Inherited Antithrombin Deficiency and Pregnancy: Maternal and Fetal Outcomes

Sabadell, Jordi; Casellas, M.; Alijotas‐Reig, Jaume; Arellano‐Rodrigo, Eduardo; Cabero, L.

doi:10.1097/ogx.0b013e3181e59e3b

Cited by 12 publications

(32 citation statements)

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“…6 These patients are also at increased risk for thrombosis. 24 Due to the nature of the test for protein C and S deficiency, arbitrary cutoff points are used resulting in substantial percentages of false-positive and false-negative diagnoses. Second, vitamin K deficiency, hepatic disease, treatment with oral anticoagulants or oral contraceptives, pregnancy itself, and the presence of autoantibodies against protein C and S, respectively, decrease protein C and S concentrations.…”

Section: What Is the Role Of Acquired Thrombophilia In Complicated Prmentioning

confidence: 99%

Thrombophilia and Pre-Eclampsia

Maat¹,

Groot²

2011

Semin Thromb Hemost

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Pre-eclampsia (P-EC) poses an increased risk for fetal and maternal morbidity and sometimes even mortality. Several risk factors have been identified, among which an important extensively studied group is formed by the early recognizable genetic factors resulting in thrombophilia. The discussion is ongoing whether the associations found for thrombophilia are true and clinically relevant. In this review, we address the association between P-EC and thrombophilia, its concerns, and the necessity of screening after a pregnancy complicated by hypertension.

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Section: What Is the Role Of Acquired Thrombophilia In Complicated Prmentioning

confidence: 99%

Thrombophilia and Pre-Eclampsia

Maat¹,

Groot²

2011

Semin Thromb Hemost

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“…Antithrombin is an anticoagulant synthesised in the liver and endothelial cells. It has an inhibitory effect on thrombin, clotting factors X, IX, XI, XII and tissue factor bound VIIa [33]. Antithrombin type Ideficiency was the first of the inherited thrombophilias to be described and is the most thrombogenic.…”

Section: Antithrombin Deficiencymentioning

confidence: 99%

“…A prospective observational study analyzed women who tested positive for antithrombin deficiency, protein C deficiency or protein S deficiency and were followed through the index pregnancy [33]. Thromboprophylactic treatment included low molecular weight heparin, unfractionated heparin and vitamin K antagonists.…”

Section: Thromboprophylaxis To Prevent Obstetric Complicationsmentioning

confidence: 99%

Pregnancy and Thrombophilia

Dawood

2013

J Blood Disord Transfus

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Thrombophilic disorders encompass a diverse group of coagulation disorders that potentiate a predisposition for thrombotic events. Amongst the known thrombophilias are antithrombin III deficiency, prothrombin G20210A gene mutation, protein S and protein C deficiency, activated protein C resistance and the antiphospholipid syndrome. Thrombophilia and its influence on pregnancy have been studied for the past 50 years. Both inherited and acquired thrombophilia have been associated with an increased risk of thrombo-embolism as well as an increased risk of pregnancy loss and adverse obstetric outcomes. Some thrombophilias (antiphosphoplipid syndrome, factor V Leiden mutation and antithrombin III deficiency confer a higher risk of both venous thrombo-embolism and obstetric complications. There is still no consensus on the optimal management of thromboprophylaxis in future pregnancies. Clearly large well designed and adequately powered multicenter randomised trials are required to clarify the management of thrombophilia in pregnancy especially with a history of adverse obstetric outcome.

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“…Inherited thrombophilias are also linked to adverse pregnancy outcomes, although the evidence is less compelling. Pregnant women with AT deficiency had a high incidence of fetal loss and other complications in several studies [2, 3]. Deficient women had a twofold higher risk of first and second trimester loss and a fivefold higher risk of late third trimester loss than women without thrombophilia [4].…”

mentioning

confidence: 99%

“…The benefit of antithrombotic therapy in women with inherited thrombophilia and fetal loss is unproven and strongly debated [11]. AT‐deficient women who received anticoagulation during pregnancy had a lower incidence of fetal loss in several nonrandomized studies [2, 3]. Current guidelines suggest antepartum and postpartum prophylaxis for AT‐deficient women to prevent VTE [5].…”

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confidence: 99%

Antiphospholipid antibodies and antithrombin deficiency: Double trouble for pregnancy

Kujovich

Merrill

2011

American J Hematol

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A 30-year-old G3P1 woman with a history of deep vein thrombosis (DVT) and recurrent pregnancy loss presented for hematology consultation in 2005. She developed a right lower extremity DVT at 13 weeks gestation during her first pregnancy in 2002, treated with enoxaparin. At 19 weeks, an obstetric ultrasound revealed a fetal demise. After a brief interruption of anticoagulation for a D&C, she developed new right leg thrombosis. A thrombophilia evaluation in 2002 included IgM anticardiolipin antibody (ACA) 64, IgG 27 (normal < 10 phospholipid [PL] units for both), normal protein C (133%) and protein S (115%) activity, and negative genetic testing for factor V Leiden. She completed a 6-month course of warfarin. Her antithrombin (AT) activity was 60% (normal 86-118%) 1 month after starting warfarin.She received enoxaparin and sporadic low-dose aspirin during her second pregnancy in 2003. Fetal growth restriction (FGR) was noted at 20 weeks. At 22 weeks, she was hospitalized with HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome requiring delivery of a nonviable neonate. Additional testing revealed a strong lupus anticoagulant (LA), mildly elevated IgG and IgM ACA, and negative prothrombin 20210G>A mutation. Placental pathology showed numerous small gross and microscopic infarcts. She received a 6-week course of postpartum anticoagulation.Her third pregnancy in 2004 ended in a miscarriage at 8 weeks, 1 month after initiation of therapeutic-dose enoxaparin (1 mg/kg bid) and low-dose aspirin.A successful pregnancy requires the development and maintenance of an adequate placental circulation. Placentalmediated pregnancy complications including recurrent fetal loss, preeclampsia, and FGR each occur in 1-5% of pregnant women. A total of 1% of women experience three or more consecutive fetal losses [1]. Hematologists are frequently consulted by women with these complications, many of whom have already undergone thrombophilia testing.Her evaluation in 2005 showed: IgG ACA 44, IgM 111, IgM beta 2 glycoprotein1 (B 2 GP1) antibody 30 (normal < 20 PL units for all 3), and a strong LA with multiple assays; LA-sensitive partial thromboplastin time (PTT) 84 sec (26-37 sec); hexagonal PL PTT 53 sec (< 8 sec); DVV confirm 1.9 (<1.4). AT activity was 60% (86-118%), AT antigen 60% (82-136%). Her liver function tests and urinalysis were normal. She provided a well-documented family history of AT deficiency. Her mother and brother had AT antigen and activity levels of 44-51%, and a history of recurrent DVT and pulmonary embolism. Repeat thrombophilia testing several months later showed similar antiphospholipid (APLA) and AT levels. She was diagnosed with AT deficiency and APLA syndrome and started on long-term warfarin.Recurrent fetal loss is a well-established complication of the APLA syndrome. Inherited thrombophilias are also linked to adverse pregnancy outcomes, although the evidence is less compelling. Pregnant women with AT deficiency had a high incidence of fetal loss and other complications in several studies ...

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Inherited Antithrombin Deficiency and Pregnancy: Maternal and Fetal Outcomes

Cited by 12 publications

References 0 publications

Thrombophilia and Pre-Eclampsia

Thrombophilia and Pre-Eclampsia

Pregnancy and Thrombophilia

Antiphospholipid antibodies and antithrombin deficiency: Double trouble for pregnancy

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