Riadh Jemaa

University of Tunis El Manar, Tunis-Ville, Tūnis, Tunisia

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Publications (85)188.89 Total impact

  • Archives of Cardiovascular Diseases Supplements 01/2015; 7(1):85. DOI:10.1016/S1878-6480(15)71729-5
  • Archives of Cardiovascular Diseases Supplements 01/2015; 7(1). DOI:10.1016/S1878-6480(15)71529-6
  • Archives of Cardiovascular Diseases Supplements 01/2015; 7(1):84. DOI:10.1016/S1878-6480(15)71728-3
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    ABSTRACT: Behçet's disease (BD) is a multisystem inflammatory disease characterized by recurrent orogenital ulceration, ocular inflammation and skin lesions. Reduced plasma nitric oxide (NO) levels in patients with BD have been implicated in the development of the endothelial abnormalities and thrombotic complications occurring in these patients. Polymorphisms in the endothelial nitric oxide synthase gene (NOS3) have been inconsistently associated with BD. This inconsistency may derive from population stratification secondary to ethnic diversity, and consideration limited to only one rather than combinations of polymorphisms. We studied three genetic variations in the NOS3 gene: a single nucleotide polymorphism in the promoter region −786T>C, in exon 7 (Glu298Asp), and a variable number of tandem repeats in intron 4 (4a4b) of the NOS3 gene in 100 unrelated Tunisian patients with BD and 148 healthy controls. In addition, we also examined the association of NOS3 gene haplotypes with BD. Analyses of the Glu298Asp, −786T>C and 4a4b polymorphisms were made by the polymerase chain reaction (PCR) restriction fragment length polymorphism technique and PCR genotyping, respectively. The distribution of the Glu298Asp genotype differed significantly between patients with BD and controls (P = 0.01). Allele Asp298 was significantly more frequent in patients with BD than in controls (P = 0.005, OR = 1.70, 95% CI 1.14–2.54). In contrast, distribution of alleles and genotypes of −786T>C and 4a4b polymorphisms was not different between the control and BD group. However, the frequency of Asp-T-4b haplotype was significantly higher in patients with BD than in healthy controls. By gender, the signification remained only for heterozygous men (P = 0.03) and homozygous women (P = 0.02). These results suggest that Glu298Asp polymorphism of the NOS3 gene is associated with BD susceptibility in Tunisian patients.
    International Journal of Immunogenetics 01/2015; 42(2). DOI:10.1111/iji.12176
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  • Atherosclerosis 08/2014; 235(2):e154. DOI:10.1016/j.atherosclerosis.2014.05.439
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    ABSTRACT: Purpose Development of a validated risk prediction model for cardiovascular death in coronary patients is a high priority for strategies of therapy. We sought to validate and recalibrate of the SCORE (Systematic coronary risk evaluation) risk chart based on Tunisian national mortality data and average major cardiovascular risk factor levels. Methods Baseline data were collected between 1997 and 2004 in 146 male patients aged 52.4 ± 9 years hospitalized with STEMI treated with fibrinolysis in 68 % of patients and not revascularized early in 32% of patients. Vital status was checked and causes of death were obtained in 2011 after a mean follow up of 9.6 years. The expected cardiovascular mortality was calculated by applying the SCORE equation for high risk populations on the basis of the level of risk factors in the total population, in the diabetic and non-diabetic population and was compared with the observed mortality in each group. Correction factor was calculated for each group. Univariate analysis was used for statistical analysis. The optimum threshold of SCORE, allowing for an optimal sensitivity and specificity, was determined by the ROC curve (receiver operating characteristic). For risk thresholds 5% and that determined from the ROC curve of the European SCORE sensitivity, specificity values were calculated. Results The total number of cardiovascular death at 10 years is 18 with a mortality of 12.3%. The average of SCORE in our population was 8.73+/-5.12% with extremes ranging from 1 to 32%. The European SCORE was strongly correlated in our cohort to the occurrence of cardiovascular death at 10 years (p <0.0001). The correction factor of SCORE is calculated to 2.7 in diabetic group, 1 in non-diabetic group and 1.4 for the total population. The ROC curve has a c index (AUC) = 0.73 corresponding to the risk threshold of 9.12%. The relative risk of cardiovascular death at 10 years of SCORE for the 9.12% threshold is calculated at 3.6. For the risk threshold for 9.12%, sensitivity was calculated at 66.7% and specificity at 68.8%. For the risk threshold for 5%, sensitivity was calculated at 94.9% and specificity at 17.96%. Conclusion SCORE is validated in coronary male Tunisian patients with and recalibrated using correction factors. Validation on a larger population and multi-ethnic remains our future desire.
