alexa Factor V Leiden Mutation as a Novel Marker in Children with Cerebral Palsy | OMICS International
ISSN: 1745-7580

Immunome Research
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Research Article

Factor V Leiden Mutation as a Novel Marker in Children with Cerebral Palsy

Doaa M Mahrous Alshareef1, Hanan Mostafa Kamel2, Waleed Mahmoud Abd el Hameed*2 and Abdel Halim E Amin3

1Departments of Pediatrics, Clinical Pathology Department, Faculty of Medicine, Minia University, Egypt

2Clinical Pathology, Clinical Pathology Department, Faculty of Medicine, Minia University, Egypt

3Obstetrics & Gynecology, Faculty of Medicine, El-Minia University, Egypt

Corresponding Author:
Waleed Mahmoud Abd el Hameed
Clinical Pathology Department, Faculty of Medicine
Minia University, Egypt
Tel: 01005200719
E-mail: [email protected]

Received date: February 08, 2016; Accepted date: March 16, 2016; Published date: March 22, 2016

Citation: Mahrous Alshareef DM, Mostafa Kamel H, Abd el Hameed WM, Amin AHE (2016) Factor V Leiden Mutation as a Novel Marker in Children with Cerebral Palsy. Immunome Res 12:107. doi:10.4172/1745-7580.10000107

Copyright: © 2016 Mahrous Alshareef M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited

Abstract

Background: Gene mutations are known to play a role in the development of cerebral palsy (CP). The aim of this study was to determine the frequency of factor V Leiden (fVL) mutation as an etiological novel marker in Egyptian children with cerebral palsy. Methods: The study included 70 children; 50 patients with cerebral palsy (Group I) and 20 healthy subjects (Group II) matched age and sex as a control group. Venous blood samples were used for DNA extraction using PCR testing. Polymerase chain reaction (PCR) primers were designed based on exon 10 sequence of human factor V gene. Key findings: There was insignificant difference between both groups regarding comparison of demographic characteristics and risk factors except for pre-term birth (26% in study group versus 5% in control group with P = 0.04). The frequency of fVL mutation was 42% in the study group, 15% in control group with significant difference between study and control groups. There was a significant association and for the first time between homozygous fVL mutation and severe type of cerebral palsy; 60% of homozygous mutations associated with severe CP versus 9% of heterozygous mutations. Conclusions: The fVL mutation is one of the major risk factors that may increase the likelihood of cerebral thrombo-embolism and subsequent cerebral palsy in Egyptian children.

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