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UBC Theses and Dissertations

The maternal predisposition to the syndrome of pre-eclampsia Alasaly, Kadria A.


Pre-eclampsia, which is characterized by maternal hypertension, proteinuria, hypoperfusion of end organs and a systemic maternal innate inflammatory response, is a leading cause of maternal mortality and morbidity world-wide. When of early-onset, pre-eclampsia is associated with fetal intrauterine growth restriction (IUGR). IUGR can occur in isolation, so-called normotensive IUGR. What is poorly understood is that some women develop the maternal syndrome of pre-eclampsia whilst others have only the fetal syndrome (normotensive IUGR), despite the fact that the initiating event in both is believed to be reduced uteroplacental perfusion. In this thesis I have asked two questions: First, could the maternal innate inflammatory response of pre-eclampsia predict an increased lifetime risk for developing the systemic inflammatory response syndrome (SIRS), as it is with later atherosclerosis (another disease of inflammation)? My hypothesis was the maternal syndrome of pre-eclampsia is a form of the systemic inflammatory response syndrome. Second, could it be that the maternal syndrome of pre-eclampsia is triggered by a reactivation of chronic infections common in the community, mainly infection with Chlamydophila pneumoniae (Chl pneumoniae) or cytomegalovirus (CMV) infections? This is especially pertinent as these infectious agents have been implicated in the development of atherosclerosis. We wanted to determine whether or not the dichotomous response of pre-eclampsia and normotensive IUGR could be explained by reactivation of chronic infection with Chl pneumoniae or CMV during preeclampsia, but not normotensive IUGR. My hypothesis was, could reactivated infectious trigger explain the differential maternal response to the shared placental pathology of pre-eclampsia and normotensive growth restriction? This would provide a link between pre-eclampsia and its attendant lifelong risk of atherosclerosis. Study designs SIRS. Cases were selected from women admitted to the intensive care unit (ICU) of St. Paul's Hospital with the diagnosis of SIRS. Controls were women without SIRS, admitted to general medical/surgical wards with the same primary diagnosis and same underlying problem (eg: pneumonia, bowel resection) but unremarkable in-hospital course (NO SIRS). The controls were matched for both age (±5 years) and ethnicity. Chl pneumoniae and CMV. Seroprevalence and levels of anti-CMV and Chl pneumoniae IgG were compared in a nested case-control study. We compared between women with early-onset preeclampsia (<34 weeks'; n=9), late-onset pre-eclampsia (>34+0 weeks'; n=29); normotensive IUGR (birthweight <3rd centile; n=33), and matched normal pregnancy (n=l13, up to 2 per case). Results SIRS. Most women in the ICU were too critically ill to be interviewed. Therefore, this study was deemed not to be feasible and was abandoned because of the low frequency of female admissions to the St Paul's ICU and, insufficient obstetric information. Chi pneumoniae and CMV . There was a significant difference in both anti-CMV and Chl pneumoniae EB antibodies between groups (Kruskal-Wallis p<0.05). Women with early-onset pre-eclampsia had higher anti-CMV levels (median: 79 [95% confidence interval 47, 164]) than women with late-onset pre-eclampsia (26 [22, 82], p<0.05), normotensive IUGR (40 [31, 72], p<0.05), and normal pregnancy (49 [45, 70], p<0.05). Women with normotensive IUGR had significantly lower anti-Chl pneumoniae antibodies (0.10 [0.08, 0.38]) than did normal pregnancy controls (0.21 [0.20, 0.28], p<0.05). Conclusions SIRS. We were unable to test the hypothesis as the study, as designed, was not feasible. Chi pneumoniae and CMV . Women with early-onset pre-eclampsia had higher levels of IgG against Chl pneumoniae and anti-CMV anti-bodies in their serum than in late-onset pre-eclampsia, normotensive IUGR, and normal pregnancy. This may provide a pathophysiological link between pre-eclampsia and the known increased risk for subsequent atherosclerosis. Could a reactivated infectious trigger explain the differential maternal response to the shared placental pathology of pre-eclampsia and normotensive intrauterine growth restriction? In addition, could the association between the maternal IgG response to Chl pneumoniae and CMV provide a link between pre-eclampsia (especially of early onset) and its attendant lifelong risk of atherosclerosis. Early-onset pre-eclampsia may truly be the 'toxaemia' of pregnancy.

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