This study aimed to identify if the clinical features of proteinuric pre-ec
lampsia or the biochemical markers of endothelial dysfunction associated wi
th this syndrome are altered according to parity in a direction that would
suggest a different pathophysiology. Groups of 27 primigravid and 35 multig
ravid women with pre-eclampsia (defined as blood pressure > 140/90 mmHg and
2+ proteinuria) were studied ante-partum, and at 6 weeks and 6 months post
-partum. Clinical markers of severity of pre-eclampsia, including blood pre
ssure, markers of renal, hepatic and coagulatory function, and biochemical
markers of endothelial dysfunction were measured. Fetal outcome was assesse
d by birthweight and birthweight percentile. Antepartum systolic blood pres
sure was 10 mmHg higher in the primigravida, and this difference was indepe
ndent of age and anti-hypertensive medication. Analysis of systolic blood p
ressure before and after delivery showed the primigravid women to have elev
ated systolic blood pressure over the whole time period (P < 0.01). The pri
migravid women had more severe hepatic dysfunction, with elevated aspartate
aminotransferase levels, but plasma creatinine, proteinuria, platelet coun
ts and haematocrit were similar, indicating that renal and coagulatory func
tion and plasma volume were affected to the same extent in the two groups a
nd were independent of parity. Birthweight was similar in the two groups, a
nd the percentage of infants weighing less than the 10th centile for gestat
ion was also similar. Biochemical markers of endothelial dysfunction, asses
sed by measuring the urinary prostacyclin metabolite 2,3-dinor-6-oxo-prosta
glandin F-1 alpha and plasma endothelin I, did not differ according to pari
ty. There were no differences in a number of other biochemical markers of p
re-eclampsia, including plasma albumin, uric acid, triacylglycerol, and tot
al, low-density lipoprotein and high-density lipoprotein cholesterol. Basop
hil, monocyte and lymphocyte counts were elevated before delivery in primig
ravid women with pre-eclampsia. The differences in lymphocyte counts persis
ted post-partum. Further studies are required to clarify the role, if any,
of monocytes, basophils and lymphocytes in the pathophysiology of pre-eclam
psia. in conclusion, the elevated systolic blood pressure and raised aspart
ate aminotransferase levels observed in primigravida suggest a more severe
form of pre-eclampsia The lack of differences in birthweight and other bioc
hemical and endothelial markers of severity of pre-eclampsia do not suggest
a different pathophysiology; however, the persistently higher white cell c
ounts in the primigravid pre-eclamptics are of interest, and might reflect
differences in immune responses in the two groups. We suggest that studies
of the pathophysiology of pre-eclampsia should include multigravida, as lon
g as there is adequate postpartum follow-up to exclude underlying disease.