Absence of Association of Thrombophilia Polymorphisms with Intrauterine Growth Restriction

Infante‐Rivard, Claire; Rivard, Georges‐Étienne; Yotov, Wagner V.; Génin, Emmanuelle; Guiguet, Marguerite; Weinberg, Clarice R.; Gauthier, Robert; Feoli-Fonseca, Juan Carlos

doi:10.1056/nejm200207043470105

Cited by 228 publications

(120 citation statements)

References 28 publications

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“…Trombofilisi olan gebelerde IUGG görülme riskinin genel olarak arttığı bilinse de Yasuda ve ark. 'nın yaptığı bir çalışmada anlamlı ilişki sadece AKA pozitif hastalarda gösterilmiştir (16) . Howley ve ark.…”

Section: Discussionunclassified

The evaluation of perinatal outcomes in pregnancies complicated with thrombophilias

Kafadar¹,

Melekoğlu²,

Evrüke³

et al. 2014

tjod

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Section: Discussionunclassified

The evaluation of perinatal outcomes in pregnancies complicated with thrombophilias

Kafadar¹,

Melekoğlu²,

Evrüke³

et al. 2014

tjod

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“…Overall 22.8% of neonates under the 10 th percentile were from mothers with thrombophilic mutations compared to 14.5% of neonates under the 10 th percentile from mothers without thrombophilic mutations (OR 1.7, 95% CI 1.1-2.7). Recently, Infante-Rivard C et al [92] did not find an association between thrombophilic mutations and IUGR < 10th percentile. In this study 493 newborns with IUGR and 472 controls and their parents were tested for thrombophilic mutations.…”

Section: Inherited Thrombophilias and Iugrmentioning

confidence: 93%

Thrombophilia and pregnancy

Brenner¹

2005

Eur J Clin Investigation

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Pregnancy is hypercoagulable state. The field of thrombophilia; the tendency to thrombosis, has been developed rapidly and has been linked to many aspects of pregnancy. It is recently that severe pregnancy complications such as severe preeclampsia intrauterine growth retardation abruptio placentae and stillbirth has been shown to be associated with thrombophilia. Recurrent miscarriage and has also been associated with thrombophilia. Finally, thromboembolism in pregnancy as in the non-pregnant state is linked to thrombophilia. In this review all aspects of thrombophilia in pregnancy are discussed, and also all prophylactic and therapeutic implications.Thrombophilias are inherited or acquired conditions which predispose an individual to thromboembolism. Deficiencies of protein S C and antithrombin are rare and each of them is found in about 3% of patients with thrombosis. Recently, three important inherited thrombophilias were discovered which are responsible of the majority of thromboembolic events in patients with otherwise no apparent risk for thrombosis. Resistance to activated protein C caused by an adenine 506 guanine (A506G) mutation in factor V (factor V Leiden) has been linked with an increased risk for venous thromboembolism [1][2][3]. Heterozygosity for the factor V (FV) Leiden mutation is found in about 5% of the population and the mutation is responsible of 20-30% of venous thromboembolism events. A recently described guanine 20210 adenine mutation in prothrombin is associated with higher plasma prothrombin concentrations and increased risk for venous thromboembolism [4] and cerebral-vein thrombosis [5]. Homozygosity for the cytosine 677 thymine (C677T) mutation in methylenetetrahydrofolate reductase (MTHFR) results in decreased synthesis of 5-methyltetrahydrofolate, the primary methyl donor in the conversion of homocysteine to methionine and the resulting increase in plasma homocysteine concentrations is a risk factor for thrombosis [6,7]. The mutation is responsible for reduced MTHFR activity and is the most frequent cause of mild hyperhomocysteinemia and can be found in 5-15% of the population.Homocysteine is an independent risk factor for atherosclerosis, stroke, peripheral vascular disease and cardiovascular diseases [8,9]. Homocysteine concentrations are affected by nutrition. A deficiency in folate, B-6, and/or B-I2 causes elevation of homocysteine. Homocysteine concentrations are also affected by genetics such as cystathionine beta-synthase deficiency (10) and C677T MTHFR gene mutation [7]. Hyperhomocysteinemia promotes vascular damage by several mechanisms. Many of the endothelial vascular changes associated with hyperhomocysteinemia can be found in preeclampsia [11][12][13][14][15]. thrombophilia is substantially increased. The risk of VTE in pregnant women may be further amplified by the type of underlying genetic predisposition, like, homozygosity for a mutation, the presence of multiple mutations (multigenic defects) or thrombophilic anomalies [16][17][18][19].Thrombophilia and ad...

