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Objective: The aim of this study was to determine whether positive results of tests for any of 5 antiphospholipid antibodies are associated with recurrent preeclampsia among women with a history of preeclampsia in a previous pregnancy. Study Design: Second-trimester serum samples were obtained from 317 women with preeclampsia in a previous pregnancy who were being followed up in a prospective treatment trial. The serum samples were measured by enzyme-linked immunoassay for immunoglobulin G and immunoglobulin M antibodies against 5 phospholipids. Positive results were analyzed with regard to preeclampsia, severe preeclampsia, intrauterine growth restriction, and preterm delivery. Results: Sixty-two of the 317 women (20%) had recurrent preeclampsia develop, 19 (6%) had severe preeclampsia, and 18 (5.8%) were delivered of infants with growth restriction. Positive results of tests for immunoglobulin G or immunoglobulin M antiphospholipid antibodies were not associated with recurrent preeclampsia. Positive results for immunoglobulin G or immunoglobulin M antibodies at the 99th percentile were also not associated with preterm delivery. Positive results at the 99th percentile for immunoglobulin G antiphosphatidylserine antibody were associated with severe preeclampsia, and positive results at the 99th percentile for immunoglobulin G anticardiolipin, antiphosphatidylinositol, and antiphosphatidylglycerol antibodies were associated with intrauterine growth restriction. The positive predictive values for these outcomes all were approximately 30%. Conclusion: Positive results of testing for antiphospholipid antibodies in the second trimester were not associated with recurrent preeclampsia among women at risk because of a history of preeclampsia. Positive results for immunoglobulin G antiphosphatidylserine antibody were associated with severe preeclampsia, and positive results for immunoglobulin G anticardiolipin, antiphosphatidylinositol, and antiphosphatidylglycerol antibodies were associated with intrauterine growth restriction. However, the positive predictive values for all these associations were modest. Testing for antiphospholipid antibodies during pregnancy is of little prognostic value in the assessment of the risk for recurrent preeclampsia among women with a history of preeclampsia. (Am J Obstet Gynecol 2001;184:825-34.)

Objective: We sought to characterize the presentation, recurrence, and outcome of venous thromboembolism during pregnancy. Study Design: We performed a 12-year, single-center, retrospective review of 38 patients with venous thromboembolism during pregnancy. The independent variables were subjected to univariate analysis (unpaired t test for normally distributed continuous variables and Fisher exact test for discrete variables). P Results: There was no significant difference for the following variables according to time of presentation (antepartum vs post partum): gestational age at delivery (37.4 ± 6.6 wk vs 38.1 ± 2.4 wk; P = .7), birth weight (3257 ± 458 g vs 3093 ± 719 g; P = .3), and mode of delivery (2 vs 4 cesarean deliveries; P = .15). There were 2 maternal deaths. All 3 women with antepartum recurrent venous thromboembolism (despite heparin prophylaxis) had findings of protein C deficiency, protein S deficiency, and lupus anticoagulant–anticardiolipin antibody, respectively. Conclusion: The gestational age at presentation appears more equally distributed throughout gestation than previously reported. Notwithstanding limited numbers, the recurrence of venous thromboembolism despite use of prophylactic heparin therapy suggests the need to reexamine the current recommendations for heparin dosing. (Am J Obstet Gynecol 1999;181:1118-21.)