    Archives of Cardiovascular Diseases Supplements 04/2014; 6:3. DOI:10.1016/S1878-6480(14)71270-4
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    ABSTRACT: Purpose The aim of the study was to Validate and to recalibrate the Framingham’s score Hard coronary heart disease (HCHD score) in a coronary Tunisian population. Methods Baseline data were collected between 1997 and 2004 in 146 patients. We excluded from the analysis all patients who died during the first 30 days of hospitalization. Vital status was checked and causes of death were obtained in 2011 after a mean follow up of 9.6 years. We also noticed myocardial infarction during the same period. The expected incidence of the composite event cardiovascular death and/or myocardial infarction was calculated by applying the HCHD equation on the basis of the level of risk factors in diabetic and non-diabetic populations and was compared with the observed incidence of the composite event in each group. Correction factor was calculated for each group. For the risk thresholds 20 % and that determined from the ROC curve of the HCHD score sensitivity, specificity values ??were calculated. Results The total number of patients who developed the composite event cardiovascular death and/or myocardial infarction was 34 (23.3%). The average of HCHD score in our population is 16.2 +/−7.2% with a range from 2 to 30%. The HCHD score is significantly associated with cardiovascular death event and/or myocardial infarction in our population (p = 0.029). The correction factor score is 2 in diabetic group, 1.1 in non-diabetics group and 1.4 for the total population. The relative risk of HCHD score is calculated to 1.59 for the composite event cardiovascular death and/or myocardial infarction at 10 years.For the risk threshold for 20%, sensitivity was calculated at 41.11% and specificity at 76.7%. Conclusion HCHD score is validated in coronary male Tunisian patients with and recalibrated using correction factors. Validation on a larger population and multi-ethnic remains our future desire.
    Archives of Cardiovascular Diseases Supplements 04/2014; 6:2. DOI:10.1016/S1878-6480(14)71265-0
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    ABSTRACT: Introduction Few studies have examined the incidence of the composite event cardiovascular death and/or myocardial infarction in long term in patients who presented with acute coronary syndrome with ST segment elevation (STEMI) treated with fibrinolysis or percutaneous angioplasty. Methods This is a prospective longitudinal trial held between August 1997 and September 2011 in La Rabta Hospital. Between August 1997 and august 2004, were randomly included 146 patients who had had a first nonfatal myocardial infarction non-fatal during the first 30 days. After a mean follow up of 9.6 years, we recorded the composite event cardiovascular death and/or myocardial infarction. Results The total number of patients who developed the composite event cardiovascular death and/or myocardial infarction was 34 (23.3%). The average time of occurrence of the composite event is 8.4+/−4.1 years. No factors of the characteristics of the population were significantly associated with nonfatal myocardial infarction at 10 years in univariate analysis. Factors significantly predictive of the composite event cardiovascular death and/or myocardial infarction at 9.6 years in univariate analysis are the same factors predictive of cardiovascular death age (p = 0.002), diabetes (p = 0.01) and multivessel coronary disease (p = 0.05). There is a tendency to correlation of the composite event at 9.6 years with history of hypertension (p = 0.06). In multivariate analysis, independent factors predictive of the composite event, cardiovascular death and/or myocardial infarction are age >55 years (OR=.53, 95% CI: 1.97, 36.96, p = 0.004), diabetes (OR=4.3, 95% CI: 1.31, 14.15, p = 0.016) and the anterior territory of the myocardial infarction (OR=5.5, 95% CI: 1.02, 29.66, p = 0.047). Conclusion In our population predictors of the composite event cardiovascular death and/or myocardial infarction in the multivariate analysis were age, anterior territory of the infarction and diabetes. Better control and management could reduce the long-term mortality.
    Archives of Cardiovascular Diseases Supplements 03/2014; 6:1. DOI:10.1016/j.gheart.2014.03.2270
