Cytokine gene polymorphism [tumor necrosis factor-alpha (-308), IL-10 (-1082), IL-6 (-174), IL-17F, 1RaVNTR] in pediatric patients with primary immune thrombocytopenia and response to different treatment modalities

Mokhtar G. ; El-Beblawy N. ; Adly A. ; Elbarbary, Nancy ; Kamal T. ; Hasan E. 


Abstract


© 2016 Wolters Kluwer Health, Inc. All rights reserved. To evaluate the association between development, progression, and response to therapy among patients with immune thrombocytopenia (ITP) and different cytokine gene polymorphisms known to be related to autoimmunity [tumor necrosis factor (TNF)-alpha, interleukin (IL)-10, IL-6, IL-17, IL-1Ra]. A total of 50 pediatric patients with ITP (20 newly diagnosed, 30 chronic) and 50 healthy controls were investigated via PCR-restriction fragment length polymorphism analysis for cytokine gene polymorphism. Compared with controls, all patients showed a higher frequency of IL-6-174 CC [P=0.0001, odds ratio (OR)=7.048, 95% confidence interval (CI)=2.18-22.7] , higher GA genotype of TNF-α (-308) (P=0.001, OR=6.469, 95% CI=2.0-20.9), higher CC genotype of IL-17F (P=0.0001, OR=55.545, 95% CI=14.4-213.2), higher GG of IL-10-1082 (P=0.029, OR=3.6, 95% CI=1.08-12.18), and A1A2 genotype of IL-1Ra VNTR (P=0.039, OR=2.374, 95% CI=1.03-5.4). IL-10 GA and IL-1Ra A1A1 genotypes were higher among chronic patients (P=0.042, P=0.001 respectively) compared with newly diagnosed ones. Best platelet response to steroid treatment was found among GC genotype of IL-6 (-174) and GG genotype of IL-10 (-1082) in all patients with ITP. This suggests that previously mentioned cytokine gene polymorphisms possibly contribute to the susceptibility of acquisition of childhood ITP. Furthermore, GA genotype of IL-10 and A1A1 genotype of IL-1Ra polymorphisms are associated with increased risk of chronic ITP. IL-6 (-174) and IL-10 (-1082) genes might play a role in the effectiveness of steroid therapy among patients with ITP.


Other data

Issue Date 1-Apr-2016
Journal Blood Coagulation and Fibrinolysis 
URI http://research.asu.edu.eg/123456789/142
DOI 3
313
http://api.elsevier.com/content/abstract/scopus_id/84961390485
27
1473-5733
10.1097/MBC.0000000000000431


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