الفهرس 
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Abstract
Preeclampsia, which affects approximately 5-10% of all pregnancies, is a pregnancy-specific disorder characterized by the onset of hypertension and proteinuria in the second half of pregnancy and it is among the leading causes of fetal and maternal morbidity and mortality.
Despite intense efforts to find mechanisms and molecules that induce preeclampsia, no specific etiological factor has been identified. Placental ischemia and endothelial damage have been considered the key pathophysiologies of preeclampsia , however, the mediators leading to these alterations have not been clearly clarified .Altered expression of cytokines has been reported in preeclampsia, but their roles in disease pathogenesis remain controversial. A generalized inflammatory response has been considered to be one of the main pathologies and plays an important role in the disease development.
Serum levels of several cytokines have been reported to be altered and the alteration in cytokines levels were thought to participate in the pathogenesis of preeclampsia . IL-16 are among those cytokines .
IL-16 is a proinflammatory cytokine that is expressed in numerous normal human tissues and cell types, including activated monocytes , dendritic cells and fibroblasts , also in non immune cells suggesting its activity beyond the immune system ,Its presence at maternal-fetal interface implies role in pregnancy .
IL-16 enhances inflammatory process by stimulating the production of proinflamatory cytokines such as IL-6, TNF-alpha , IL-1 alpha and IL-15 by monocytes ,and upregulation of IL-2 receptor alpha on T-cells.
In addition, it inhibits IL-4 and IL-5 release from T-cells , thus impairs T-helper 2 immunity and alters Th1/ Th2 balance.
This case control study was designed to determine whether abnormal levels of IL-16 in maternal plasma correlate with the diagnosis of preeclampsia. Seventeen patients with mild preeclampsia and another seventeen patients with sever were enrolled in the study group while seventeen patients served as control.
Blood samples were taken from each participant after taking informed concent for determination of IL-16 levels in maternal plasma by ELIZA technique. There was no significant statistical difference between the study and control groups as regards the demographic data including maternal age and parity but gestational age was found to be significantly different between groups at sample drawing.
The current study showed that serum level of IL-16 was significantly higher in preeclampsia than in control. This finding is in accordance with the proposal that preeclampsia is associated with greater inflammatory response than observed in normal pregnancy and the findings that serum IL-16 is markedly elevated in preeclampsia adds evidence supporting this proposal. Elevated serum IL-16 is possibly due to the activation of monocytes and macrophages as result of enhanced maternal response to placental debris. IL-16, as well as other proinflammatory cytokines, reactive oxygen species and enzymes released by activated immunocytes, might be among the mediators leading to endothelial dysfunction and thus it may be associated with the pathogenesis of preeclampsia.