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    ABSTRACT: Background: Elevated total plasma homocysteine (tHcy) is an established risk factor for occlusive vascular disease and is thought to increase the risk of pregnancy loss, birth defects, and cognitive impairment in the elderly. Objectives: To determine tHcy standard values and the prevalence of hyperhomocysteinemia (HHC) and to examine their association with demographic and life style factors in the Greater Tunis population. Methods: This cross-sectional study included 2712 subjects (1228 males and 1484 females) aged 35 - 70 years, living in the Greater Tunis region. tHcy was analyzed by a fluorescent polarizing immunoassay method. HHC was considered as tHcy >= 15 mu mol/L. Results: HHC was observed in 23.7% of subjects. Plasma tHcy was higher in males than females (median (5th - 95th percentile): 13.5 [8.75 - 26.3] mu mol/L vs. 10.7 [6.94 - 19.6] mu mol/L). The tHcy concentration was significantly increased in smokers, alcoholics, in subjects with vitamin B-12 and folate deficiencies, and hyperuricemia. In multivariate analysis, HHC was associated with male gender, vitamin B-12 deficiency, clearance of creatinine, alcohol consumption, and hyperuricemia. Conclusions: HHC is common in Tunisian adults. Male gender, advanced age, renal insufficiency, low vitamin B-12 status, hyperuricemia, and alcohol consumption are the main determinants of HHC in this population.
    Clinical laboratory 01/2014; 60(6):897-902. DOI:10.7754/Clin.Lab.2013.130723
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    ABSTRACT: Background and aims Peroxisome proliferator-activated receptor-γ co-activator-1α (PGC-1α) is a transcriptional co-activator involved in adaptive thermogenesis, skeletal muscle metabolism, fatty acid oxidation, and gluconeogenesis. Several studies have suggested that the common PGC-1α polymorphism Gly482Ser (rs8192678) may be associated with risk of type 2 diabetes (T2D), with conflicting results. The aim of this study was to analyze whether the Gly482Ser variant is a risk factor for development of T2D in Tunisian population. Methods In a case–control study 487 unrelated patients with type 2 diabetes and 402 apparently healthy controls were recruited from January 2008 to August 2010. The Gly482Ser polymorphism was determined by PCR-RFLP analysis. Results A significant difference in genotypes distribution was observed between patients (Gly/Gly: 34.1%; Gly/Ser: 47.1%; Ser/Ser: 18.5%) and controls (Gly/Gly: 43.8%; Gly/Ser: 42.3%; Ser/Ser: 13.9%) (χ2 = 9.44, p = 0.009). The T2D patient group showed a significant higher frequency of the Ser allele compared to the controls (43% vs. 34%; OR: 1.35, 95% [CI]: 1.11–1.65, p = 0.002). The association between the Gly482Ser polymorphism and T2D remained significant after adjustment for other well-established cardiovascular risk factors. Conclusions In the current study, a significant and independent association between the Gly482Ser polymorphism (rs8192678) of the PGC-1α gene and T2D in the Tunisian population was found.
    Diabetes and Metabolic Syndrome Clinical Research and Reviews 11/2013; DOI:10.1016/j.dsx.2013.10.011
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    ABSTRACT: Controversial results regarding the association of eNOS gene (NOS3) polymorphisms with myocardial infarction (MI) have been reported. This study investigated the relationship of the -786T>C (rs2070744), 894G>T (rs1799983) and 4a4b polymorphisms of the NOS3 gene with the presence of MI in the Tunisian population. In addition, we also examined the association of NOS3 gene haplotypes with MI in Tunisian subjects. A total of 303 patients with MI and 225 controls were included in the study. The 894G>T and -786T>C single nucleotide polymorphisms were analyzed by PCR-RFLP, and 4a4b polymorphism just for PCR. There was significant linkage disequilibrium between the three NOS3 polymorphisms (p<0.0001). The genotype distribution and allele frequency of NOS3 4a4b, but not -786T>C and 894G>T, polymorphism was significantly different between MI patients and controls. The univariate logistic regression analysis showed a significant association of the 4a4b polymorphism and MI according to co-dominant, dominant and recessive models (co-dominant model OR: 4.38, 95%CI: 1.24-15.41; p=0.021, dominant model OR: 1.66, 95%CI: 1.14-2.42); p=0.007, and recessive model OR: 3.85, 95%CI: 1.10-13.47; p=0.035). The multivariate analysis, adjusted for traditional cardiovascular risk factors, revealed that the NOS3 4a4a genotype was an independent predisposing factor to MI, according to the models considered. In addition, a haplotype 7 (C-T-4a), (OR=12.05, p=0.010) was a risk factor of MI after controlling for classical risk factors. These finding suggest that the 4a4b polymorphism of the NOS3 gene was associated with MI in Tunisian patients.
    Cytokine 10/2013; DOI:10.1016/j.cyto.2013.09.005
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    ABSTRACT: Tumor necrosis factor α (TNFα) plays a key role in orchestrating the complex events involved in inflammation and immunity. Accordingly, TNF α has been implicated in a wide range of autoimmune and infectious diseases, but also in conditions such as obesity and insulin resistance. The aim of the present study was to investigate the association between the -863C/A polymorphism in the promoter of the TNFα gene and type 2 diabetes in the Tunisian population. The polymorphism -863C/A in the TNFα gene was determined in 211 type 2 diabetes patients and 345 healthy controls using the Polymerase Chain Reaction-Restriction Fragment Length Polymorphism (PCR-RFLP) analysis. A significant difference in genotype distribution and allele frequency was observed between patients and controls. Patients with type 2 diabetes had significantly higher frequency of the CA+AA genotypes compared to controls [35.5% vs. 22.3%; OR (95%CI), 1.91 (1.31-2.8); p=0.001]. The type 2 diabetes patient group showed a significant higher frequency of the A allele compared to the controls (0.19 vs. 0.11; p=0.001). After adjustment by a stepwise logistic regression method, hypertension, dyslipidemia, and CA+AA genotype were found to be significantly associated with T2D. The present study showed a significant and independent association between the -863C/A polymorphism of the TNFα gene and type 2 diabetes in the Tunisian population.
