TNF-alpha -308G>A and IL-6 -174G>C polymorphisms in Tunisian patients with coronary artery disease.

OBJECTIVE: Our aim was to evaluate the contribution of tumor necrosis factor (TNF)-alpha -308G>A and interleukin (IL)-6 -174G>C gene promoter variants to the presence of coronary artery disease (CAD) in Tunisians. DESIGN AND METHODS: Study subjects comprised 418 angiographically proven CAD patients and 406 age-, gender-, and ethnic origin-matched controls. Genotyping was performed using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) analysis. RESULTS: There were no significant differences in the allelic distribution of TNF-alpha -308A (19.6% vs. 19.0%, P=0.73), and IL-6 -174C (15.6% vs. 14.3%, P=0.47) promoter polymorphisms between CAD patients and control subjects, respectively. In addition, single locus analysis revealed no differences in genotype frequencies between the two study groups, and the combined distribution of both genotypes did not differ significantly between controls and CAD patients (P>0.05). CONCLUSION: There is no allelic or genotypic association of TNF-alpha -308G>A and IL-6 -174G>C promoter polymorphisms with CAD in Tunisians, thereby confirming an ethnic-selective contribution of both gene variants to CAD presence.

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

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-alpha (TNF-alpha), 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-alpha -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-alpha -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-alpha -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.

[Homocysteinaemia and degenerative complications in non insulin dependent diabetes mellitus]. / Homocysteinemie et complications degeneratives chez les diabetiques de type 2.

Type 2 diabetes mellitus (non insulin-dependent diabetes mellitus: NIDDM) is known to be associated with degenerative complications. Although, the pathophysiology of such complications is well known, the role of homocysteine (Hcy) is still discussed. The aim of the present study was to evaluate the relationship between the homocysteine levels and the NIDDM related complications in a group of NIDDM patients. Our study population consisted of 41 NIDDM patients including 13 subjects (G1) without complications (group controls), 17 patients (G2) with microangiopathy and 11 patients (G3) with coronary deficiency. Plasmatic homocysteine, glycemia, glycated haemoglobin (HbA1C) and lipidic parameters were essessed in all patients. Our results showed that mean levels of plasmatic homocysteine were within the normal range (10.4 +/- 3.3 micromol/l, 9.9 +/- 5.5 micromol/l and 14.8 +/- 10.4 micromol/l in G1, G2 and G3 respectively). Nevertheless, moderate hyperhomocysteinaemia was found in 36% in the coronary group (G3), 17.3% in patients with microangiopathy (G2) and 7.7% in controls. These preliminary results showed that cardiovascular complications in NIDDM patients may be related to high levels of homocysteine.

[Acquired isolated factor VII deficiency and bronchogenic carcinoma. A case report]. / Deficit acquis, isole en facteur VII et cancer bronchique. A propos d'un cas.

An acquired factor VII deficiency was identified in a 63-year-old man with bronchogenic carcinoma. Initial studies indicated a normal activated partial thromboplastin time and a prolonged prothrombin time. The factor VII level was 6%. No evidence of a factor VII inhibitor or inactivator was demonstrable. However, on account of the initial normal laboratory test of emostases, the partial correction of the prothrombin time with 50% normal plasma in vitro and the family history, the congenital deficiency in factor VII was ruled out. Whatever the mechanism involved, this factor VII deficiency was related to malignancy.