title: Reduced placental growth and hCG secretion in vitro induced by antiphospholipid antibodies but not by anti-Ro or anti-La: studies on sera from women with SLE/PAPS.
abstract: Systemic lupus erythematosus (SLE) and primary anti-phospholipid syndrome (PAPS) are autoimmune diseases causing recurrent pregnancy loss. We hypothesized that anti-phospholipid antibodies (aPL), but not anti-Ro and anti-La antibodies, might have a role through direct placental damage. We cultured human placental explants in sera from women with SLE/PAPS with different antibodies. These sera were found to reduce placental growth and increase trophoblastic apoptosis. No effect was found on estradiol or progesterone secretion, but inhibition in betahCG secretion was detected. BetahCG was reduced in women with a history of recurrent pregnancy loss or thromboembolic events, and was also the most sensitive marker when examining the effects of specific antibodies. High titers of aPL were found to cause the largest reduction in betahCG. Anti-Ro and anti-La did not induce placental damage. A strong correlation was found between the rise in the number of different antibodies in the sera and the incidence of recurrent pregnancy loss, which was also accompanied by a decline in the betahCG levels. In conclusion, aPL, but not anti-Ro or anti-La, may cause placental damage in vitro. Thus betahCG levels might constitute a predictive marker for the risk of placental damage and pregnancy loss in women with SLE/PAPS.
authors.affiliation: Laboratory of Teratology, Department of Anatomy and Cell Biology, Hebrew University, Hadassah Medical School, Jerusalem, Israel.
authors.forename: N
authors.initials: N
authors.lastname: Schwartz
authors.forename: Y
authors.initials: Y
authors.lastname: Shoenfeld
authors.forename: O
authors.initials: O
authors.lastname: Barzilai
authors.forename: R
authors.initials: R
authors.lastname: Cervera
authors.forename: J
authors.initials: J
authors.lastname: Font
authors.forename: M
authors.initials: M
authors.lastname: Blank
authors.forename: S
authors.initials: S
authors.lastname: Yacobi
authors.forename: N
authors.initials: N
authors.lastname: Patlas
authors.forename: A
authors.initials: A
authors.lastname: Cohen
authors.forename: D
authors.initials: D
authors.lastname: Mevorach
authors.forename: A
authors.initials: A
authors.lastname: Ornoy
mesh_terms: D000974:Antibodies, Antinuclear / Q000502:physiology*; D017152:Antibodies, Antiphospholipid / Q000502:physiology*; D016736:Antiphospholipid Syndrome / Q000097:blood / Q000276:immunology*; D001324:Autoantigens / Q000276:immunology; D006063:Chorionic Gonadotropin / Q000378:metabolism*; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000276:immunology*; D010929:Placentation; D012261:Ribonucleoproteins / Q000276:immunology; D000097585:SS-B Antigen
chemical_list: D000974:Antibodies, Antinuclear; D017152:Antibodies, Antiphospholipid; D001324:Autoantigens; D006063:Chorionic Gonadotropin; D012261:Ribonucleoproteins; D000097585:SS-B Antigen; C035356:SS-A antibodies; C035357:SS-B antibodies