Use of Low Molecular Weight Heparin in Pregnancy

Melissari, E.; Parker, Christopher J.; Wilson, N.; Monte, Giovanni Dal; Kanthou, Chryso; Pemberton, K. D.; Nicolaides, Kypros H.; Barrett, J.; Kakkar, Vijay V.

doi:10.1055/s-0038-1646338

Cited by 178 publications

(103 citation statements)

References 23 publications

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“…Alcanzan su nivel máximo a las 4 horas durante el embarazo (33,34), con una vida media de 4 a 5 horas (35). Se monitorizan mediante la cuantificación de niveles de antifactor Xa, no poseen traspaso placentario (26,36,37) y no se les asocian efectos adversos fetales (38). Tienen mayor actividad contra el factor Xa, y se unen menos a proteínas plasmáticas, células endoteliales y macrófagos, con lo que aumentan su biodisponibilidad, vida media y actividad anticoagulante.…”

Section: Tabla I Indicaciones De Distintos Niveles De Anticoagulaciónunclassified

Anticoagulación Y Embarazo

M³

et al. 2006

Rev. chil. obstet. ginecol.

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RESUMENSe comentan los aspectos clínicos del tratamiento anticoagulante en la paciente embarazada. PALABRAS CLAVES: Anticoagulantes, trombosis, trombofilia, embarazo SUMMARYThe clinical aspects of the anticoagulant treatment in pregnant patient are commented.KEY WORDS: Anticoagulants, thrombosis, thrombophilia, pregnancy Documentos INTRODUCCIÓNEl embarazo humano normal se asocia con alteraciones importantes en todos los componentes de la triada de Virchow, de tal forma que el efecto procoagulante se vuelve dominante (1). El embarazo es un estado de hipercoagulabilidad en el que se puede incrementar hasta en cinco veces el riesgo de eventos tromboembólicos (2). Los cambios en el sistema de coagulación comienzan en el momento de la concepción y sólo terminan 8 semanas postparto (3).En mujeres con trombofilia, el riesgo durante el embarazo se incrementa hasta el doble de un embarazo normal (4). También poseen riesgo aumentado de desprendimiento placentario, preeclampsia, restricción del crecimiento intrauterino, muerte fetal in útero y probablemente aborto (5).La terapia anticoagulante se indica durante el embarazo para la prevención y tratamiento del embolismo sistémico en pacientes portadoras de válvulas cardiacas mecánicas y valvulopatías con fibrilación auricular (6.) Habitualmente también, para la prevención de complicaciones durante el embarazo en mujeres con anticuerpos antifosfolípidos y otras trombofilias que han presentado complicaciones con anterioridad (7).El objetivo de esta comunicación es presentar los aspectos básicos del tratamiento anticoagulante durante el embarazo. Indicaciones de anticoagulaciónA pesar del aumento del riesgo de trombosis durante el embarazo y posparto, la mayoría de las mujeres no requieren anticoagulación. Aunque algunos expertos recomendarían tromboprofilaxis en todas las embarazadas con trombofilia hereditaria, la anticoagulación no es necesaria si no existe historia personal de tromboembolismo o una mala historia obstétrica (7). Las excepciones son las mujeres con deficiencia de antitrombina, mutación homocigota para el factor V de Leiden, mutación homocigota para el gen de protrombina G20210A o heterocigota para ambas mutaciones (heterocigota compuesta) (8). En la mayoría de

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Section: Tabla I Indicaciones De Distintos Niveles De Anticoagulaciónunclassified

Anticoagulación Y Embarazo

M³

et al. 2006

Rev. chil. obstet. ginecol.

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“…The risk of osteoporosis is lower in pregnant women treated with LMWH than with UFH [166]. Insertion of a vena caval filter may be indicated in pregnant women.…”

Section: Secondary Prophylaxis In Women With Previous Thrombosismentioning

confidence: 99%

“…After therapeutic administration of LMWH for 10-14 days, a prophylactic dose of LMWH should be continued throughout the pregnancy and then replaced with heparin for 6-8 weeks post-partum as described for UFH [140,164,168]. Published studies indicate that the effective maintenance dose of enoxaparin is 40 mg once daily and of dalteparin, 5000 IU once daily [163][164][165][166][167]175,176]. However, in certain thrombophilic conditions these doses should be increased depending on the risk of recurrent VTE.…”

Section: Secondary Prophylaxis In Women With Previous Thrombosismentioning

confidence: 99%

“…LMWHs exhibit a number of advantages over unfractionated heparin (UFH), including improved bioavailability, a longer half-life, ease of administration, no monitoring requirement and fewer side-effects [163][164][165][166][167][168][169]. Animal and human studies have shown that LMWHs are not teratogenic or fetotoxic and do not cross the placenta [170].…”

Section: The Management Of Thrombophilia During Pregnancymentioning

confidence: 99%

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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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“…[16][17][18][19] Several studies have suggested the safety and efficacy of LMWH during pregnancy. 13,20,21 In addition, the risk of adverse heparin-induced thrombocytopenia and osteoporosis after LMWH treatment is greatly reduced compared with UFH. [20][21][22][23][24][25] In our previous work, we showed that the messenger RNA and protein expression of the proteoglycan decorin (DCN) was reduced in PE-and FGR-affected placentae compared with controls.…”

Section: Introductionmentioning

confidence: 99%

Antiangiogenic effects of decorin restored by unfractionated, low molecular weight, and nonanticoagulant heparins

et al. 2017

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Key Points• UFH, LMWH, and NAC restored angiogenesis in decorin-reduced endothelial cells.• NAC treatment was similar to, or better than, UFH or LMWH at improving endothelial angiogenesis without increasing anticoagulant activity.Pregnancies affected by preeclampsia (PE) or fetal growth restriction (FGR) display increases in thrombin generation and reductions in angiogenesis and cell growth. There is significant interest in the potential for low molecular weight heparins (LMWHs) to reduce the recurrence of PE and FGR. However, LMWH is associated with an increased risk of bleeding. Therefore, it is of vital importance to determine the exact molecular function of heparins in pregnancy if they are used as therapy for pregnant women. We aimed to determine this using our model Therefore, NAC could potentially be a better therapeutic option for prevention of PE/FGR in high-risk women, without the risk of the adverse effects of traditional anticoagulants.

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Use of Low Molecular Weight Heparin in Pregnancy

Cited by 178 publications

References 23 publications

Anticoagulación Y Embarazo

Anticoagulación Y Embarazo

Thrombophilia and pregnancy

Antiangiogenic effects of decorin restored by unfractionated, low molecular weight, and nonanticoagulant heparins

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