Studies in rheumatologic and hematologic populations suggest that anti-beta(2)-glycoprotein I antibodies are more specific for the clinical manifestations of antiphospholipid syndrome than anticardiolipin antibodies. However, the association between anti-beta(2)-glycoprotein I and pregnancy loss remains uncertain. We sought to determine whether anti-beta(2)-glycoprotein I is associated with the obstetric features of antiphospholipid syndrome.Sera from 4 groups of women were studied: (1) 152 healthy fertile control subjects, (2) 141 subjects with unexplained recurrent spontaneous abortions, (3) 58 subjects with unexplained fetal deaths, and (4) 73 subjects with well-characterized antiphospholipid syndrome. Serum anticardiolipin and anti-beta(2)-glycoprotein I levels were determined by enzyme-linked immunoassay.Patients with antiphospholipid syndrome had significantly higher levels of immunoglobulin G and immunoglobulin M anticardiolipin and anti-beta(2)-glycoprotein I than the other 3 groups (P.0001). However, women in the recurrent spontaneous abortion, fetal death, and fertile control groups had similar levels of each antibody. Similarly, there were no differences in the proportion of women with positive test results for each autoantibody in these 3 groups. Linear regression analysis showed significant correlation between anticardiolipin immunoglobulin G and beta(2)-glycoprotein I immunoglobulin G (R (2) = 0.544786, P =.0001) and anticardiolipin immunoglobulin M and beta(2)-glycoprotein I immunoglobulin M (R (2) = 0.525048, P =.0001).Both anticardiolipin and anti-beta(2)-glycoprotein I are associated with antiphospholipid syndrome. However, testing for anti-beta(2)-glycoprotein I does not identify additional patients with either recurrent spontaneous abortions or unexplained fetal deaths who initially have negative test responses for anticardiolipin. This is likely because of the strong correlation between the 2 autoantibodies. Our data do not support routine testing for anti-beta(2)-glycoprotein I in addition to testing for antiphospholipid antibodies in women with recurrent pregnancy loss and unexplained fetal death.

Objective: In patients with a history of severe preeclampsia, an increased frequency of hemostatic abnormalities has recently been suggested in small studies without control groups. Our purpose was to investigate the prevalence of such abnormalities in a large patient group with a history of severe hypertensive disorder in pregnancy, in comparison with an appropriate control group. Study Design: A total of 345 patients with a history of severe preeclampsia were investigated at a minimum of 10 weeks post partum for the presence of activated protein C resistance, the associated factor V mutation, hyperhomocysteinemia and anticardiolipin antibodies. The control group consisted of 67 healthy women with a history of uncomplicated pregnancies only. Blood was obtained during the second half of a normal menstrual cycle, and none of the patients or control subjects used oral contraceptives. Results: Of all patients, 11.3% had activated protein C resistance (control subjects 1.5%, P = .025). Only half of these patients had the factor V mutation. Hyperhomocysteinemia was present in 12.1% of all patients, in comparison with 4.5% in the control group ( P = .115). Anticardiolipin antibodies were observed in 20.9% of the patients, whereas these antibodies were found in 7.5% of the control subjects ( P = .016). In general, the prevalence of these abnormalities was 1.5 to 2 times higher in patients who were delivered before 28 weeks, in comparison with patients who were delivered after 28 weeks. Conclusions: Hemostatic abnormalities, associated with an increased risk of thrombosis, are present in approximately 40% of patients with a history of severe preeclampsia, which is almost 4 times higher than in control subjects. These findings might suggest a cause of preeclampsia and could have implications in subsequent pregnancies and general health. (Am J Obstet Gynecol 1999;180:1146-50.)

OBJECTIVE: Initial studies showed that passive immunization with human immunoglobulin G fractions containing antiphospholipid antibodies can result in murine fetal loss. We intended to use the murine model to study mechanisms of fetal loss associated with antiphospholipid antibodies. However, we have since found variable effects of antiphospholipid antibodies on murine pregnancy. The objective of this study was to determine the consistency of murine pregnancy loss from antiphospholipid antibody containing immunoglobulin G fraction. STUDY DESIGN: Pregnant C3H/HeN (mated with C57B1/6 males) and BALB/c (mated with BALB/c males) mice were passively immunized with antiphospholipid antibody containing human immunoglobulin G fraction from 20 women with antiphospholipid syndrome. The mice received either a single dose of 10 to 30 mg on day 12 of pregnancy or 10 mg per day on days 12 to 14 of gestation. Some mice receiving each dose of immunoglobulin G fraction were bled to confirm serum levels of anticardiolipin antibodies. Mice were killed on day 15 and the fetal status was determined. RESULTS: Overall, passive immunization with individual antiphospholipid antibody containing immunoglobulin G fractions resulted in 801 live pups (75%), 232 fetal deaths (22%), and 38 resorptions (3%) in 131 mice. The effect of immunoglobulin G fractions from individual patients was highly variable. Immunoglobulin G fraction from eight women resulted in high rates of fetal loss. However, in spite of high levels of anticardiolipin antibodies, fetal outcome was normal in mice immunized with immunoglobulin G fraction from the majority of women. The rate of fetal death did not uniformly increase with increasing doses of immunoglobulin G fraction and was unrelated to the donor's medical history. Fetal outcome was similar for both C3H/HeN and BALB/c mice. CONCLUSIONS: Human antiphospholipid antibodies have variable effects on murine pregnancy outcome. Characterization of antiphospholipid antibodies that do and do not cause murine fetal loss may provide insight into epitopes relevant to fetal loss associated with antiphospholipid syndrome.

