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

dc.contributor.authorGhazouani, Lakhdar
dc.contributor.authorAbboud, Nesrine
dc.contributor.authorAddad, Faouzi
dc.contributor.authorKhalfallah, Ali Ben
dc.contributor.authorBrahim, Nsiri
dc.contributor.authorMediouni, Mounira
dc.contributor.authorY Almawi, Wassim
dc.contributor.authorMahjoub, Touhami
dc.date.accessioned2022-02-24T05:37:59Z
dc.date.accessioned2023-08-19T08:52:02Z
dc.date.available2022-02-24T05:37:59Z
dc.date.available2023-08-19T08:52:02Z
dc.date.issued2009-10
dc.description.abstractBackground: 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.en_US
dc.identifier.citationGhazouani, L., Khalifa, S., Abboud, N., Addad, F., Khalfallah, A., Brahim, N., Mediouni, M., Almawi, W. & Mahjoub, T. (2009). –308G>A and –1031T>C tumor necrosis factor gene polymorphisms in Tunisian patients with coronary artery disease. Clinical Chemistry and Laboratory Medicine, 47(10), 1247-1251.en_US
dc.identifier.doihttps://doi.org/10.1515/CCLM.2009.287
dc.identifier.urihttps://edms.wexl.in/handle/1/2759
dc.language.isoenen_US
dc.publisherWalter de Gruyteren_US
dc.subjectAtherosclerosisen_US
dc.subjectCoronary artery diseaseen_US
dc.subjectPolymorphismsen_US
dc.subjectTumor necrosis factoren_US
dc.title–308G> A and–1031T> C tumor necrosis factor gene polymorphisms in Tunisian patients with coronary artery diseaseen_US
dc.title.alternativeClinical chemistry and laboratory medicineen_US
dc.typeArticleen_US

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