OBJECTIVES: We have previously shown that the levels of circulatory fetal DNA are elevated in preeclampsia and that these increases correspond to disease severity. Several reports have indicated that increased levels of antiphospholipid (anti-PL) and anti-DNA antibodies may be associated with preeclampsia, in particular with the severe forms of the disorder. Since the release of cell-free DNA by the placenta is attributed to some form of cell death or damage and as anti-PL and anti-double-stranded DNA (dsDNA) antibodies have been proposed to lead to placental damage, we have studied the relationship between these parameters in preeclampsia. METHODS: Circulating fetal DNA levels in samples taken from pregnant women with mild (n = 12) or severe (n = 12) preeclampsia and from normal pregnant controls (n = 35) were quantified using a Taqman real-time Polymerase Chain Reaction (PCR) assay. The Anti-PL antibodies (IgG and IgM) were assayed by anticardiolipin ELISA and by commercial anti-beta2-Glycoprotein I (GPI) ELISA kits. Anti-dsDNA antibodies (IgG and IgM) were analyzed by a commercially available anti-dsDNA ELISA kit. RESULTS: No correlation could be drawn with the quantity of circulatory fetal DNA in the samples analyzed and corresponding anti-PL or anti-dsDNA antibody levels. Furthermore, no significant difference existed between the levels of these antibodies in the two study groups and the control cohort. CONCLUSION: Our data suggest that the mechanism leading to the increased release of cell-free circulatory DNA from the placenta does not involve trophoblast damage mediated by these agents. Our analysis also questions the reported involvement of anti-PL and anti-DNA antibodies in preeclampsia.
OBJECTIVES: We have previously shown that the levels of circulatory fetal DNA are elevated in preeclampsia and that these increases correspond to disease severity. Several reports have indicated that increased levels of antiphospholipid (anti-PL) and anti-DNA antibodies may be associated with preeclampsia, in particular with the severe forms of the disorder. Since the release of cell-free DNA by the placenta is attributed to some form of cell death or damage and as anti-PL and anti-double-stranded DNA (dsDNA) antibodies have been proposed to lead to placental damage, we have studied the relationship between these parameters in preeclampsia. METHODS: Circulating fetal DNA levels in samples taken from pregnant women with mild (n = 12) or severe (n = 12) preeclampsia and from normal pregnant controls (n = 35) were quantified using a Taqman real-time Polymerase Chain Reaction (PCR) assay. The Anti-PL antibodies (IgG and IgM) were assayed by anticardiolipin ELISA and by commercial anti-beta2-Glycoprotein I (GPI) ELISA kits. Anti-dsDNA antibodies (IgG and IgM) were analyzed by a commercially available anti-dsDNA ELISA kit. RESULTS: No correlation could be drawn with the quantity of circulatory fetal DNA in the samples analyzed and corresponding anti-PL or anti-dsDNA antibody levels. Furthermore, no significant difference existed between the levels of these antibodies in the two study groups and the control cohort. CONCLUSION: Our data suggest that the mechanism leading to the increased release of cell-free circulatory DNA from the placenta does not involve trophoblast damage mediated by these agents. Our analysis also questions the reported involvement of anti-PL and anti-DNA antibodies in preeclampsia.