الفهرس Only 14 pages are availabe for public view
 |  | from | 120 |  |  |
| | | from | 120 | | |
Abstract
Preeclampsia and atherosclerosis share many risk factors and pathophysiologic features, accumulating evidence suggests a strong association between C.pneumoniae and atherosclerosis. Accordingly a similar association between C. pneumoniae and preeclampsia may also exists. Preeclampsia thought to be a 2 stages disorder, the first is abnormal placentation and placental Ischaemia, the second stage is systemic endothelial dysfunction most probably caused by factors released from Ischaemic placenta. These factors may be neutrophils. Neutrophils supposed to be activated during their passage in placental vessels, activated neutrophils may lead to endothelial damage by releasing inflammatory mediators.
The cause of abnormal placentation is uncertain, it may be immunological, inflammatory or genetically determined. There is clinical and biochemical evidence of endothelial cell dysfunction during preeclampsia. Altered levels of NO, elevated thromboxane A2/prostacyclin ratio, deficiency of antithrombotic factors and platelet activation all are found in preeclampsia and are mediated by injured endothelial cells.
Whether C. pneumoniae may have a role in the pathogenesis of preeclampsia is uncertain. However it is postulated that
C. pneumoniae may be implicated in preeclampsia through many ways. It may be involved in abnormal placentation seen in preeclampsia. Also, it may be responsible for atherosis frequently seen in placental vessels by mechanisms resemble those occurring in atherosclerosis. C. pneumoniae can lead to endothelial dysfunction in different ways, lipopolysaccharide when bound to low
density lipoprotein cholesterol render it toxic to endothelium,
C. pneumoniae infection, also induce production of several cytokines, cytokines are potent inducers of neutrophil free radical generation. Cytokines and free radicals also stimulate platelet activation.
In this study the seroprevalence of C. pneumoniae IgG was compared between 46 preeclamptic primigravidae and 46 healthy matched controls. Venous blood was collected and serum was stored at -20C. Antibodies to C. pneumoniae (IgG) were determined using Enzyme Linked Immuno-Sorbent Assay (ELISA) (Vircell, Espain).
There was increased percentage of C. pneumoniae IgG in preeclamptic women (37%) than in control group (22%). Suggesting a relation between preeclampsia and exposure to C. pneumoniae. The difference was statistically significant (P value < 0.05).
A further prospective case control study is recommended to confirm the relation between preeclampsia and C. pneumoniae and to determine the time of infection that may be implicated the pathogenesis of preeclampsia, and possible role of antichlamydial therapy in the prevention of the disease.