 2 and 3 affected arteries, respectively (r = 0.174, P < 0.01). The frequency of CC genotype was significantly higher in patients with coronary heart disease (7.48%) than in controls (1.62%, P < 0.01), with adjusted odds ratio of 4.367 (95% confidence interval: 1.178 to 16.191, P < 0.01), so was the C allele (23.2% vs. 14.9%, P < 0.05).ConclusionsHigh plasma homocysteine thiolactone adducts and the CC 311 genotype of paraoxonase-2 gene may be the emerging risk factor for coronary heart disease.
