Anti-fibrillin-1 autoantibodies in normal pregnancy and recurrent pregnancy loss.

PROBLEM: The aim of this study was to investigate anti-fibrillin-1 autoantibody in patients with a history of recurrent pregnancy loss (RPL) and during normal pregnancy. METHOD OF STUDY: Anti-fibrillin-1 IgG and IgM antibodies were measured by a home made ELISA in serum samples of 48 medically and obstetrically normal pregnant women, classified to three trimester groups, 15 female patients with RPL and 26 healthy non-pregnant women classified to two control subgroups: (a) women who had already had at least one previous successful pregnancy and (b) women who had never been pregnant. Differences in anti-fibrillin-1 autoantibodies between the groups were analyzed for statistical significance (P<0.05) with one-way analysis of variance (ANOVA) and multiple comparison test - Post Hoc test, Least Significant Difference method. RESULTS: Anti-fibrillin-1 IgM autoantibodies were significantly decreased in the second and third trimester pregnant women compared to the nulligravida controls. RPL patients had significantly increased anti-fibrillin-1 IgM antibody compared to control group (a). CONCLUSION: Fibrillin-1 degradation seems to be decreased during the second and third trimester of normal pregnancy. Increased anti-fibrillin-1 IgM antibodies in RPL patients may be a secondary phenomenon of increased fibrillin-1 degradation and contribute to the pathogenesis of pregnancy losses.

Levels of platelet-leukocyte aggregates in women with both thrombophilia and recurrent pregnancy loss.

The aim of our study was to investigate the significance of platelet-leukocyte aggregates (PLA) in women with recurrent pregnancy loss (RPL) as well as to identify association between common thrombophilic factors and whole blood levels of PLA in these patients. We measured PLA by whole blood flow cytometry in 66 nonpregnant women with hereditary and/or acquired thrombophilia and RPL, classified to 3 study groups, according to the type of losses (first, second, and third trimester) and 35 age-matched healthy controls. Platelet-leukocyte aggregates levels in all study groups were significantly increased compared to the control group (median values 2.13%, 2.32%, and 2.41%, vs median value in the control group 1.39%, P < .05 for all comparisons). Women with a single thrombophilic factor and women with combination of thrombophilic factors did not differ significantly as regards the PLA levels (2.13% vs 2.27%, P = .4). This study suggests that PLA may have a role in the pathogenesis of RPL in women affected by hereditary or acquired thrombophilia.

Flow cytometric investigation of CD40-CD40 ligand system in preeclampsia and normal pregnancy.

Our aim was to investigate the CD40-CD40 ligand system in preeclamptic women. We also studied CD62P and platelet-monocyte aggregates, which have been closely linked to the CD40-CD40L system. Platelet expression of CD40L and CD62P and expression of CD40 on monocytes and platelet-monocyte aggregates were determined by flow cytometry in whole blood from 23 preeclamptic women, 23 normotensive pregnant women, and 23 nonpregnant women. The preeclamptic women showed a significant increase in CD40L and CD62P on platelets and in CD40 on monocytes when compared with normotensive pregnant women and nonpregnant women (all P < .001). There was a significant increase in platelet-monocyte aggregates in preeclamptic women (P < .001) and normotensive pregnant women (P = .003) compared with nonpregnant women. Preeclampsia is associated with activation of the CD40-CD40L system. The activation of this system may contribute to the development or maintenance of the proinflammatory and prothrombotic milieu found in preeclampsia.

Upregulation of the CD40-CD40 ligand system in pre-eclampsia.

OBJECTIVE: To investigate the CD40-CD40 ligand (CD40L) system in women with pre-eclampsia. METHODS: Expression of CD40 on monocytes and expression of CD40 and CD40L on platelets were determined by whole blood flow cytometry in 23 women with pre-eclampsia and in 23 normotensive pregnant women. Serum levels of soluble CD40L in both groups of women were measured by enzyme-linked immunosorbent assay. RESULTS: There was a significantly higher expression of CD40 and CD40L on platelets and CD40 on monocytes in the women with pre-eclampsia compared with normotensive pregnant women (P<0.001 for all comparisons). The serum concentration of soluble CD40L was significantly higher in women with pre-eclampsia compared with normotensive pregnant women (P=0.012). CONCLUSION: Pre-eclampsia is associated with activation of the CD40-CD40L system. The activation of this system may contribute to the development or maintenance of the proinflammatory and prothrombotic responses, increased cytokine production, and endothelial cell dysfunction found in pre-eclampsia.