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Egypt J Pediatr Allergy Immunol, (April 2012), Volume No. 10, Issue 01  
 
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Egypt J Pediatr Allergy Immunol 2012 ; 10 ( 01 ) : 13-18 -
, ESP - 21  
Original articles
Platelet activating factor and monocyte chemoattractant protein-1 in children with refractory epilepsy
Sahar A. Abd El-Aziz   Rasha A. Alm El-Din          
Background: Epilepsy is an important common and diverse group of symptom complexes characterized by recurrent spontaneous seizures. It is estimated that about 5-10% of all cases of epilepsy eventually become refractory. It has been suggested that inflammation plays a role in epilepsy. In refractory epilepsy, an inflammatory response is produced that leads to rapid release of pro-inflammatory cytokines as platelet activating factor (PAF) and monocyte chemoattractant protein-1 (MCP-1). Objective: The aim of the present study was to evaluate the plasma levels of the monocyte chemoattractant protein-1 (MCP-1) and platelet activating factor (PAF) in children with refractory epilepsy to explore their role in the pathogenesis of refractory epilepsy. Methods: The present study was carried out in Tanta University Hospital, Pediatric Department, Neurology unit. Forty (40) children with idiopathic refractory epilepsy (25 males and 15 females) their age ranging between 4- 15 years were included in the study. The control group consisted of thirty healthy children, 20 males and 10 females aged 5 years to 13 years. The serum levels of MCP-1 and PAF were measured for children with refractory epilepsy and the control children. Results: Children with refractory epilepsy had significantly higher serum levels of PAF (P value<0.001) and significantly higher serum level of MCP-1 (P value<0.001) in comparison to the control children. Also there was a significant correlation between the duration of refractory epilepsy and the serum levels of PAF and MCP-1. Conclusion: Higher serum levels of the proinflammatory cytokines PAF and MCP-1 in children with refractory epilepsy suggest that both, PAF and MCP-1, may play a role in the pathogenesis of refractory epilepsy.