Intrauterine Death and Circulating Anticoagulant (“Antithromboplastin”)

Nilsson, Inga Marie; Åstedt, Birger; Hedner, Ulla; Berezin, David

doi:10.1111/j.0954-6820.1975.tb04897.x

Cited by 275 publications

(34 citation statements)

References 18 publications

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“…The first such case report suggesting this correlation was published in 1975 and described the presence of a circulating anticoagulant in a woman with recurrent abortions. 11 This anticoagulant was later found to be the lupus anticoagulant. Since that time many studies have confirmed the association of ADs such as antiphospholipid syndrome, 12 rheumatoid arthritis 13 and systemic lupus erythematosus, 14,15 with miscarriage.…”

Section: Autoimmune Diseases and Miscarriagementioning

confidence: 98%

Thyroid autoimmunity and miscarriage

Kaprara¹,

Krassas²

2008

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The relation of thyroid autoimmunity to miscarriage is an important issue that has attracted the interest of many investigators. A number of papers have been published so far, which include healthy women, women with recurrent miscarriage and those undergoing assisted reproductive techniques. Most studies have shown a significant positive association between the presence of thyroid autoantibodies and miscarriage rate. It is of interest that women with high titers do not show a higher miscarriage rate when compared with women having low titers, although, there is no general agreement on this issue. There are three possible explanations for the assumed association of thyroid autoimmunity with miscarriage: 1) pregnancy loss is an epiphenomenon and not a direct effect of the thyroid autoantibodies, the presence of thyroid autoantibodies reflecting a generalized activation of the immune system; 2) delayed conception from the presence of thyroid autoantibodies; hence, when women with thyroid autoimmunity become pregnant, face a higher risk of miscarriage because of older age; and 3) the pregnancy loss is secondary to a subtle deficiency in thyroid hormone concentrations or a lower capacity of the thyroid to adequately adapt to the demands of pregnancy.

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Section: Autoimmune Diseases and Miscarriagementioning

confidence: 98%

Thyroid autoimmunity and miscarriage

Kaprara¹,

Krassas²

2008

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“…A higher incidence of RPL has been documented for both low-risk and high-risk pregnancies with antiphospholipid antibodies (aPL; (Empson et al 2002;Subrt et al 2008). Antiphospholipid antibodies are thought to lead to fetal loss by causing thrombosis of the placental vessels, although the observed variability in placental pathology somehow argues against such a direct involvement (Nilsson et al 1975;Salafia and Cowchock 1997). Lowered expression of ANXA5 in placentas of M2 haplotype carriers ) could be potentially responsible for reduced coverage of phospholipid trophoblast surfaces and hence lead to an increase in the number of exposed available antigenic determinants for the generation of aPL.…”

Section: Apl Antibodies and M2 Haplotype Of Anxa5mentioning

confidence: 99%

Hereditary thrombophilic risk factors for recurrent pregnancy loss

Bogdanova

Markoff²

2010

J Community Genet

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This review summarizes current knowledge about the role of hereditary hypercoagulation factors predisposing to thrombophilia-associated recurrent fetal loss. Thrombophilias are a major cause of adverse pregnancy outcome, playing a role in the etiology of up to 40% of cases worldwide. Hereditary thrombophilic predispositions to recurrent pregnancy wastage include genetic lesions in blood coagulation factors II and V as well as natural anticoagulants antithrombin, protein C, and protein S. Furthermore, methylenetetrahydrofolate reductase gene variants conferring higher thrombophilia risk in combination with these mutations and the newly described annexin A5 gene M2 promoter allele are associated with repeated fetal loss. The review gives a concise description of the molecular defects arising from the genetic changes, of the role these factors play in the timing and definition of fetal loss, and risk estimates from available studies and meta-analysis. This knowledge is instrumental for a more precise assessment of individual risks for repeated fetal loss and should guide therapeutic strategies, where relevant. Since the average childbearing age increases in Western societies, the importance of a timely diagnosis of fetal loss predisposition is increasing.

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“…Since then, the association between the presence of aPL and the occurrence of repeated spontaneous abortions has been extensively reported [2][3][4][5][6][7]. Antiphospholipid antibodies are a leading cause of pregnancy loss and pregnancy-related morbidity.…”

Section: Apl Antibodies and Pregnancy Lossmentioning

confidence: 99%

Role of Tissue Factor in the Maternal Immunological Attack of the Embryo in the Antiphospholipid Syndrome

Girardi

2009

Clinic Rev Allerg Immunol

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Recurrent fetal loss affects 1-5% of women of childbearing age. Immunological mechanisms may account for 40% of recurrent miscarriages, and in particular, the antiphospholipid syndrome (APS) appears to be implicated in 7-25% of the cases. Because antiphospholipid (aPL) antibodies have thrombogenic properties, fetal loss in patients with APS has been ascribed to thrombosis of placental vessels. However, we have shown that inflammation, specifically activation of complement with generation of the anaphylotoxin C5a, is an essential trigger of fetal injury. Thrombosis and inflammation are linked in many clinical conditions. Tissue factor (TF), the major cellular initiator of the coagulation protease cascade, plays important roles in both thrombosis and inflammation, and its expression is increased in patients with APS. Here we describe how TF, acting as a proinflammatory molecule, induces trophoblast injury and fetal death in a mouse model of APS. Importantly, we will discuss how TF contributes to C5a-induced oxidative burst in neutrophils leading to trophoblasts and fetal injury in APS. The finding that TF is an important effector in aPL-induced inflammation may allow the development of new therapies to abrogate the inflammatory loop caused by tissue factor and improve pregnancy outcomes in patients with aPL antibodies. Statins downregulate TF-induced inflammation and rescued the pregnancies in aPL-treated mice, suggesting they may be a good treatment for women with aPL-induced pregnancy complications.

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Intrauterine Death and Circulating Anticoagulant (“Antithromboplastin”)

Cited by 275 publications

References 18 publications

Thyroid autoimmunity and miscarriage

Thyroid autoimmunity and miscarriage

Hereditary thrombophilic risk factors for recurrent pregnancy loss

Role of Tissue Factor in the Maternal Immunological Attack of the Embryo in the Antiphospholipid Syndrome

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