Postnatal Screening for Thrombophilia in Women With Severe Pregnancy Complications

Alfirević, Z̄arko; Mousa, H.; Martlew, Vanessa; Briscoe, Lesley; Perez-Casal, Marga; Toh, Cheng Hock

doi:10.1097/00006250-200105000-00021

Cited by 43 publications

(76 citation statements)

References 24 publications

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“…[15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32] Our findings in a large white population provide a clear demonstration of the strong association of severe PE with thrombophilia. Diagnosis of PE and assessment of its severity were in strict accordance with the American College of Obstetricians and Gynecologists criteria.…”

Section: Discussionmentioning

confidence: 86%

Thrombophilia Is Significantly Associated With Severe Preeclampsia

Mello

Parretti²,

Marozio³

et al. 2005

Hypertension

140

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Abstract-The role of thrombophilia in the pathogenesis of preeclampsia is controversial. The aim of this case-controlled study was to determine whether thrombophilia increases the risk of preeclampsia or interferes with its clinical course. A total of 808 white patients who developed preeclampsia (cases) and 808 women with previous uneventful pregnancies (controls) matched for age and parity were evaluated for inherited and acquired thrombophilia (factor V Leiden; factor II G20210A; methylenetetrahydrofolate reductase C677T; protein S, protein C, and antithrombin III deficiency; anticardiolipin antibodies; lupus anticoagulant; and hyperhomocysteinemia). Odds ratios (ORs) with 95% confidence intervals (CIs) for risk of being carriers of thrombophilia in cases compared with controls and for risk of maternal life-threatening complications and adverse perinatal outcomes in preeclamptic patients with or without thrombophilia were calculated. Women with severe preeclampsia (406 cases) had a higher risk (OR, 4.9; 95% CI, 3.5 to 6.9) of being carriers of either an inherited or acquired thrombophilic factor, except for protein S, protein C, and antithrombin deficiency. In women with mild preeclampsia (402 cases), only prothrombin and homozygous methylenetetrahydrofolate reductase gene mutations were significantly more prevalent than in the controls. Thrombophilic patients with severe preeclampsia are at increased risk of acute renal failure (OR, 1.8; 95% CI, 1.5 to 2.2), disseminated intravascular coagulation (OR, 2.7; 95% CI, 1.1 to 6.4), abruptio placentae (OR, 2.6; 95% CI, 1.2 to 6.0) and perinatal mortality (OR, 1.7; 95% CI, 1.5 to 2.2) compared with nonthrombophilic preeclamptic patients. Our study demonstrates a significant association between maternal thrombophilia and severe preeclampsia in white women. Thrombophilia also augments the risk of life-threatening maternal complications and adverse perinatal outcomes in preeclamptic patients.

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Section: Discussionmentioning

confidence: 86%

Thrombophilia Is Significantly Associated With Severe Preeclampsia

Mello

Parretti²,

Marozio³

et al. 2005

Hypertension

140

View full text Add to dashboard Cite

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“…Furthermore, 20-50% of women who had late pregnancy losses were carriers of FV Leiden compared with less than 5% of control parous women. Others failed to demonstrate any association between FV Leiden or PRT G20210A SNPs with recurrent idiopathic miscarriage [21][22][23], as similar carrier frequencies for either SNP were seen in patients and controls. Herein we investigate the relationship between recurrent miscarriages and FV Leiden and prothrombin G20210A mutations in 200 women with 3 or consecutive miscarriages of unknown etiology, compared to 200 parous women with uncomplicated pregnancies and deliveries.…”

