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Turk J Haematol. 2011 Sep 05;28(3):170-5. doi: 10.5152/tjh.2011.50.

The role of tumor necrosis factor-alpha -308 G/A and transforming growth factor-beta 1 -915 G/C polymorphisms in childhood idiopathic thrombocytopenic purpura.

Turkish journal of haematology : official journal of Turkish Society of Haematology

Emel Okulu, Talia İleri, Vildan Koşan Çulha, Fatih Mehmet Azık, Yonca Eğin, Zümrüt Uysal, Nejat Akar

Affiliations

  1. Department of Pediatrics, Faculty of Medicine, Ankara University, 06100 Dikimevi, Ankara, Turkey, Phone: +90 312 595 63 90 E-mail: [email protected].

PMID: 27264363 DOI: 10.5152/tjh.2011.50

Abstract

OBJECTIVE: To increase our understanding of the etiology of idiopathic thrombocytopenic purpura (ITP) some cytokine gene polymorphisms were analyzed for susceptibility to the disease. The aim of this study was to investigate the role of tumor necrosis factor-alpha (TNF-α) -308 G/A and transforming growth factor-beta 1 (TGF-β1) -915 G/C polymorphisms in the development and clinical progression of childhood ITP.

METHODS: In all, 50 pediatric patients with ITP (25 with acute ITP and 25 with chronic ITP) and 48 healthy controls were investigated via LightCycler® PCR analysis for TNF-α -308 G/A and TGF-β1 -915 G/C polymorphisms.

RESULTS: The frequency of TNF-α -308 G/A polymorphism was 20%, 16%, and 22.9% in the acute ITP patients, chronic ITP patients, and controls, respectively (p>0.05). The frequency of TGF-β1 -915 G/C polymorphism was 16%, 8%, and 8.3% in the acute ITP patients, chronic ITP patients, and controls, respectively (p>0.05). The risk of developing ITP and clinical progression were not associated with TNF-α -308 G/A (OR: 0.738, 95% CI: 0.275-1.981, and OR: 0.762, 95% CI: 0.179-3.249) or TGF-β1 -915 G/C (OR: 1.5, 95% CI: 0.396-5.685, and OR: 0.457, 95% CI: 0.076-2.755) polymorphisms.

CONCLUSION: The frequency of TNF-α -308 G/A and TGF-β1 -915 G/C polymorphisms did not differ between pediatric ITP patients and healthy controls, and these polymorphisms were not associated with susceptibility to the development and clinical progression of the disease.

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