Factor XII congenital deficiency and early spontaneous abortion

Schved, J.F.; Gris, J.-C.; Neveu, S.; Dupaigne, D; Marès, P.

doi:10.1016/s0015-0282(16)60866-x

Cited by 29 publications

(30 citation statements)

References 6 publications

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“…Schved et al 1 reported the cases of three young women with a FXII deficiency and a clinical history of spontaneous abortion. Braulke et al 2 reported on eight patients with moderately reduced level of FXII found among 43 patients with repeated abortions.…”

Section: Introductionmentioning

confidence: 99%

Autoantibodies to Factor XII and Kininogen‐Dependent Antiphosphatidylethanolamine Antibodies in Patients with Recurrent Pregnancy Loss Augment Platelet Aggregation

Satō¹,

Sugi²,

Sakai³

2015

American J Rep Immunol

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Antibodies to LDC27 and IPP30 markedly increased aggregation of normal platelets stimulated by γ-thrombin. Augmentation of SSPA formation was more frequent in the patients with RPL who were positive for anti-FXII than in the control group (P = 0.003). This study strongly supports the hypothesis that aPE and anti-FXII may cause RPL due to disruption of the normal antithrombotic effects of kininogens and FXII.

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Section: Introductionmentioning

confidence: 99%

Autoantibodies to Factor XII and Kininogen‐Dependent Antiphosphatidylethanolamine Antibodies in Patients with Recurrent Pregnancy Loss Augment Platelet Aggregation

Satō¹,

Sugi²,

Sakai³

2015

American J Rep Immunol

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“…The thrombotic hemostasis defects associated with RMS include lupus anticoagulants and anticardiolipin antibodies (these two comprising the antiphospholipid syndromes associated with fetal wastage syndrome) (42)(43)(44) ; Factor XII deficiency (45); dysfibrinogenemias associated with thrombosis (46); protein C deficiency (47); protein S defects; antithrombin deficiency (48); heparin cofactor II deficiency (49); and fibrinolytic defects associated with thrombosis, including plasminogen deficiency ; tissue plasminogen activator (t-PA) deficiency; and elevated plasminogen activator inhibitor Type 1 (PAI-1) (50,51), including PAI-1 polymorphisms (52). Also, although sticky platelet syndrome has been known for more than a decade and leads to a wide variety of arterial and venous events, only recently has it become apparent that this defect is a common cause of RMS (2,53), and, like other new defects, including factor V Leiden, 5,10-MTHFR mutations and prothrombin G20210A gene mutation, it should be added to the prothrombotic disorders associated with RMS (2).…”

Section: Discussionmentioning

confidence: 99%

Recurrent Miscarriage Syndrome due to Blood Coagulation Protein/Platelet Defects: Prevalence, Treatment and Outcome Results

Bick

2000

Clin Appl Thromb Hemost

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Although first-time miscarriages are usually caused by chromosomal defects, about 55% of recurrent miscarriages are caused by procoagulant defects that induce thrombosis and infarction of placental vessels. Of recurrent miscarriages, about 7% are caused by chromosome defects, 15% to hormonal defects, and 10% to 15% to anatomical defects. Recurrent miscarriage involves more than 500,000 women in the United States each year. During the past 4 years, 179 patients, prescreened for chromosomal, hormonal, and anatomical defects, and found to harbor none, underwent hemostasis defect evaluation. A total of 160 of these have been analyzed. A hemostasis defect was found in 150 of 160 women (n = 94% of screened women). The mean age was 33 years; the mean number of miscarriages before referral was three. All women with a procoagulant defect (149) were treated with preconception ASA at 81 mg/d, and unfractionated porcine heparin at 5000 U every 12 hours was added immediately postconception; both agents were used to term delivery. Only two of 149 patients failed therapy. The defects found were as follows: antiphospholipid syndrome, 67%; sticky platelet syndrome, 21%; tissue plasminogen activator (TPA) deficiency, 9%; factor V Leiden, 7%; high PAI-1, 6%; protein S, 5%; high LP(a), 3%; AT, 2%; protein C, 1%. Thirty-eight patients had more than one defect. In the group with antiphospholipid syndrome, 24% only had a subgroup antibody (antiphosphatidyl-serine, -inositol, -ethanolamine, -choline, -glycerol) or antiphosphatidic acid antibody, in the absence of anticardiolipin antibody or lupus anticoagulant. This finding is similar to that recently reported in early age ischemic stroke patients (<50 years old). In summary, about 55% of patients with recurrent miscarriage harbor a procoagulant defect to account for placental vascular occlusion. More than 98% will have a normal term delivery with preconception aspirin (ASA) and addition of postconception heparin to term. Patients should be screened by an obstetrician or by reproductive specialists for hormonal and anatomic defects before initiating a procoagulant evaluation; if such prescreening is done, the yield of a defect is high and appropriate therapy leads to an excellent outcome.

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“…Neben einer Verminderung des Faktor-XII (Schved et al 1989;Braulke et al 1993) werden auch eine verminderte APC-Resistenz bzw. der Nachweis des Faktor-V-Leiden als begünsti-201 Reproduktionsmedizin (1999) 15: 200±211 Springer-Verlag 1999 Immune therapy of recurrent abortion B. Hinney, H. Neumeyer…”

Section: Reproduktionsgenetik Zusammenfassungunclassified

Immune therapy of recurrent abortion

Hinney

Neumeyer

1999

Reproduktionsmedizin

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Factor XII congenital deficiency and early spontaneous abortion

Cited by 29 publications

References 6 publications

Autoantibodies to Factor XII and Kininogen‐Dependent Antiphosphatidylethanolamine Antibodies in Patients with Recurrent Pregnancy Loss Augment Platelet Aggregation

Autoantibodies to Factor XII and Kininogen‐Dependent Antiphosphatidylethanolamine Antibodies in Patients with Recurrent Pregnancy Loss Augment Platelet Aggregation

Recurrent Miscarriage Syndrome due to Blood Coagulation Protein/Platelet Defects: Prevalence, Treatment and Outcome Results

Immune therapy of recurrent abortion

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