Genetic thrombophilic defects (Factor V Leiden, prothrombin G20210A, MTHFR C677T) in women with recurrent fetal loss

Maternal thrombophilia (inherited and acquired) has recently been identified as a major cause of thrombembolism, but it may also contribute to adverse pregnancy outcomes and recurrent pregnancy loss. To determine the association of specific inherited thrombophilias and recurrent fetal loss (RFL), three gene mutations (Factor V Leiden, prothrombin G20210A, MTHFR C677T) were investigated. The prevalence of the thrombophilic markers was compared in 156 women with history of fetal loss in different trimester of pregnancy and 80 matched controls. At least one thrombophilic defect was found in 28.2% of total study group women compared with 16.2% in controls (p=0.06; OR-2.02) and in 50% of women with RFL in third trimester (p=0.008; OR-5.15). Factor V Leiden was more common in the group of women with fetal loss in third trimester (37.5%) compared to the controls (6.2%) (p=0.002; OR-9.0). Presence of FVL was associated with a significant increased risk for RFL in second and third trimester (OR-6.25; P<0.001) and significant protection for RFL in first trimester (OR-0.16; P<0.001). Mutation prothrombin G20210A or MTHFR C677T was more common in group of women with fetal loss in first trimester compared to the controls (28.3% vs. 11.2% respectively; p=0.009; OR-3.11). The presence of either of these mutations was associated with no significant increased risk for RFL in first trimester (OR-2.5). Genetic thrombophilic defects are common in women with RFL and are associated with late fetal loss. This association is manifest by FVL rather than total number of defects involved.     

Genetic mutations, acquired coagulation system disorders and obstetric pathology. Personal experience

BACKGROUND: To evaluate the incidence of thrombophilic disorders such as Factor II mutation, Leiden factor V and MTHFR genotype, and anti-phospholipid anti-bodies syndrome in women with or without pregnancy related problems. METHODS: Sixty-three patients (group A) with pregnancy complications were included in the study and tested for Factor V mutation, Factor II mutation, 5-10 MTHFR reductase mutation and anti-phospholipid antibodies syndrome. The incidence of disorders was compared with thirty-six pregnancies without complications (control study, group B). RESULTS: Hemostasis thrombophilic like disorders, were significantly high (p=0.001 vs group B). Nobody in both groups was homozygous for Leiden mutation or prothrombin mutation (Factor II). The prevalence of Factor V mutation in heterozygosis was significantly (p=0.01) higher in group A in comparison with group B. The MTHFR mutation in homozygosis was found in 21.4% of group A while in the control group it was 11%. Factor II mutation in heterozygosis and anti-phospholipid antibodies were found only in group A. CONCLUSIONS: It is important to evaluate the hemocoagulation patterns in women with a history of complicated pregnancies.     

Mesenteric vein thrombosis in a pregnant patient heterozygous for the factor V (1691 G --> A) Leiden mutation

Factor V Leiden mutation is a risk factor for the development of thromboembolic events in pregnancy. Thrombosis of the mesenteric vein is a fairly infrequent condition complicating pregnancy. In this paper, we described a pregnant patient with mesenteric vein thrombosis who was heterozygous for the factor V Leiden mutation.     

Factor V Leiden and factor II G20210A in preeclampsia and HELLP syndrome

BACKGROUND: The association of factor V and factor II mutations with preeclampsia and hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome, and a possible role of the two thrombophilic mutations in the pathogenesis of the diseases have been previously investigated. The results, however, are still inconclusive and contradictory. METHODS: A case-control study was performed over an interval of 24 months, on 111 subjects with preeclampsia and 111 normal pregnant women matched for age and parity, without previous thromboembolic disorders. The subjects were tested for the mutation A1691G in the factor V gene (R506Q or Leiden mutation) and the mutation A20210G in the factor II (prothrombin) gene. The Student's t-test and the chi2-test were applied when appropriate, and odds ratios and 95% confidence intervals were calculated. RESULTS: Fourteen patients with preeclampsia (12.6%) had at least one of the two mutations, as compared with six controls (5.4%). Factor V Leiden was found in eight patients with preeclampsia (7.2%) and in five controls (4.5%). Factor II G20210A was detected in eight preeclamptic women (7.2%) and in one normal pregnant woman (0.9%)(p = 0.041). In the subgroup of 32 preeclamptic subjects with HELLP syndrome, factor V Leiden was found in three patients (9.3%) and factor II G20210A in two (6.2%). CONCLUSIONS: The prevalence of factor V and factor II mutations is increased in patients with preeclampsia; the thrombophilic mutations may interact with other pathogenic factors to determine the clinical features of the disease and of its complications.     