    Diabetes research and clinical practice 10/2013; 102(2). DOI:10.1016/j.diabres.2013.09.015
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    ABSTRACT: We investigated the interaction between the G protein beta3 subunit (GNB3) C825T variant and angiotensin converting enzyme (ACE) Insertion/Deletion (I/D) polymorphism in hypertensive Tunisian population. Analyses of ACE and GNB3 genotypes were performed in 388 hypertensive patients and 425 healthy controls by polymerase chain reaction-restriction fragment length polymorphism. The plasma ACE activity was determined by a spectrophotometric method. The ACE genotype distribution and allele frequencies were not significantly different between the hypertensive and normotensive subjects (p > 0.05). This polymorphism was not associated with hypertension (HTA) (OR = 0.93, 95% CI = 0.75 - 1.15; p = 0.50). In cases, subjects carrying the DD genotype exhibited higher plasma ACE activity than those with ID and II genotypes (p = 0.001). In this group, a linear regression analysis revealed that the ACE I/D polymorphism is independently associated with plasma ACE activity (p = 0.017). The genotypic distribution and allelic frequencies of the GNB3 C825T polymorphism were not significantly different between the two groups. This polymorphism was found to have no effect on the risk of HTA (OR = 1.14, 95% CI = 0.93 - 1.39; p = 0.21). We did not observe a significant interaction between the GNB3 gene and the ACE gene with HTA. In this study, the I/D polymorphism is a significant independent predictor for variability of plasma ACE activity but the ACE I/D and GNB3 C825T polymorphisms are not significant factors for HTA in the Tunisian population. Moreover, we found no interaction between ACE D allele and GNB3 825T allele solely or combined with respect to HTA in the Tunisian population.
    Clinical laboratory 01/2013; 59(1-2):85-92. DOI:10.7754/Clin.Lab.2013.111105
  • Archives of Cardiovascular Diseases Supplements 01/2013; 5(1). DOI:10.1016/S1878-6480(13)71169-8
  • Archives of Cardiovascular Diseases Supplements 01/2013; 5(1). DOI:10.1016/S1878-6480(13)71165-0
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    ABSTRACT: Background: Hypertension is a polygenic disease. Various singlenucleotide gene polymorphisms of renin angiotensin system have been explored in hypertension. Angiotensin II, the major biologically active component of this system, exerts its effect via two pharmacologically distinct subtypes of angiotensin II receptors, the angiotensin II type 1 receptor and the angiotensin II type 2 receptor. Aim: To examine whether the 3123 C/A polymorphism of angiotensin II type 2 receptor gene is involved in hypertension in a sample of Tunisian population. Methods: Atotal of 403 normotensive subjects and 382 hypertensive patients were included in the study. Genotyping was performed by polymerase chain reaction followed by Alu I restriction digestion. Results: The frequency of "A" genotype was not significantly different between the two groups in men (¯2=1.18; p=0.16). The estimated odds prevalence for hypertension ("A" versus "C") was 0.77 (95% CI 0.49 to 1.22, p=0.27). After adjustment for confounding factors, the OR for hypertension remained no significant (OR: 1.49, 95% CI: 0.84-2.63, p=0.16). In women, genotype distributions for C3123A variant in hypertensive patients were not significantly different from normotensive subjects (¯2=3.16; p=0.20). Multiple logistic regression analysis showed that the AA genotype was not significantly associated with hypertension (OR: 1.09, 95% CI: 0.58-2.06, p=0.77). Conclusion: In the present study, we showed that the 3123 C/A polymorphism of AGT2R gene is not a significant factor for hypertension in a sample of Tunisian population.
    La Tunisie médicale 08/2012; 90(8):619-24.
  • World Congress of Cardiology Scientific Sessions; 05/2012

Publication Stats

671 Citations
188.89 Total Impact Points

Institutions

  • 2011–2015
    • University of Tunis El Manar
      Tunis-Ville, Tūnis, Tunisia
  • 2004–2015
    • La Rabta Hospital Tunis
      Tunis-Ville, Tūnis, Tunisia
  • 1997
    • Faculté des Sciences de Tunis
      Tunis-Ville, Tūnis, Tunisia
    • French Institute of Health and Medical Research
      Lutetia Parisorum, Île-de-France, France
  • 1995
    • Queen's University Belfast
      Béal Feirste, N Ireland, United Kingdom