OBJECTIVE: Our goal was to determine whether women with clinical features of antiphospholipid syndrome but negative test results for lupus anticoagulant and anticardiolipin antibodies have pathogenic antibodies not identified by currently used methods. STUDY DESIGN: Sera were obtained from women with clinical features associated with antiphospholipid antibodies who had negative test results for lupus anticoagulant and anticardiolipin antibodies (antiphospholipid syndrome–like). We studied (1) the effect of passive immunization with their purified immunoglobulin G fraction on murine pregnancy ( n = 35) and (2) the presence of antiphospholipid antibodies other than lupus anticoagulant or anticardiolipin antibodies ( n = 39). Sera were also retested for anticardiolipin antibodies and lupus anticoagulant. RESULTS: Fetal loss occurred in 235 of 1088 (22%) pups in 137 mice immunized with immunoglobulin G fraction from antiphospholipid syndrome–like women compared with 23 of 402 (6%) pups in 53 control mice. Immunoglobulin G from 11 study patients resulted in the loss of at least one third of the exposed pups. Five women had positive levels of antiphosphatidylserine antibodies (>99th percentile). All levels were low positive, and three women also had low-positive levels of anticardiolipin antibodies on repeat testing. Five of the 11 (45%) women whose immunoglobulin G fractions caused at least 33% fetal loss also had positive test results for antiphospholipid antibodies. CONCLUSIONS: A subset of women with clinical disorders suspicious for antiphospholipid syndrome but who had negative test results for lupus anticoagulant and anticardiolipin antibodies by current methods have serum immunoglobulin G that is pathogenic to murine pregnancy. Testing for pathogenic immunoglobulin G may provide additional means to identify women with an as yet uncharacterized immune condition. The clinical relevance of low levels of antiphospholipid antibodies in these women remains unproved. (Am J Obstet Gynecol 1997;176:628-33.)

OBJECTIVE: Antiphospholipid antibodies are associated with clinical intrauterine growth restriction. In this study we investigated whether immunoglobulin M monoclonal antibodies against phosphatidylserine or cardiolipin or cross-reactive with both phospholipids would induce intrauterine growth restriction in an experimental model of the antiphospholipid antibody syndrome. STUDY DESIGN: Balb/c or CD-1 mice were injected intraperitoneally on day 8 of pregnancy with three immunoglobulin M monoclonal antibodies that differentiated between cardiolipin- and phosphatidylserine-dependent antigens or with control immunoglobulin M monoclonal antibodies against irrelevant antigens. The animals were killed on day 15 of pregnancy and placental and fetal weights were measured. RESULTS: Monoclonal antibody 3SB9b, which reacted in enzyme-linked immunosorbent assays with phosphatidylserine but not cardiolipin, induced a significant reduction in both fetal and placental weights. Monoclonal antibodies BA3B5C4, which was cross-reactive with cardiolipin and phosphatidylserine, and D11A4, which reacted with cardiolipin, did not alter fetoplacental weights. CONCLUSION: An antiphospholipid antibody that reacts with phosphatidylserine induces significant fetal and placental intrauterine growth restriction in a mouse model for the antiphospholipid antibody syndrome, but those that react with cardiolipin do not. (AM J OBSTET GYNECOL 1996;174:700-7.)

