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Aly A Yousef,1 Faisal Y Mohamed,2 Naglaa F Boraey,3 Nagwa E Akeel,4 Attia A Soliman,4 Nevin M Waked,5 Mustafa IA Hashem,4 Hassan Shehata,4 Dalia S Fahmy,6 Ali Ismael,7 Lamya M Ibrahim,8 Mohamed AM Ibrahim,9 Hanan F Salem,10 Sherif M Yousry,11 Sherif F Osman,12 Rania A Fouad,13,14 Eman T Enan,15,16 Mohammed A Attia,17,18 Mona R Afify,19 Nancy MS Zeidan,20 Mohamed Nashat21 1Department of Pediatrics, Faculty of Medicine, Helwan University, Helwan, Egypt; 2Department of Pediatrics, Faculty of Medicine, Ain-Shams University, Cairo, Egypt; 3Department of Pediatrics, Faculty of Medicine, Sohag University, Sohag, Egypt; 4Department of Pediatrics, Faculty of Medicine, Zagazig University, Zagazig, Egypt; 5Department of Pediatrics, Faculty of Medicine, October 6 University, October 6, Egypt; 6Department of Rheumatology, Faculty of Medicine, Zagazig University, Zagazig, Egypt; 7Department of Internal Medicine, Faculty of Medicine, Zagazig University, Zagazig, Egypt; 8Department of Clinical Pathology, Faculty of Medicine, Mansoura University, Mansoura, Egypt; 9Department of Clinical Pathology, Faculty of Medicine, Sohag University, Sohag, Egypt; 10Department of Anesthesia, Faculty of Medicine, Banha University, Banha, Egypt; 11Department of Clinical Pathology, Faculty of Medicine, Cairo University, Cairo, Egypt; 12Department of Radiology, Texas Tech University Health Sciences Center, El Paso, TX, USA; 13Department of Medical Biochemistry, College of Medicine, El-Mareefa University, Riyadh, Kingdom of Saudi Arabia; 14Department of Medical Biochemistry, Faculty of Medicine, Zagazig University, Zagazig, Egypt; 15Department of Pathology, College of Medicine, El-Mareefa University, Riyadh, Kingdom of Saudi Arabia; 16Department of Pathology, Faculty of Medicine, Mansoura University, Mansoura, 35516, Egypt; 17Department of Clinical Pharmacology, College of Medicine, El-Mareefa University, Riyadh, Kingdom of Saudi Arabia; 18Department of Clinical Pharmacology, Faculty of Medicine, Mansoura University, Mansoura, 35516, Egypt; 19Department of Medical microbiology and Parasitology, Faculty of Medicine, University of Jeddah, Jeddah, 21589, Saudia Arabia; 20Department of Pediatrics, Faculty of Medicine, Cairo University, Cairo, Egypt; 21Department of Pediatrics, Faculty of Medicine, Aswan University, Aswan, EgyptCorrespondence: Faisal Y MohamedFaculty of Medicine, Ain-Shams University, Cairo, EgyptTel +201113363638Email Faisalyousef69@gmail.comBackground: Plasminogen activator inhibitor-1 (PAI-1) is a key molecule residing at the nexus between thrombosis and inflammatory processes. Recently, PAI-1 and its gene expression have emerged as a potential candidate for autoimmune disorders such as SLE.Objective: To investigate whether the PAI-1 4G/5G polymorphism at position − 675 could be a genetic marker for susceptibility to childhood-onset SLE and development of lupus nephritis among Egyptian children and adolescents.Methods: Three hundred fifty patients diagnosed with childhood-onset SLE and 350 well-matched healthy controls were included in this multi-center study. All subjects were genotyped for the PAI-1 promoter 4G/5G polymorphism at position − 675 using PCR– restriction fragment length polymorphism (RFLP). Serum PAI-1 levels were measured by ELISA.Results: The PAI-1 (- 675) 4G/4G genotype was more represented in c-SLE patients, as compared to the control group (38% vs 23%; OR =2.7; [95% CI: 1.47– 2.9]; P < 0.001). Patients carrying the PAI-1 4G/4G genotype or 4G allele were more likely to develop lupus nephritis (OR: 3.38; [95% CI: 1.9– 5.9]; P < 0.001, for the 4G/4G genotype and OR: 2.6; [95% CI: 1.85– 3.67]; for the 4G allele; P < 0.01). The PAI-1 4G/4G genotype was associated with higher PAI-1 serum concentrations (mean; 86.6± 22.7 ng/mL) as compared to those with a 4G/5G genotype (mean; 48.3± 16.5 ng/mL) and the lowest for the 5G/5G genotype (mean; 34.7± 11.4 ng/mL); P = 0.004.Conclusion: The PAI-1 4G/5G polymorphism may confer susceptibility to childhood-onset SLE and development of lupus nephritis among Egyptian children and adolescents. Moreover, the PAI-1 4G/4G genotype and 4G allele were associated with higher PAI-1 serum levels and higher disease activity scores.Keywords: plasminogen activator inhibitor-1, PAI-1, gene polymorphism, SLE, children, adolescents

