Abstract
Objective: To determine the levels and isotypes of aCl, as well as anti beta 2 glycoprotein 1 (antiβ2-GP1) antibodies in serum and amniotic fluid of pregnant patients with SLE and/or APLS, and healthy pregnant women serving as a control group. Material and Methods: We analyzed serum and amniotic fluid of pregnant patients with SLE and/or APLS, and of healthy pregnant women through ELISA. Results were compared using a Student’s T test. Results: 6 of 13 patients (46.1%), 5 with SLE and one with primary APLS had antiphospholipid antibodies in amniotic fluid. Two patients had IgG aCl and 4 patients had antiβ2-GP1 (one of them also showing IgM) in amniotic fluid. In serum, 4 patients (30%) had antiphospholipid antibodies present (one IgG aCl and three anti β2-GP1) as opposed to none in the control group having antiphospholipid antibodies in amniotic fluid. Only one control had IgM aCl in serum. Antiβ2-GP1 in the amniotic fluid of patients showed a statistically significant value when compared to controls. Conclusion: aCl and antiβ2-GP1 may be present in the amniotic fluid of patients with and without a history of fetal loss. The presence of IgM aCl and antiβ2-GP1 in amniotic fluid suggests its localized production.
Highlights
The presence of anticardiolipin antibodies in maternal serum has been linked with recurrent fetal loss and adverse neonatal outcomes such as intrauterine growth retardation
Among the resulting damage inflicted by these antibodies are decidual vasculopathy, placental vessel thrombosis and placental infarction [2]. It has been suggested [3] that aCl are responsible for intrauterine stroke or neonatal convulsions [4]. These authors have suggested that immunoglobulin G (IgG) crosses the placental barrier and reaches the fetal circulation and can be the cause of thrombosis in the fetus
The presence of maternal aCl in amniotic fluid (AF) and umbilical cord blood of babies whose mothers have antiphospholipid antibody syndrome has been demonstrated (APS) [5], no other antibodies are documented, for instance anti beta 2 glycoprotein 1 antibodies, a protein that is importantly involved in the pathogenesis of APS
Summary
The presence of anticardiolipin antibodies (aCl) in maternal serum has been linked with recurrent fetal loss and adverse neonatal outcomes such as intrauterine growth retardation. These complications are associated to placental insufficiency and seem to be the consequence of the interaction between antiphospholipid antibodies and the placental tissue [1]. Among the resulting damage inflicted by these antibodies are decidual vasculopathy, placental vessel thrombosis and placental infarction [2]. It has been suggested [3] that aCl are responsible for intrauterine stroke or neonatal convulsions [4]. The presence of maternal aCl in amniotic fluid (AF) and umbilical cord blood of babies whose mothers have antiphospholipid antibody syndrome has been demonstrated (APS) [5], no other antibodies are documented, for instance anti beta 2 glycoprotein 1 (antiβ2-GP1) antibodies, a protein that is importantly involved in the pathogenesis of APS
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