Study of Plasma Factors Associated With Neutrophil Activation and Lipid Peroxidation in Preeclampsia

Abstract

Abstract-Neutrophil activation occurs in women with preeclampsia and is resolved after delivery. The present study examined whether circulating factors in plasma of women with preeclampsia caused neutrophil activation and lipid peroxidation. Twenty-one women with proteinuric preeclampsia were matched for age and gestational age with 19 normal pregnant women. Plasma was collected from all subjects before delivery and at 6 weeks postpartum and incubated with autologous white-cell buffy coat collected at the postpartum visit. Neutrophil activation was assessed by level of CD11b and CD18 expression after incubation with autologous antepartum or postpartum plasma. Lipid peroxidation was assessed by measurement of F 2 -isoprostanes in plasma, plasma-white cell incubates, and urine. Neutrophil CD11b and CD18 expression was not differentially altered by incubation with plasma from either women with preeclampsia or normal pregnant women and was similar between groups when incubation was performed with plasma collected after delivery. In preeclampsia, plasma F 2 -isoprostanes were significantly increased before and after delivery compared with controls. Plasma F 2 -isoprostanes were increased 2-fold after incubation of plasma with buffy coat, but preeclamptic women had higher levels compared with those of controls when either pregnant or postpartum plasma was used. In pregnant preeclamptics, plasma F 2 -isoprostanes were positively correlated with lymphocyte count. Six weeks after delivery, plasma F 2 -isoprostanes in the preeclamptic women were significantly positively associated with lymphocyte count and cholesterol and negatively associated with albumin. In conclusion, the present study does not suggest that a stable circulating factor causes neutrophil activation in preeclampsia. However, lipid peroxidation is elevated before and after delivery in women with preeclampsia, which suggests that these women may have an underlying predisposition to increased oxidative stress that may be driven by or contribute to a persistent low-grade inflammatory response. (Hypertension. 2001;38:803-808.)

STUDY OF SERUM CALCIUM, MAGNESIUM & URINE MICROALBUMIN LEVELS IN NORMAL & PRE-ECLAMPTIC GESTATION & TO COMPARE WITH NON-GESTATIONAL VALUE.

“…It may be due to loss of protein in the urine. Lower protein and albumin level in preeclampsia subjects was also found by Anne Barden et al [14].…”

Study of serum lipid profile in pregnancy induced hypertension

“…A significantly higher level of beta-lipoprotein was also reported by many workers in third trimester of gestational proteinuric hypertension (12,19,20). Some scientists observed significantly higher mean titre of autoantibodies to MDA-LDL, the IgG antibodies to an epitope of oxidized LDL, in preeclamptic patients, as enhanced lipid peroxidation is involved in the foam cell formation of decidua in the pathogenesis of toxaemia of pregnancy (20,21). Hypooestro genaemia, predominance of smaller and denser serum LDL particles and significant concentration of soluble vascular cell adhesion molecule-1 (VCAM-1) are supposed to be important contributors for endothelial dysfunction in PIH (1,9,12).…”

Neutrophils induce proangiogenic T cells with a regulatory phenotype in pregnancy

“…The differentiation of niT cells is reliant on AnxA1-facilitated transfer of FOXO1 contained in neutrophil apoptotic bodies to T cells during activation; niT cells are required to maintain normal pregnancy outcomes as depletion of neutrophils during pregnancy leads to smaller embryo sizes and abnormal placentation in mice. Whereas the presence of activated neutrophils in the maternal circulation has been reported to be detrimental in pregnancy complications, including preeclampsia (22,48), our observations suggest that a regulatory nonactivated proapoptotic neutrophil phenotype promoted by pregnancy hormones might be essential for normal placentation, including its vascular development. The cytokine milieu that results from niT-cell generation could favor the establishment of a proangiogeneic environment, with both IL-10 and IL-17 promoting vessel development (21,49) and IL-17 promoting trophoblast invasion (27,50), both key processes in spiral artery remodelling (26).…”