Is proteinuric pre-eclampsia a different disease in primigravida and multigravida?

Citation
Ae. Barden et al., Is proteinuric pre-eclampsia a different disease in primigravida and multigravida?, CLIN SCI, 97(4), 1999, pp. 475-483
Citations number
25
Categorie Soggetti
Medical Research General Topics
Journal title
CLINICAL SCIENCE
ISSN journal
01435221 → ACNP
Volume
97
Issue
4
Year of publication
1999
Pages
475 - 483
Database
ISI
SICI code
0143-5221(199910)97:4<475:IPPADD>2.0.ZU;2-P
Abstract
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.