308G>A and –1031T>C tumor necrosis factor gene polymorphisms in Tunisian patients with coronary artery disease

• Published in: Clinical chemistry and laboratory medicine Vol. 47; no. 10; pp. 1247 - 1251
• Main Authors: Ghazouani, Lakhdar, Khalifa, Sonia-Ben-Hadj, Abboud, Nesrine, Addad, Faouzi, Khalfallah, Ali Ben, Brahim, Nsiri, Mediouni, Mounira, Almawi, Wassim Y., Mahjoub, Touhami
• Format: Journal Article
• Language: English
• Published: Berlin Walter de Gruyter 01.10.2009; De Gruyter
• Subjects: African Continental Ancestry Group - genetics; atherosclerosis; Biological and medical sciences; Cardiology. Vascular system; Case-Control Studies; coronary artery disease; Coronary Artery Disease - genetics; Coronary heart disease; Female; Gene Frequency; General aspects; Genetic Predisposition to Disease; Haplotypes; Heart; Humans; Investigative techniques, diagnostic techniques (general aspects); Male; Medical sciences; Middle Aged; Polymorphism, Single Nucleotide; polymorphisms; Promoter Regions, Genetic; tumor necrosis factor; Tumor Necrosis Factor-alpha - genetics; Tunisia; Tunisia; Africa; Human; coronary artery disease; Genetic variability; Cytokine; Cardiovascular disease; Genotype; Coronary heart disease; polymorphisms; Vascular disease; Medicine; Tumor necrosis factor; Atherosclerosis; Clinical biology; Polymorphism
• ISSN: 1434-6621; 1437-4331
• DOI: 10.1515/CCLM.2009.287

Background: Recent research has shown that inflammation plays a key role in coronary artery disease (CAD) and other manifestations of atherosclerosis. Several lines of evidence support a key role for tumor necrosis factor-α (TNF-α), a potent immunomodulator and pro-inflammatory cytokine, in the development of atherosclerosis and in complications of CAD. Methods: We investigated the possible association between CAD and the TNF gene promoter polymorphisms –308G>A and –1031T>C in a Tunisian population. We compared the distribution of these polymorphisms between 418 patients with CAD and 406 healthy controls using polymerase chain reaction restriction fragment length-polymorphism analysis. Results: The frequency of the TNF-α –308A allele in the control group was similar to that observed in CAD patients [p=0.78; odds ratio (OR)=1.15; 95% confidence interval (CI)=0.86–1.55], but higher than those described in other Europeans, such as in the French, Finnish and Spanish. Concerning the TNF-α –1031T/C polymorphism, the same distribution was observed between patients with CAD and controls (p=0.12; OR=1.27; 95% CI=0.94–1.72). In addition, the genotype and allele frequencies of control individuals were comparable to those previously reported in healthy Tunisian controls and other ethnic groups. Haplotype analysis (TNF-α –308G>A and –1031T>C) demonstrated no significant association between TNF haplotypes and CAD. Conclusions: We conclude that TNF promoter gene polymorphisms at position –308G>A and –1031T>C do not play a major role in the pathogenesis of CAD in the Tunisian population. Clin Chem Lab Med 2009;47:1247–51.