Tarek M Farid

National Research Center, Egypt, Al Qāhirah, Al Qāhirah, Egypt

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Publications (5)0.94 Total impact

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    ABSTRACT: Introduction. The production of tumor necrosis factor (TNF)-α has been deeply deregulated in systemic lupus erythematosus. We evaluated the association of -863C>A and -1031T>C polymorphisms of the TNF gene with susceptibility to and clinical manifestations of juvenile systemic lupus erythematosus. Materials and Methods. This study was performed on 70 juvenile patients with systemic lupus erythematosus (mean age, 13.0 ± 4.2 years). Ninety age-and sex-matched children served as a controls. All participants were genotyped for the TNF -863C>A and -1031T>C polymorphisms by polymerase chain reaction-restriction fragment length polymorphism method. Analysis of serum TNF-α was done by solid-phase sandwich enzyme immunoassay. Results. The mean serum TNF-α was significantly higher in the SLE patients compared to controls (P < .001). Regarding all participants, the mean serum TNF-α was significantly higher in children with -863AA genotype compared to carriers of -863C allele (P < .001). The TNF -863AA genotype frequencies were significantly higher in the patients group compared with the controls (P = .005) and were associated with increased risk for SLE development (odds ratio, 4.05; 95% confidence interval, 1.38 to 13.13; P = .005). The -863AA variant was associated with nephritis (P < .001) and Raynaud phenomenon (P = .001). Conclusions. The -863A allele of the TNF gene can be used as a genetic marker for SLE susceptibility and was associated with high TNF-α production, Raynaud phenomenon, and nephritis in juvenile SLE Egyptian patients.
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    ABSTRACT: Introduction. The production of tumor necrosis factor (TNF)-α has been deeply deregulated in systemic lupus erythematosus. We evaluated the association of -863C>A and -1031T>C polymorphisms of the TNF gene with susceptibility to and clinical manifestations of juvenile systemic lupus erythematosus. Materials and Methods. This study was performed on 70 juvenile patients with systemic lupus erythematosus (mean age, 13.0 ± 4.2 years). Ninety age-and sex-matched children served as a controls. All participants were genotyped for the TNF -863C>A and -1031T>C polymorphisms by polymerase chain reaction-restriction fragment length polymorphism method. Analysis of serum TNF-α was done by solid-phase sandwich enzyme immunoassay. Results. The mean serum TNF-α was significantly higher in the SLE patients compared to controls (P < .001). Regarding all participants, the mean serum TNF-α was significantly higher in children with -863AA genotype compared to carriers of -863C allele (P < .001). The TNF -863AA genotype frequencies were significantly higher in the patients group compared with the controls (P = .005) and were associated with increased risk for SLE development (odds ratio, 4.05; 95% confidence interval, 1.38 to 13.13; P = .005). The -863AA variant was associated with nephritis (P < .001) and Raynaud phenomenon (P = .001). Conclusions. The -863A allele of the TNF gene can be used as a genetic marker for SLE susceptibility and was associated with high TNF-α production, Raynaud phenomenon, and nephritis in juvenile SLE Egyptian patients.
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    ABSTRACT: Introduction. The production of tumor necrosis factor (TNF)-α has been deeply deregulated in systemic lupus erythematosus. We evaluated the association of -863C>A and -1031T>C polymorphisms of the TNF gene with susceptibility to and clinical manifestations of juvenile systemic lupus erythematosus. Materials and Methods. This study was performed on 70 juvenile patients with systemic lupus erythematosus (mean age, 13.0 ± 4.2 years). Ninety age-and sex-matched children served as a controls. All participants were genotyped for the TNF -863C>A and -1031T>C polymorphisms by polymerase chain reaction-restriction fragment length polymorphism method. Analysis of serum TNF-α was done by solid-phase sandwich enzyme immunoassay. Results. The mean serum TNF-α was significantly higher in the SLE patients compared to controls (P < .001). Regarding all participants, the mean serum TNF-α was significantly higher in children with -863AA genotype compared to carriers of -863C allele (P < .001). The TNF -863AA genotype frequencies were significantly higher in the patients group compared with the controls (P = .005) and were associated with increased risk for SLE development (odds ratio, 4.05; 95% confidence interval, 1.38 to 13.13; P = .005). The -863AA variant was associated with nephritis (P < .001) and Raynaud phenomenon (P = .001). Conclusions. The -863A allele of the TNF gene can be used as a genetic marker for SLE susceptibility and was associated with high TNF-α production, Raynaud phenomenon, and nephritis in juvenile SLE Egyptian patients.
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    ABSTRACT: Accurate diagnosis of acute kidney injury (AKI) is problematic especially in critically-ill patients in whom renal function is in an unsteady state. Our aim was to evaluate the role of serum (S.) cystatin C as an early biomarker of AKI in critically-ill children. S. creatinine and S. cystatin C were measured in 32 critically-ill children who were at risk for developing AKI. AKI was defined by both: Risk,-injury,-failure,-loss, and-endstage renal disease (RIFLE) classification and glomerular filtration rate (GFR) <80 ml/min/1.73 m(2). GFR was estimated by both Schwartz formula and S. cystatin C-based equation. S. cystatin C was not statistically higher in AKI patients compared with non-AKI by RIFLE classification (median 1.48 mg/l vs. 1.16 mg/l, P = 0.1) while S. creatinine was significantly higher (median 0.8 mg/dl vs. 0.4 mg/dl, P = 0.001). On estimating GFR by the two equations we found, a lag between rise of S. cystatin C and creatinine denoted by lower GFR by Schwartz formula in four patients, on other hand, six patients had elevated S. cystatin C with low GFR despite normal creatinine and GFR, denoting poor concordance between the two equations and the two markers. The ability of S. creatinine in predicting AKI was superior to S. cystatin with area under the curve (AUC) 0.95 with sensitivity and specificity (100% and 84.6%, respectively) using the RIFLE classification. The same findings were found when using Schwartz formula. S. cystatin C is a poor biomarker for diagnosing AKI in critically-ill children.
    Indian Journal of Critical Care Medicine 03/2013; 17(2):92-8.
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    ABSTRACT: The production of tumor necrosis factor (TNF)-alpha has been deeply deregulated in systemic lupus erythematosus. We evaluated the association of -863C>A and -1031T>C polymorphisms of the TNF gene with susceptibility to and clinical manifestations of juvenile systemic lupus erythematosus. This study was performed on 70 juvenile patients with systemic lupus erythematosus (mean age, 13.0 ± 4.2 years). Ninety age- and sex-matched children served as a controls. All participants were genotyped for the TNF -863C>A and -1031T>C polymorphisms by polymerase chain reaction-restriction fragment length polymorphism method. Analysis of serum TNF-alpha was done by solid-phase sandwich enzyme immunoassay. The mean serum TNF-alpha was significantly higher in the SLE patients compared to controls (P < .001). Regarding all participants, the mean serum TNF-alpha was significantly higher in children with -863AA genotype compared to carriers of -863C allele (P < .001). The TNF -863AA genotype frequencies were significantly higher in the patients group compared with the controls (P = .005) and were associated with increased risk for SLE development (odds ratio, 4.05; 95% confidence interval, 1.38 to 13.13; P = .005). The -863AA variant was associated with nephritis (P < .001) and Raynaud phenomenon (P = .001). The -863A allele of the TNF gene can be used as a genetic marker for SLE susceptibility and was associated with high TNF-alpha production, Raynaud phenomenon, and nephritis in juvenile SLE Egyptian patients.
    Iranian journal of kidney diseases 11/2011; 5(6):392-7. · 0.94 Impact Factor