Specific antiphospholipid antibodies (aPL) eluted from placentae of pregnant women with aPL-positive sera

Author:

Katano K.1,Aoki K.1,Ogasawara M.1,Sasa H.1,Hayashi Y.1,Kawamura M.1,Yagami Y.1

Affiliation:

1. Department of Obstetrics and Gynecology, Nagoya City University Medical School, Mizuho-ku, Nagoya, 467, Japan

Abstract

The mechanism by which antiphospholipid antibodies (aPL) cause recurrent pregnancy loss remains unclear. It has however been reported that aPL may affect cytotrophoblasts in vitro and thus direct placental damage might occur. Therefore, we investigated whether aPL are bound directly to placental tissues in patients with immunoglobulin G (IgG) -aPL positive sera. The material investigated comprised the placentae of six patients with a history of recurrent pregnancy loss and subclinical autoimmune disorder and one with systemic lupus erythematosus, who were treated with a combination of prednisolone and aspirin. Normal controls consisted of placentae derived from six women, negative for serum aPL, with no medical or obstetrical complication during their pregnancy. Five kinds of IgG- and IgM-antiphospholipid (anti-PS, PI, PA, PG and CL) antibodies were eluted from the placentae of both patients and controls, which were measured by enzyme-linked immunosorbent assay. IgG-aPL were detected in the placental eluates of four of seven (57%) patients, whereas IgM-aPL were not found in any. With respect to the pregnancy outcome of the four patients with IgG-aPL-positive placental eluates, one experienced intrauterine fetal death (IUFD) at 23 weeks of gestation and three demonstrated intrauterine growth retardation (IUGR). In contrast, the remaining three patients, evaluated negative for IgG-aPL in placental eluates, gave birth to one baby with IUGR and two appropriate-for-date babies. The placentae of the four mothers with IgG-aPL-positive placental eluates pathologically showed severe thrombotic findings. These results suggest that IgG-aPL can directly bind to placental tissue and might cause pathologic damage resulting in IUFD or IUGR.

Publisher

SAGE Publications

Subject

Rheumatology

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