Objective: The origins of pre-eclampsia/eclampsia lie in a mismatch between feto-placental demands and utero-placental supply, a situation that also arises in normotensive intrauterine growth restriction (IUGR). Could reactivated chronic infection be both a trigger for these differential maternal responses to the same underlying pathology and a link between pre-eclampsia and its attendant lifelong risks of atherosclerosis?
Design: Nested case-control study.
Setting: Tertiary obstetric centre.
Population: Cases of pre-eclampsia, normotensive IUGR and controls.
Methods: A nested case-control study of serum from a population-based bank was performed. Seroprevalence and levels of anti-cytomegalovirus (CMV) and Chlamydophila pneumoniae immunoglobulin G (IgG) were compared (non-parametrically) between women with early onset pre-eclampsia (<34 weeks of gestation, n = 9), late onset pre-eclampsia (> or =34 + 0 weeks of gestation, n = 29), normotensive IUGR (birthweight less than third centile, n = 33) and matched normal pregnancy (n = 113, up to 2 per case).
Results: There was a significant difference in both anti-CMV and Chl. pneumoniae antibodies between groups (Kruskal-Wallis test, P < 0.05). Women with early onset pre-eclampsia had higher anti-CMV levels (median: 79, 95% confidence interval [95% CI] = 47, 164) than women with late onset pre-eclampsia (26 [95% CI = 22, 82], P < 0.05), normotensive IUGR (40 [95% CI = 31, 72], P < 0.05) and normal pregnancy (49 [95% CI = 45, 70], P < 0.05). Women with normotensive IUGR had significantly lower anti-Chl. pneumoniae antibodies (0.10 [95% CI = 0.08, 0.38]) than did normal pregnancy controls (0.21 [95% CI = 0.20, 0.28], P <0.05).
Conclusions: The anti-CMV and anti-Chl. pneumoniae antibodies were higher in early onset pre-eclampsia 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.