Autoimmunity and pregnancy loss

Fausett, M. Bardett; Branch, D. Ware

doi:10.1001/jama.264.11.1453

Cited by 12 publications

(2 citation statements)

References 98 publications

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“…APS is characterized by recurrent thromboembolic phenomena, thrombocytopenia, and serologic evidence of anti phospholipid antibodies (aPA) is also de ned by recurrent fetal loss, high rates of intrauterine fetal growth retardation and increased incidence of prematurity. 1,3,4 Antiphospholipid antibodies (aPA), such as antiphosphatidyl serine and anticardiolipin have direct effects on fecundity and on the outcome of pregnancy, as was proven in animal models. 5 To demonstrate direct effects of the antibodies on embryos, several investigators have exposed embryos in in vitro systems to sera of women with recurrent abortions.…”

Section: Introductionmentioning

confidence: 98%

“…Autoimmune causes have been suggested as a factor in some of these cases. 1 Systemic lupus erythematosus (SLE), an autoimmune disease, with or without antiphospholipid syndrome (APS), affects young women and has an adverse impact on reproduction and fetal outcome causing recurrent pregnancy loss (RPL). Only 68% fetal survival and as high as 44% of preterm deliveries have been reported in SLE/APS patients.…”

Section: Introductionmentioning

confidence: 99%

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The effects of antiphospholipid antibodies obtained from women with SLE/APS and associated pregnancy loss on rat embryos and placental explants in culture

Ornoy

Yacobi

Matalon

et al. 2003

Lupus

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Recurrent fetal loss occurs in approximately 1% of women. Autoimmune causes have been suggested as a factor in some of these cases. High rates of intrauterine fetal growth retardation and increased incidence of prematurity is associated with systemic lupus erythematosus (SLE) and the antiphospholipid syndrome (APS). We found in previous studies that sera from SLE/APS patients when used as a culture medium for rat embryos were found to reduce embryonic growth and development, induce a high rate of embryonic anomalies and death and damage the yolk sac morphologically and functionally. In order to investigate the direct effect of IgG purified from women with SLE/APS on the growth and viability of embryos, we cultured 11.5-day-old rat embryos in their yolk sacs in the presence of IgG purified from SLE/APS patients with recurrent pregnancy loss (RPL). The IgG affected directly the embryo and yolk sac, reducing their growth. The purified IgG positive for anticardiolipin/anti-DNA antibodies reduced yolk sac and embryonic growth more than sera negative for these antibodies but positive for antiphosphatydilserine and for antilaminin. Monoclonal antiphosphatydilserine reduced yolk sac growth but the embryos remained intact. Following the observed damage to the yolk sac we cultured human placental explants at 5.5-8 weeks of pregnancy in sera from SLE/APS patients for 96 hours and found that these sera reduced placental trophoblastic cell growth, reduced their proliferation rate and increased their rate of apoptosis. Successful treatment of the women resulted in a correction of the damage induced in the cultured rat embryos and in the cultured placental explants.

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Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

The effects of antiphospholipid antibodies obtained from women with SLE/APS and associated pregnancy loss on rat embryos and placental explants in culture

Ornoy

Yacobi

Matalon

et al. 2003

Lupus

View full text Add to dashboard Cite

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Maternal autoimmune diseases and immunologically induced embryonic and fetoplacental damage

Ornoy

Chen

Silver

et al. 2004

Birth Defects Research

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BACKGROUND:Autoimmune diseases are a group of illnesses in which autoantibodies are produced against various organs, presenting with a variety of clinical symptoms. In this review, we discuss the different aspects of autoimmune diseases in pregnancy. We also describe experimental models that help to understand the etiology and pathogenesis of the effects of this maternal disease on the developing embryo, fetus and placenta. METHODS:The possible direct effects of sera or IgG obtained from women with systemic lupus erythematosus/antiphospholipid syndrome (SLE/APS) and recurrent pregnancy loss (RPL) were examined on cultured 10.5-and 11.5-day-old rat embryos and on cultured human placental explants, as compared to sera from healthy women or synthetic medium that were used as controls. In addition, we examined the effects of the sera obtained from these women after successful treatment that allowed the birth of normal infants. RESULTS: We observed increased embryonic death and anomalies in embryos cultured on sera and IgG from SLE/APS women. Similarly, when human placental explants were cultured on these sera, trophoblastic cell growth was reduced and apoptotic rate was increased. Successful treatment also reduced the damage caused by the sera from these women in the cultured embryos and placentas. CONCLUSIONS: Our results, and the cited studies, point to the important role of the placental damage in the etiology of RPL associated with SLE/APS. Animal models, both in vivo and in vitro, as well as cultured early human placental explants can be used successfully to understand some of the pathogenic aspects of SLE/APS and RPL.

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Increased fetal abortion rate in autoimmune thyroid disease is related to circulating TPO autoantibodies in an autoimmune thyroiditis animal model

Lee

Lau

et al. 2009

Fertility and Sterility

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Autoimmunity and pregnancy loss

Cited by 12 publications

References 98 publications

The effects of antiphospholipid antibodies obtained from women with SLE/APS and associated pregnancy loss on rat embryos and placental explants in culture

The effects of antiphospholipid antibodies obtained from women with SLE/APS and associated pregnancy loss on rat embryos and placental explants in culture

Maternal autoimmune diseases and immunologically induced embryonic and fetoplacental damage

Increased fetal abortion rate in autoimmune thyroid disease is related to circulating TPO autoantibodies in an autoimmune thyroiditis animal model

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