Several large-scale prospective prophylactic studies of pre-eclampsia have now been completed and despite being disappointing in regard to successful prophylaxis, have yielded useful data in relation to the clinical epidemiology of pre-eclampsia. The low-dose aspirin study of 1995 (Sibai et al., 1995) revealed that systolic blood pressure at entry, prepregnancy obesity, the number of previous abortions or miscarriage and smoking history were risk factors for development of pre-eclampsia. Cigarette smoking during pregnancy was associated with a reduced incidence of pre-eclampsia. However, race was not a risk factor for pre-eclampsia in this study. A multivariate logistic regression equation based on these four factors could define a tenth of the population at very high risk and another tenth of the population at very low risk. In the subsequent CPEP study (Sibai et al., 1997) risk factors for pre-eclampsia were found to be body mass index, systolic blood pressure and diastolic blood pressure. However, maternal age, blood group and rhesus factor, alcohol use, previous abortion or miscarriage, private insurance and calcium supplementation were not associated with significant risk of development of pre-eclampsia. In a recent review of 13 cohort studies comprising 1.4 million women, O'Brien etal. (2003) found that the risk of developing pre-eclampsia doubled for every 5—7 kg m—2 increase in prepreg-nancy body mass index. A family history of pre-eclampsia has long been known to be associated with increased risk of developing it (Chesley et al., 1968). It has been estimated (Cincotta and Brennecke, 1998) that a positive family history has a 20—30% risk of developing pre-eclampsia. These risk factors may be of value in counseling women but importantly target those women for detailed biochemical investigation or inclusion in clinical trials.
The prospective low-dose aspirin in high-risk pregnancy study (Caritis et al., 1998) showed that the incidence of pre-eclampsia in women with chronic hypertension was 25%, pregestational diabetes 22%, multifetal gestations 16% and previous pre-eclampsia 19%. Although the rate of pre-eclampsia in these at-risk women is great, the calculated contribution of these conditions to the overall numbers of pre-eclampsia can be calculated to be 14% in nullipara, 45% among women of all parities, but would account for the majority of pre-eclampsia in multiparous women (R. Levine, personal communication). Hence, most nullipa-rous women, a group which contributes to the majority of cases of pre-eclampsia, are at low risk of developing it from these conditions.
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