Section: Introductionmentioning

confidence: 99%

Association between adverse pregnancy outcomes and maternal factor V G1691A (Leiden) and prothrombin G20210A genotypes in women with a history of recurrent idiopathic miscarriages

et al. 2005

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Thrombophilia was implicated in the development of pregnancy complications, including recurrent idiopathic pregnancy loss, and is aggravated in women who are carriers of factor V G1691A (FV Leiden) and prothrombin (PRT) G20210A single-nucleotide polymorphisms (SNPs). Previous studies examined the role of FV-Leiden and PRT G20210A in recurrent pregnancy loss with conflicting results. Here we examined the prevalence of FV Leiden and PRT G20210A SNPs, in 200 women with 3 or more consecutive early (n = 87), late (n = 41), or early-late (n = 72) recurrent pregnancy losses, and 200 age-matched fertile parous control women. APC resistance (APCR) was detected functionally (measuring the activated clotting time triggered by activated factor X in presence of a fixed amount of purified APC), and FV-Leiden and PRT G20210A genotypes were assessed by PCR. The frequency of the mutant FV (0.1400 vs. 0.0276; P < 0.001) but not PRT 20210 (0.0100 vs. 0.0225; P = 0.159) allele was higher in patients than controls, respectively. APC resistance with factor V Leiden was seen in 27% of patients compared to 11.5% of controls, while APC resistance without factor V Leiden was seen in 12.5% of patients compared to 9.5% of controls. Regression analysis demonstrated that the significant predictors for early abortion was FV Leiden; those for late abortion were oral contraceptive, APCR, and FV Leiden; and predictors for early-late abortions were oral contraceptives, obesity, FV Leiden, and smoking. APC resistance and FV Leiden, as well as combination of both, are common thrombotic defects seen in women with idiopathic recurrent pregnancy loss, thus testing for these is recommended in women who have experienced recurrent miscarriages. Am.

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“…8,[11][12][13] The role of genetic and acquired thrombophilias in the pathogenesis of PAS is quite controversial and not completely understood. 14 -16 Maternal thrombophilias, both genetic and acquired, have been widely investigated in their association with various pregnancy complications, [17][18][19][20][21] but their role in PAS is not clear.…”

mentioning

confidence: 99%

Factor V Leiden and Antiphospholipid Antibodies in Either Mothers or Infants Increase the Risk for Perinatal Arterial Ischemic Stroke

Simchen

Gal

Lubetsky

et al. 2009

Stroke

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Background and Purpose-The objective was to investigate the role of infant and maternal thrombophilia in a cohort of mothers and infants presenting with perinatal arterial ischemic stroke. Methods-Forty-seven infants with clinically and radiologically confirmed perinatal arterial ischemic stroke underwent thrombophilia workup: factor V Leiden (FVL), PII20210A mutation, Methylene-tetrahydrofolate reductase 677T polymorphism, protein C, protein S, antithrombin, FVIII, and antiphospholipid antibodies. Thrombophilia data were available for 23 mother-infant pairs and compared with control populations to evaluate the risk for PAS. Results-Thirty of 47 (64%) infants and 15 of 22 mothers (68%) had evidence of thrombophilia. In 18 of 23 (78%) mother-infant pairs, there was at least 1 thrombophilic risk factor, but 15 pairs were mismatched in pathology. Among infants, FVL, protein C deficiency, and presence of antiphospholipid antibodies prevailed (OR, 4.2; 95% CI, 1.5-11.3; OR, 12.2; 95% CI, 2.5-59.9; OR, 4.1; 95% CI, 1.4 -12.2, respectively). Interestingly FVL prevailed in almost one-third of mothers (OR, 8.5; 95% CI, 4.1-17.5) and 18% of mothers had antiphospholipid antibodies (OR, 3.8l; 95% CI, 1.5-10.0). Conclusions-Maternal

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Postnatal Screening for Thrombophilia in Women With Severe Pregnancy Complications

Cited by 43 publications

References 24 publications

Thrombophilia Is Significantly Associated With Severe Preeclampsia

Thrombophilia Is Significantly Associated With Severe Preeclampsia

Association between adverse pregnancy outcomes and maternal factor V G1691A (Leiden) and prothrombin G20210A genotypes in women with a history of recurrent idiopathic miscarriages

Factor V Leiden and Antiphospholipid Antibodies in Either Mothers or Infants Increase the Risk for Perinatal Arterial Ischemic Stroke

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