OBJECTIVE: Our purpose was to determine whether anticardiolipin antibodies induced by immunization with β 2 -glycoprotein I cause fetal death in mice. STUDY DESIGN: Female BALB/c mice were immunized with β 2 -glycoprotein I in a carbohydrate adjuvant or with carbohydrate adjuvant alone. The mice were mated with BALB/c malee and killed on day 11 to 13 of pregnancy, and the fetal status was determined. Posttreatment blood samples were obtained for measurement of anticardiolipin and anti-β 2 -glycoprotein I antibodies and platlet counts. RESULTS: Anticardiolipin and anti-β 2 -glycoprotein I antibodies developed in all mice immunized with β 2 -glycoprotein I. Fetal death occurred in 17 of 145 gestational sacs (12%) in 18 mice immunized with β 2 -glycoprotein I compared with 24 of 177 (14%) sacs in 21 control mice. There were no morphometric or histologic differences between gestational tissues, and platelet counts were similar for each group. CONCLUSIONS: The induction of high levels of anticardiolipin antibodies in BALB/c mice by β 2 -glycoprotein I immunizations did not result in fetal death or thrombocytopenia. These nonpathogenic β 2 -glycoprotein I-induced anticardiolipin antibodies should prove useful in the characterization of clinically relevant epitopes for antiphospholipid syndrome.

Objective: We compared the use of aspirin alone with combined therapy (prednisone plus aspirin) in antiphospholipid antibody-positive obstetric patients with prior adverse pregnancy outcome. Study Design: Thirty-nine patients meeting specific laboratory and clinical inclusion criteria were randomized to receive either combined therapy (prednisone plus low-dose aspirin, n = 17) or aspirin alone ( n = 22). The daily aspirin dose was 81 mg; prednisone was begun at 20 mg/day and increased or decreased on the basis of observed changes in serial antibody levels. Perinatal outcomes were compared between groups. Evaluation of treatment-related maternal complications and serial antibody titers was also accomplished. Results: Thirty-four randomized subjects were evaluable (prednisone plus low-dose aspirin, n = 12 vs aspirin only, n = 22); no perinatal losses were observed in the study cohort. Preterm delivery was experienced by significantly more patients receiving prednisone plus low-dose aspirin than aspirin only (8/12 vs 3/22, respectively; p = 0.003), and prednisone exposure appeared to be an independent risk factor for preterm birth. Conclusions: The use of prednisone therapy in conjunction with low-dose aspirin does not appear to improve outcome and may provoke obstetric complications in antiphospholipid antibody-positive patients.

Objectives: A prospective, controlled multicenter study was performed to estimate the obstetric risks of antiphospholipid antibodies (the lupus anticoagulant and anticardiolipin antibodies). In addition, the risks of prior thrombosis, obstetric history, systemic lupus erythematosus, and high-dose prednisone treatment were evaluated. Study Design: After screening for antiphospholipid antibodies in patients with lupus erythematosus or women with prior fetal loss(es), 59 subsequent pregnancies with and 54 without these antibodies were followed. Results: The presence of the lupus anticoagulant and a history of at least three spontaneous abortions could predict fetal loss ( p = 0.032 and 0.001, respectively). In live born infants, a low birth weight could be predicted by the presence of anticardiolipin antibodies ( p = 0.034), prior intrauterine fetal death ( p = 0.025), and treatment with high-dose prednisone ( p = 0.002). No relationships were seen between antiphospholipid antibodies and small-for-gestational-age newborns and pregnancy-induced hypertension or preeclampsia. The disappearance of antiphospholipid antibodies during pregnancy was not correlated with live birth. Conclusion: It is concluded that the presence of antiphospholipid antibodies is a risk factor for adverse pregnancy outcome.

