الفهرس 
ChlamydiaOnly 14 pages are availabe for public view
 |  | from | 150 |  |  |
| | | from | 150 | | |
Abstract
P
reeclampsia and atherosclerosis share many risk factors and pathophysiologic features. Accumulating evidence suggest a strong association between C.pneumoniae and atherosclerosis. Accordingly a similar association between C.pneumoniae and preeclampsia may also exist.
Preeclampsia can be considered a two stage disorder, with the first Stage involving abnormal placentation and the second being the abnormal maternal adaptation to the pregnancy that results in systemic dysfunction. Past, persistent or recurrent infection with C. pneumoniae may contribute to abnormal vascular function, atherosis and the abnormal placental perfusion that marks the first stages of Preeclampsia.
The cause of the abnormal placentation is uncertain; it may be immunological, inflammatory or genetically determined. There is ample clinical and biochemical evidence of endothelial cell dysfunction during preeclampsia. Altered levels of NO, elevated thromboxane-A2/ prostacycline 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 pathogensis 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 placenta vessels by mechanisms resemble those occurring in atherosclerosis.
C.pneumoniae can lead to endothelial dysfunction in different ways, Lipopolysaccaride when bound to LDL-C render it toxic to endothelium. Chlamydia pneumoniae infection also induced production of several cytokines. Cytokines are potent inducers of neutrophils free radical generation. Cytokines and free radicals also stimulate platelet activation.
Many studies were done considering the relation between C.pneumoniae infection and Preeclampsia. Some of these studies were found a positive correlation between C. pneumoniae and Preeclampsia and some of them found a negative correlation between C.pneumoniae and Preeclampsia.
This study was designed in a prospective manner to search for the Link between C.pneumoniae infection and development of Preeclampsia. The study population was 93 pregnant women more than 20th weeks gestation, venous blood was collected and plasma was stored at -20C. who were tested for C.pneumoniae IgG antibodies using ELISA technique.
17 out of 30 normotensive pregnant women showed negative seroconversion and 20 out of 63 preeclamptic women showed positive seroconversion. 56.7% of women showed no seroconversion developed Preeclampsia while 31.7% of women showed seroconversion developed Preeclampsia.
This correlation was statistically non significant may be due to small numbers of women who developed seroconversion.
There were no statistically significant differences between the three groups concerning age and gestational age.
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 pathogensis of preeclampsia and possible role of antichlamydial therapy in prevention of the disease.