SUMMARYIt has been reported tiiat the binding of some antiphospholipid antibodies (APA) to phospholipids requires llic presence of /frglycoprotein I (/(:-GPI), Using a new ELISA. in which well coaled phosphoiipids were treated witiiaeonstantamount of"puriiied/^-GPI. we tried to detect liie presence of APA which binds lo phosphoiipid//^;-GPI eomplex or to phospholipids sueh as eardioiipin (CA) and phnsphittidylserine (PS) in preeeiampsia. and to check for cliniciii abnormaiilies in iintibodypositivc eases. Serum satnples were taken from 43 cases of preeeiampsia. ineiuding 26 cases of the severe lype. and 47 normal pregnant women. Positive rates of antieardioiipin antibody (ACA) by ELISA using CA/^:-GPI complex in miid. severe and totai preeeiampsia were 200%, i7-4% and 18-4% respeetively. No antibody-positive eases were found in normal pregnancies. ACA was deteeted tntieh more frequently when eardiolipin,7?:-GPI complex was used in ELISA eompared with ELISA wiihout /(-GPI. Positive rales of anliphosphatidylserine antibody (APSA) in mild, severe and totai preeclampsia were 5-9%. li-5'^ and 9-3% respectively. APSA was aiso deteeted mueh more frequently when the phosphatidylserine,//^-GP! eomplex was used in ELISA. The frequency of inirauierine growth retardation (lUGR) in liie ACA-positive subjeets was higher than that of ACA negatives. We suggest that Lhe ACA and APSA which bind lo phospholipiiJ//f2-OPI complex are delectable in preeclampsia, and that these antiphospholipid antibodies arc rciated to fctai growth.

Summary In order to investigate the pathophysiologica! significance of anti-endothelial cell antibody (AECA) in pre-eclampsia, the effects of AECA on endothelin-1 (ET-I) and prostaglandin I-, (PGI-,) release from cultured human umbilical vein endothelial cells (HUVEC) was evaluated. Serum samples were taken from 85 pre-eclamptic and 20 normal pregnant women. Anti-endothelial cell antibody was measured by ELISA using HUVEC. The release of ET-1 and 6-keto PGEl-a, a stable metabolite of PGI,, from HUVEC were evaluated after incubation with IgG-AECA-positive sera and IgG isolated from AECA-positive sera. The incidence of IgG-and IgM-AECA was 24.7 and R.2%, respectively. The release of ET-I in the medium containing IgG-AECA-positive sera was significantly greater than in the medium containing IgG-AECA-negative sera. There was signiticant correlation between the levels of IgG-AECA and the release of ET-1 from endothelial cells. The ET-1 relea.se by IgG isolated from AECA-positive sera was greater than that from AECAnegative .sera. However, the release of 6-keto PGFI-a by AECA-positive sera was not significantly different from that of AECA-negative sera. ]( is concluded that IgG-AECA in pre-eclampsia increases ET-I release from endothelial cells and that AECA may affect local vascular function in this disorder.

The results suggest that one cause of preeclampsia is the production of antiphospholipid antibodies that bind to placental villous membrane antigens.

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The presence of anti‐ssDNA and anti‐dsDNA antibodies and their clinical significance in preeclampsia were studied. Serum samples were taken from 38 cases of preeclampsia including 19 severe cases, and from 26 normal pregnant women. Anti‐ssDNA and anti‐dsDNA antibodies were measured by using an enzyme‐linked im‐munosorbent assay (ELISA). Only 1 of the 38 preeclampsia tested positively for the anti‐dsDNA and none of 26 normal pregnant women showed positive results. Although 15 out of the 38 cases (39.4%) of preeclampsia tested positively the anti‐ssDNA antibody, none of the 26 normal pregnant women showed positive results. Five of 19 (26.3%) mild preeclampsia cases tested positively. In severe cases, 10 of 19 (52.6%) tested positively. The frequency of the anti‐ssDNA antibody is related to the severity of such symptoms as hypertension and proteinuria. However, we could not confirm that the presence of the anti‐ssDNA antibody is related to the appearance of intrauterine growth retardation (IUGR) in preeclampsia. This study demonstrated a high incidence of autoantibodies, such as the anti‐ssDNA antibody, in preeclampsia, and indicates a close relationship between this antibody and the severity of preeclamptic symptom. We concluded that the autoantibodies, such as the anti‐DNA antibody, might be produced in preeclampsia, and that the abnormal B‐cell activation might occur in the pathophysiology of preeclampsia.