In vitro effect of anticardiolipin autoantibodies upon total and pulsatile placental hCG secretion during early pregnancy

• Published in: American journal of reproductive immunology (1989) Vol. 29; no. 4; p. 206
• Main Authors: Shurtz-Swirski, R, Inbar, O, Blank, M, Cohen, J, Bakimer, R, Barnea, E R, Shoenfeld, Y
• Format: Journal Article
• Language: English
• Published: Denmark 01.05.1993
• Subjects: Abortion, Habitual - etiology; Animals; Antibodies, Anticardiolipin - pharmacology; Antibodies, Monoclonal - pharmacology; Antiphospholipid Syndrome - complications; Antiphospholipid Syndrome - etiology; Antiphospholipid Syndrome - physiopathology; Chorionic Gonadotropin - secretion; Female; Humans; In Vitro Techniques; Mice; Models, Biological; Placenta - immunology; Placenta - secretion; Pregnancy; Pregnancy Complications - etiology; Thromboembolism - etiology
• ISSN: 1046-7408
• DOI: 10.1111/j.1600-0897.1993.tb00588.x

The anticardiolipin syndrome is characterized among other features by recurrent thromboembolic events, thrombocytopenia, and recurrent fetal loss associated with high IgG titers of anticardiolipin antibodies and/or the presence of lupus anticoagulant. The mechanisms for the fetal loss in this syndrome have not yet been clearly elucidated, although several hypothesis based on experimental data have been put forward. We wanted to evaluated the effect in vitro of anticardiolipin antibodies on the secretion of human chorionic gonadotropin. Employing our previous experience with placental explants, we studied the effect of several mouse monoclonal and human polyclonal purified anticardiolipin antibodies (ACA), which were shown by us to induce experimental antiphospholipid syndrome (APLS), to affect the pulsatile secretion of beta human choriogonadotropin. The mouse monoclonal ACA antibodies caused an increase in the pulsatility of beta human choriogonadotropin, while human polyclonal ACA derived from patients with ACA had an inhibitory effect. These studies with placental explants show that ACA may have an additional effect on placental hormone secretion and thus affect the fate of the embryo.