Objective We investigated whether levels of annexin A5 (AnxA5), AnxA5 anticoagulant activity and binding, and anti-AnxA5 antibodies might be altered in women with previous histories of recurrent spontaneous pregnancy losses (RSPL) when tested during pregnancy. Study design Ninety pregnant women with histories of 3 or more RSPL (cases) and 150 women without adverse pregnancy histories (controls) were assayed for these AnxA5 parameters. Results There were no significant differences between cases and controls in AnxA5 levels (median, 23.1 ng/mL [range, 2.1-201.1 ng/mL] vs 19.7 ng/mL [2.1-151.5 ng/mL]; P = .20), AnxA5 anticoagulant activity (183% [101%-236%] vs 168% [128%-256%]; P = .39) and binding (6.0 ng/aliquot PL [2.1-19.5 ng/aliquot PL) vs 6.1 ng/aliquot PL [1.6-16.8 ng/aliquot PL]; P = .72), and anti-AnxA5 antibody levels. Conclusions AnxA5 parameters do not distinguish between cases and controls when tested during pregnancy. The pregnant state itself appears to be associated with altered levels of AnxA5 parameters.

Studies in rheumatologic populations suggest that immunoglobulin A antiphospholipid antibodies are strongly associated with the clinical manifestations of antiphospholipid syndrome. However, the association between immunoglobulin A antiphospholipid antibodies and pregnancy loss is uncertain. We determined whether immunoglobulin A antiphospholipid antibodies, specifically anti-beta(2)-glycoprotein I and anticardiolipin, are associated with the obstetric features of antiphospholipid syndrome.Sera from 4 groups of women were studied: (1) 133 women who experienced unexplained recurrent spontaneous abortion, (2) 48 women who experienced unexplained fetal death, (3) 145 healthy fertile control subjects, and (4) 67 women with well-characterized antiphospholipid syndrome. Serum immunoglobulin A, immunoglobulin G, and immunoglobulin M anti-beta(2)-glycoprotein I and anticardiolipin antibodies were determined by enzyme-linked immunoassay.Groups of women who experienced unexplained recurrent spontaneous abortion and unexplained fetal death had a higher proportion of women who had positive test results for immunoglobulin A anti-beta(2)-glycoprotein I antibodies than fertile control subjects (P.01, chi-square test); these subjects also had higher levels of autoantibody (P = .001, Kruskal-Wallis). Women who experienced recurrent spontaneous abortion had a higher proportion of women with positive test results for immunoglobulin A anticardiolipin antibodies compared to fertile control subjects (P.05, chi-square test); this group also had higher levels of autoantibody (P = .0065, Kruskal-Wallis test). Linear regression analysis showed significant correlation between anti-beta(2)-glycoprotein I immunoglobulin A and anti-beta(2)-glycoprotein I immunoglobulin G (R = .609; P =.0001) and less correlation between anticardiolipin immunoglobulin A and anticardiolipin immunoglobulin G (R = .093; P = .065).Immunoglobulin A anti-beta(2)-glycoprotein I antibodies are more common in women who experience unexplained recurrent spontaneous abortion and unexplained fetal death whose initial test results are negative for lupus anticoagulant and immunoglobulin G anticardiolipin antibodies compared to fertile control subjects. Therefore, these antibodies may identify additional women with clinical features of antiphospholipid syndrome who are not identified through traditional testing. It is unclear whether these antibodies are directly pathogenic, a result of the pregnancy losses, or markers for an underlying, yet uncharacterized autoimmune disorder.

OBJECTIVE: Our purpose was to determine whether patients with severe early-onset preeclampsia have hemostatic or metabolic abnormalities that are associated with a tendency to vascular thrombosis. STUDY DESIGN: A total of 101 patients with a history of severe early-onset preeclampsia were tested at least 10 weeks post partum for the presence of hyperhomocysteinemia (methionine loading test), protein C, protein S, and antithrombin III deficiency, activated protein C resistance, lupus anticoagulant, and immunoglobulin G and/or M anticardiolipin antibodies. RESULTS: Of the 101 patients, 39 (38.6%) had chronic hypertension. Of the 85 patients tested for coagulation disturbances, 21 (24.7%) had protein S deficiency. Of the 50 patients tested for activated protein C resistance, 8 (16.0%) were positive. Of the 79 patients tested for hyperhomocysteinemia, 14 (17.7%) had a positive methionine loading test. Finally, 95 patients were tested for anticardiolipin antibodies; 27 (29.4%) had detectable immunoglobulin G and/or M anticardiolipin antibodies. CONCLUSION: Patients with a history of severe early-onset preeclampsia should be screened for protein S deficiency, activated protein C resistance, hyperhomocysteinemia, and anticardiolipin antibodies, since these results may have an impact on counseling for and pharmacologic management in future pregnancies.