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“…Studies have provided contradictory results for the risk of IUGR in pregnancies in women with thrombophilia. 25 Thrombophilia was found in 61.4% of patients with IUGR with higher prevalence of PT G20210A and MTHFR (C677T) in women with severe IUGR.…”

Section: Pre-eclampsia and Intrauterine Growth Retardation (Iugr)mentioning

confidence: 98%

Management of Hereditary Hypercoagulable Disorders

Bockenstedt¹

2006

Hematology

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The clinical management of individuals with hereditary hypercoaguable disorders has evolved from initial broad recommendations of lifelong anticoagulation after first event of venous thromboembolism to a more intricate individualized risk-benefit analysis as studies have begun to delineate the complexity of interactions of acquired and hereditary factors which determine the predilection to thrombosis. The contribution of thrombophilic disorders to risk of thrombotic complications of pregnancy, organ transplantation, central venous catheter and dialysis access placement have been increasingly recognized. The risk of thrombosis must be weighed against risk of long-term anticoagulation in patients with venous thromboembolism. Thrombophilia screening in select populations may enhance outcome. Initial DecisionsThe clinical management of individuals with hereditary hypercoagulable disorders has evolved from initial broad recommendations of lifelong anticoagulation after first event of venous thromboembolism (VTE) to a more intricate, individualized risk-benefit analysis as the complexity of interactions of acquired and hereditary factors that determine the predilection to thrombosis are now recognized. Important behind stratifying risk of recurrent events is the necessity of correctly identifying hereditary thrombophilic disorders, especially in circumstances in which laboratory results, e.g., mildly low antithrombin III (ATIII) or protein S levels, may be more indicative of a temporary acquired deficiency. The relevance of thrombophilic testing is debated, but most clinicians agree that prothrombotic assessment should be considered in individuals with unprovoked thrombosis at age less than 40 years, individuals who have had thrombosis at an unusual anatomic site or who have had repeated thromboses, or when the family history suggests multiple affected individuals. For review of the laboratory assessment of thrombophilia see references [1][2][3] . The following discussion is not meant to be comprehensive, but serves to highlight a few of the clinical management decisions important in the care of the thrombophilic patient. Therapeutic considerations involving individuals with antiphospholipid syndrome (APS) will be included where pertinent. Duration of anticoagulant therapyThe decision to extend therapy beyond 6-12 months after an incident thrombotic event must be made on an individual basis. Patients with a transient risk factor such as oral contraceptive use, postsurgical state or limb immobilization have a low risk of recurrence of thrombosis once anticoagulation has been completed. (For review see 4,5 .) Identifying the individual with moderate to high risk of recurrent thrombosis is important to prevent the unnecessary risk of hemorrhage from long-term anticoagulation. From studies of patients with a first VTE (both with and without diagnosed hereditary thrombophilia), one third of patients with unprovoked VTE will have a reoccurrence over the next 10 years and 6% of patients with VTE develop postphlebitic syndrom...

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Absence of Association of Thrombophilia Polymorphisms with Intrauterine Growth Restriction

Abstract: Our findings do not indicate that there are associations between maternal or newborn polymorphisms associated with thrombophilia and an increased risk of intrauterine growth restriction.

Cited by 228 publications

References 28 publications

The evaluation of perinatal outcomes in pregnancies complicated with thrombophilias

The evaluation of perinatal outcomes in pregnancies complicated with thrombophilias

Thrombophilia and pregnancy

Management of Hereditary Hypercoagulable Disorders

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