BACKGROUND Pneumonia is the foremost cause of child death worldwide. M-ficolin is encoded by the FCN1 gene and represents a novel link between innate and adaptive immunity. OBJECTIVES To investigate the FCN1 -144 C/A (rs10117466) polymorphism as a potential marker for pneumonia severity and adverse outcome namely complications or mortality in the under-five Egyptian children. METHODS This was a prospective multicenter study that included 620 children hospitalized with World Health Organization-defined severe pneumonia and 620 matched healthy control children. Polymorphism rs10117466 of the FCN1 gene promoter was analyzed by PCR-SSP, while serum M-ficolin levels were assessed by ELISA. RESULTS The FCN1 A/A genotype and A allele at the -144 position were more frequently observed in patients compared to the control children (43.4% vs 27.6%; odds ratio [OR]: 1.62; [95% confidence interval {CI}: 1.18-2.2]; for the A/A genotype) and (60.8% vs 52.5%; OR: 1.4; [95% CI: 1.19-1.65]; for the A allele); P

BackgroundRecently, the interleukin-17A ( IL-17A) gene has emerged as a potential candidate gene for autoimmune disorders, including systemic lupus erythematosus (SLE).ObjectivesThis study aimed to investigate whether IL-17A polymorphisms at rs2275913 G/A, rs8193036 C/T and rs3748067 C/T could be susceptibility markers for juvenile-onset SLE (JSLE) and lupus nephritis (LN) in Egyptian children and adolescents.MethodsIn this multi-centre study, we genotyped 320 patients diagnosed with JSLE and 320 matched control children for three IL-17A polymorphisms at rs2275913 G/A, rs8193036 C/T and rs3748067 C/T using TaqMan probe-based real-time polymerase chain reaction. Meanwhile, IL-17A serum levels were assessed using ELISA.ResultsThe IL-17 rs2275913 A/A genotype and A allele were more represented in JSLE patients compared to the control group (21% vs. 7%, odds ratio (OR) = 3.8, 95% confidence interval (CI) 1.78–5.5, p = 0.001, pBonf = 0.003 for the A/A genotype; 37% vs. 29%, OR = 1.4, 95% CI 1.11–1.8, p = 0.003, pBonf = 0.009 for the A allele. No significant difference was found for IL-17 rs8193036 and rs3748067 single nucleotide polymorphisms (SNPs) in genotype distribution or allele frequencies ( p>0.05). Patients carrying the IL-17 rs2275913 A/A genotype and A allele were more likely to develop LN (OR = 5.64, 95% CI 2.39–13.77, pBonf = 0.001 for the A/A genotype; OR = 2.73, 95% CI 1.84–4.07, pBonf = 0.02 for the A allele).ConclusionThe IL-17 rs2275913 A allele and A/A genotype were associated with high IL-17 serum levels and may contribute to susceptibility to JSLE and the development of LN in Egyptian children and adolescents. However, no significant association was evident between the studied IL-17A SNPs and other clinical phenotypes, disease activity scores or laboratory profile of JSLE.

Plasminogen activator inhibitor-1 (PAI-1) is a key molecule residing at the nexus between thrombosis and inflammatory processes. Recently, PAI-1 and its gene expression have emerged as a potential candidate for autoimmune disorders such as SLE.To investigate whether the PAI-1 4G/5G polymorphism at position -675 could be a genetic marker for susceptibility to childhood-onset SLE and development of lupus nephritis among Egyptian children and adolescents.Three hundred fifty patients diagnosed with childhood-onset SLE and 350 well-matched healthy controls were included in this multi-center study. All subjects were genotyped for the PAI-1 promoter 4G/5G polymorphism at position -675 using PCR- restriction fragment length polymorphism (RFLP). Serum PAI-1 levels were measured by ELISA.The PAI-1 (- 675) 4G/4G genotype was more represented in c-SLE patients, as compared to the control group (38% vs 23%; OR =2.7; [95% CI: 1.47-2.9];The PAI-1 4G/5G polymorphism may confer susceptibility to childhood-onset SLE and development of lupus nephritis among Egyptian children and adolescents. Moreover, the PAI-1 4G/4G genotype and 4G allele were associated with higher PAI-1 serum levels and higher disease activity scores.

To measure blood lead levels in children (5-14 y) with bronchial asthma, and correlate with asthma severity.Cross-sectional analytical.Pediatric Allergy and Immunology Clinic of a Childrens hospital in Cairo, Egypt.200 children (127 males) with bronchial asthma and 125 age- and sex-matched healthy controls (80 males).Blood lead levels were measured by atomic absorption spectrophotometer technique, and were subsequently correlated with asthma severity.No significant difference in mean (SD) blood lead levels was observed between children with asthma [13.3 (4.8) ug/dL] and control group [11.4 (3.9) ug/dL]. 190 children (58.5%) had elevated blood lead levels (10 ug/dL), with no significant difference between patients (60%) and controls (56%). Patients with elevated blood lead levels had significantly higher frequency of eosinophilia (66.7%) and increased total immunoglobulin E (83.3%) compared to other patients with blood lead levels10ug/dL (10% and 43.8%, respectively). Patients of asthma with elevated blood lead levels had higher grades of severity of asthma compared to those with blood lead levels10 ug/dL.Blood lead levels are not significantly associated with diagnosis of asthma but elevated blood lead levels seem to be associated with increased asthma severity and higher frequency of eosinophilia and elevated immunoglobulin E levels.