Our purpose was to determine whether anticardiolipin antibody-positive sera alter platelet adherence to vascular endothelium by a platelet activating factor-dependent mechanism.Anticardiolipin antibody-positive sera were used in an in vitro platelet-endothelial adherence assay. Confluent endothelial monolayers were randomly assigned for exposure to a 20% concentration of experimental and control sera. Platelets were radiolabeled with chromium 51, and adherence was assessed by quantification of endothelium-associated gamma emission.Inducible platelet adherence was observed by endothelial cell preincubation with sera from anticardiolipin antibody-positive donors compared with anticardiolipin antibody-negative control experiments (n = 12, platelet adherence 6.4% +/- 1.3% vs 4.5% +/- 1.1%, respectively; p = 0.02). Compared with endothelial cell incubations alone, coincubation of platelets with anticardiolipin antibody-positive sera consistently augmented primary adherence (n = 6, p = 0.042). Furthermore, platelet-adherence induced by antibody-positive sera was consistently attenuated by specific platelet-activating factor antagonists in a dose-dependent fashion (p0.001) and was restored by exogenously administered platelet-activating factor.Anticardiolipin antibody-induced platelet adherence may constitute an important prerequisite for vascular thrombosis in antibody-positive patients. The findings from this in vitro model suggest direct involvement of platelet-activating factor in this process.

OBJECTIVE: To investigate the binding of antibodies against negatively charged phospholipids (antiphospholipid antibodies) to human placenta, we tested the reactivity of three mouse monoclonal antiphospholipid antibodies against first-trimester human placenta. STUDY DESIGN: Formalin-fixed and frozen sections of first-trimester placentas were stained by immunoperoxidase with three mouse monoclonal antibodies. Each monoclonal antibody reacted differently with cardiolipin and phosphatidylserine, 3SB9b reacted with phosphatidylserine, D11A4 reacted with cardiolipin, and BA3B5C4 reacted with both. RESULTS: 3SB9b reacted strongly with the syncytiotrophoblastic layer of both formalin-fixed and frozen placental tissue. Sporadic reactivity was observed against the cytotrophoblastic layer. BA3B5C4 reacted strongly and specifically with cytotrophoblastic cells. D114A reacted minimally or, more commonly, not at all. CONCLUSION: The trophoblastic layer directly in contact with the maternal circulation is most reactive with antiphospholipid antibodies that react with phosphatidylserine rather than cardiolipin, suggesting that the trophoblasts may potentially be directly damaged by antiphospholipid antibodies through mechanisms unrelated to thrombosis. In addition, the differential reactivity of 3SB9b and BA3B5C4 suggests that the antigenic conformation involving phosphatidylserine on the cytotrophoblast is altered concurrent with fusion into the syncytium.

