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A Journal on Pediatrics, Neonatology, Adolescent Medicine,
Child and Adolescent Psychiatry
Indexed/Abstracted in: CAB, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,532
Minerva Pediatrica 2015 August;67(4):279-84
The role of prothrombotic factors in children with hemiplegic cerebral palsy
Türedi Yildirim A. 1, Sütçü R. 2, Köroğlu M. 3, Deli̇baş N. 4, Ki̇şi̇oğlu N. 5, Akar N. 6, Ergürhan İlha İ. 7 ✉
1 Department of Pediatric Hematology, School of Medicine, Celal Bayar University, Manisa, Turkey;
2 Department of Biochemistry, School of Medicine, Izmir Katip Çelebi University, Izmir, Turkey;
3 Department of Radiology, School of Medicine, Suleyman Demirel University, Isparta, Turkey;
4 Department of Biochemistry, School of Medicine, Suleyman Demirel University, Isparta, Turkey;
5 Department of Statistics, School of Medicine, Suleyman Demirel University, Isparta, Turkey;
6 Department of Pediatric Molecular Genetics, School of Medicine, Ankara University, Ankara, Turkey;
7 Department of Pediatric Oncology, Ankara Oncology Training and Research Hospital, Ankara, Turkey
AIM: Hemiplegic cerebral palsy (HCP) is a condition occurring as a consequence of a non-progressive damage of the brain with incomplete anatomical and physical development during the early period of life. Its etiology is multifactorial, with the cause remaining unexplained in the majority of cases. This study aims to investigate whether thrombophilic factors correlates with the etiology in children with HCP.
METHODS: We included 36 children with HCP in the patient group, and 41 healthy children with no neurologic disorders in the control group. No significant difference was found between the two groups in terms of factor V leiden, methylenetetrahydrofolate reductase and prothrombin 20210A mutation frequency and protein C, protein S and antithrombin III levels.
RESULTS: Homocysteine levels were significantly higher in the group of patients with HCP as compared to the control group (P=0.012). Because we could not identify the origin of hyperhomocysteinemia as congenital or acquired, the impact of hyperhomocysteinemia on HCP was considered insignificant. Each thrombophilic disorder was assessed in terms of relatedness to atrophy, periventricular leukomalacia, infarct, congenital anomaly and porencephalic cyst, respectively. No significant correlation was detected between thrombophilic disorders and cranial imaging findings.
CONCLUSION: Our study has shown that thrombophilic factors are not involved in the etiology of HCP.