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Preeclampsia is an important cause of maternal and perinatal morbidity and mortality characterised by elevated blood pressure, fluid retention and protein in the urine. When convulsions and coma are superimposed, the condition is known as eclampsia. The origins of preeclampsia lie in a mismatch between foeto-placental demands and the ability of the utero-placental arteries to supply those demands. This situation also arises in intrauterine growth restriction in a mother with normal blood pressure, (the foetal syndrome of preeclampsia in isolation). von Dadelszen & Magee, 2002 pose the question why should there be this differential response to the same underlying pathology and review the evidence that infection may be a trigger. They point out that there is increasing evidence for an inflammatory model of preeclampsia.  Evidence for an infectious trigger is principally indirect, consisting of:

• similarities between the acute atherosis of preeclampsia and atherosclerosis

• the increased likelihood of developing cardiovascular disease later in life following a preeclampsia pregnancy

• the association between chronic infection and atherogenesis.

In pursuit of this hypothesis, von Dadelszen et al., 2003 compared the seroprevalence of antibody to cytomegalovirus and C. pneumoniae immunoglobulin G in women with early onset pre-eclampsia (<34 weeks of gestation, n = 9), late onset pre-eclampsia (>/=34 + 0 weeks of gestation, n = 29), normotensive intrauterine growth restriction (birthweight less than third centile, n = 33) and matched normal pregnancy (n = 113, up to 2 per case). Women with early onset preeclampsia had significantly higher (Kruskall Wallis test, P <0.05)  antibodies to cytomegalovirus than women with late onset preeclampsia,  intrauterine growth restriction or normal pregnancy. C. pneumoniae antibodies were significantly lower in women with intrauterine growth restriction  (median: 0.10 [95% CI = 0.08, 0.38]) than did normal pregnancy controls (0.21 [95% CI = 0.20, 0.28], P <0.05).Antibodies against both organisms were higher in early onset pre-eclampsia than in late onset pre-eclampsia, intrauterine growth restriction and normal pregnancy. It was suggested there may be  a pathophysiological link between pre-eclampsia and the known increased risk for subsequent atherosclerosis.

[Comment: As discussed elsewhere [see: chronic infections]  the high exposure of  populations to C. pneumoniae infection (also cytomegalovirus) makes it extremely difficult to infer causal relationships from seroprevalence studies.  The finding that C. pneumoniae antibodies were lower in women with intrauterine growth restriction is unexpected in the context of the hypothesis that the authors are exploring. This is a new field of study and more research is clearly indicated]. 

[MEW] August 2003

NEXT: Conclusions

von Dadelszen, P. & Magee, L. A. (2002). Could an infectious trigger explain the differential maternal response to the shared placental pathology of preeclampsia and normotensive intrauterine growth restriction? Acta Obstetrica Gynecologica Scandinavica 81, 642 - 648.

von Dadelszen, P., Magee, L. A., Krajden, M., Alasaly, K., Popovska, V., Devarakonda, R. M., Money, D. M., Patrick, D. M. & Brunham, R. C. (2003). Levels of antibodies against cytomegalovirus and Chlamydophila pneumoniae are increased in early onset pre-eclampsia. British Journal of Obstetrics and Gynaecology 110, 725 - 730.