Our purpose was to determine whether beta 2-glycoprotein I-dependent anticardiolipin antibodies may represent a superior marker of reproductive risk than do conventional antiphospholipid antibodies.The incidence of beta 2-glycoprotein I-dependent and beta 2-glycoprotein I-independent anticardiolipin antibodies and of six conventional antiphospholipid antibodies was statistically compared between study groups with and without autoantibody-associated features of reproductive failure. Sera from 356 women were randomly selected from the frozen sera bank at the Center for Human Reproduction, Chicago. They included sera from 259 patients with autoantibody-associated features of reproductive failure such as unexplained infertility, endometriosis, and repeated pregnancy loss and 97 infertile controls. Autoantibody levels by a modified enzyme-linked immunosorbent assay for beta 2-glycoprotein I-dependent and beta 2-glycoprotein I-independent anticardiolipin antibodies and a standard enzyme-linked immunosorbent assay for anticardiolipin antibody and five other antiphospholipid antibodies were then compared.Patients demonstrated a significantly higher incidence of beta 2-glycoprotein I-dependent anticardiolipin antibodies (5.4%) than did controls (0%) in a modified enzyme-linked immunosorbent assay (p = 0.01). No such difference was, however, noted for beta 2-glycoprotein I-independent anticardiolipin antibodies or any one of six antiphospholipid antibodies. Two or more among six antiphospholipid antibodies, especially if involving anticardiolipin antibodies, antiphosphatidylserine and antiphosphatidylinositol, as assayed by standard enzyme-linked immunosorbent assay, were significantly more often (p = 0.02) positive in the patients (5.0%) than in the controls (0%). Moreover, positivity in two of those three antiphospholipid antibodies correlated in 59% of cases to positivity in the beta 2-glycoprotein I-dependent anticardiolipin antibody.As a single test beta 2-glycoprotein I-dependent anticardiolipin antibody appears to be superior to cofactor-independent anticardiolipin antibody or any other single conventional antiphospholipid antibody for the detection of autoantibody-associated conditions of reproductive failure. A broadly based panel of conventional antiphospholipid antibodies, especially if inclusive of anticardiolipid antibody, antiphosphatidylserine, and antiphosphatidylinositol, may, however, achieve similar results.

OBJECTIVE: The purpose of this study was to compare the effectiveness of low-molecular-weight heparin with regular heparin in the prevention of fetal resorption in mice with the antiphospholipid syndrome. STUDY DESIGN: Antiphospholipid syndrome was passively induced in ICR mice by injecting them with anticardiolipin antibodies on the first day of pregnancy. Subsequently, these mice were treated with low-molecular-weight heparin in two different doses, with regular heparin, and with a placebo. On gestational day 17 the mice were killed by cervical dislocation, and the pregnancy outcome was evaluated. Statistical analysis was performed by means of a one-way analysis of variance using Bonferroni's t test. RESULTS: Treatment with low-molecular-weight heparin resulted in a resorption rate of 22.4% as opposed to 41.4% in mice with antiphospholipid syndrome that were given regular heparin and 51.7% in nontreated controls. CONCLUSION: We conclude that low-molecular-weight heparin can prevent fetal resorptions in mice with antiphospholipid syndrome.

OBJECTIVES : Anticardiolipin antibodies are estimated to occur in 2.2% of all pregnancies and areassociated with adverse outcomes including thrombotic events, fetal wastage, intrauterine growth retardation, and preterm delivery. We studied 32 human immunodeficiency virus-seropositive gravidas (1) to determine the prevalence of anticardiolipin antibodies in pregnant women infected with human immunodeficiency virus-1 and (2) to investigate the association between the presence of anticardiolipin antibodies and pregnancy outcome, disease status, and perinatal transmission of human immunodeficiency virus-1. STUDY DESIGN : Serum samples obtained at the first prenatal visit were analyzed for anticardiolipinimmunoglobulin M and immunoglobulin G by enzyme-linked immunosorbent assay. Relevant antepartum, intrapartum, and postpartum data, including maternal CD4+ lymphocyte subsets, human immunodeficiency virus p24 antigen determinations, Venereal Disease Research Laboratory test, hematocrit, platelet counts, and placental pathologic tissue of the anticardiolipin antibody-positive and anticardiolipin antibody-negative groups were compared. RESULTS : Test results for 17 (53%) of patients were positive for anticardiolipin antibody: 4 had onlyimmunoglobulin M, 1 had only immunoglobulin G, and the remaining 12 had both antibodies. The patients in the anticardiolipin antibody-positive group were delivered of infants with a mean gestational age of 39 weeks and mean birth weight of 2983 gm. In the anticardiolipin antibody-negative group 15 deliveries had a mean gestational age of 36.3 weeks and a mean birth weight of 2330 gm. CONCLUSIONS : We conclude that there is a high prevalence of anticardiolipin antibodies in patients whohave human immunodeficiency virus, which is not associated with adverse maternal or neonatal outcome, maternal human immunodeficiency virus status, or perinatal transmission of human immunodeficiency virus-1. (Am J Obstet Gynecol 1992;167:1080–5.)