Thrombophilia is common in women with idiopathic pregnancy loss and is associated with late pregnancy wastage

OBJECTIVE: To describe the characteristics of thrombophilia in women with idiopathic pregnancy loss. DESIGN: Prospective observational study. SETTING: Tertiary referral center in a teaching academic hospital. PATIENT(S): One hundred forty-five patients with repeated pregnancy loss and 145 matched controls. INTERVENTION(S): Prospective assessment of thrombophilia in patients and controls. MAIN OUTCOME MEASURE(S): Prevalence of activated protein C (APC) resistance, protein C, protein S, and antithrombin III deficiencies, antiphospholipid antibodies, factor V Leiden, factor II G20210A, and MTHFR C677T mutations. RESULT(S): At least one thrombophilic defect was found in 66% of study group patients compared with 28% in control group patients. Combined thrombophilic defects were documented in 21% of women with pregnancy loss compared with 5.5% of control patients. Late pregnancy wastage occurred more frequently in women with thrombophilia compared with women without thrombophilia (160/429 [37%] vs. 39/162 [24%], respectively). APC resistance was documented in 39% of women with pregnancy loss compared with 3% of the control patients. APC resistance without factor V Leiden mutation was documented in 18% of women with pregnancy loss compared with none of the controls. While factor V Leiden mutation was more common in women with pregnancy loss (25% vs. 7.6%), factor II G20210A and homozygosity for MTHFR C677T contributed to pregnancy loss only in the presence of other thrombophilia. CONCLUSION(S): Thrombophilia was found in the majority (66%) of women with idiopathic pregnancy loss. APC resistance with or without factor V Leiden mutation is the most common thrombophilic defect, and combined thrombophilia is a frequent finding in women with pregnancy loss. Thrombophilia is associated with increased frequency of late pregnancy wastage.     

Factor V Leiden and prothrombin 20210 G-A mutations in controls and in patients with thromboembolic events during pregnancy or the puerperium

Factor V Leiden and prothrombin 20210 G-A mutations are independent risk factors for venous thrombosis. We studied the frequency of these mutations in 35 patients who had thromboembolic events during pregnancy and puerperium, and in 32 women who had a history of uncomplicated pregnancy, delivered either vaginally or by cesarean section, and did not have a past history of thromboembolism. Factor V Leiden mutation was present in 7 patients (20%) in the study group. Of these 7 patients, 1 was homozygote, whereas the remaining 6 were heterozygote for the mutation. Prothrombin 20210 G-A mutation was present in 2 patients (5.7%) in the study group. In the control group none of the 32 patients was positive for the factor V Leiden and prothrombin 20210 G-A mutations. Our findings indicate that the factor V Leiden mutation is an important risk factor for thromboembolic disease during pregnancy or puerperium.     

Combined inherited thrombophilia and adverse pregnancy outcome

Inherited thrombophilia has been suggested as a possible condition of increased susceptibility to adverse pregnancy outcomes. In our prospective study, we investigated the association between combined inherited thrombophilia and adverse pregnancy outcome in the South-Western Greek population. Three hundred and ninety-six healthy Greek women with spontaneous pregnancies were investigated for combinations of the three commonest thrombophilic mutations (Factor II G20210A, Factor V Leiden and MTHFR C677T) and followed for adverse pregnancy outcomes. Statistical analysis was performed by Pearson's chi-square test. Four women (1%) had the FV Leiden/MTHFR T677T double genotype and two women (0.5%) had the FII G20210A/MTHFR T677T double genotype. Although the small number of cases of combined inherited thrombophilia, it seems that the presence of FV Leiden/MTHFR T677T double genotype increases the risk for placental abruption.     

Increased prevalence of thrombophilia among women with severe ovarian hyperstimulation syndrome

OBJECTIVE: To determine the prevalence of markers of thrombophilia in women hospitalized for severe OHSS. DESIGN: Prospective study. SETTING: Academic research center. PATIENT(S): Women undergoing induction of ovulation complicated by severe OHSS (n = 20) and women undergoing induction of ovulation without development of severe OHSS (n = 41). INTERVENTION(S): Blood samples to test for markers of thrombophilia were obtained during the luteal phase of the treatment cycle. MAIN OUTCOME MEASURE(S): Blood samples were analyzed for markers of thrombophilia, such as plasma levels of antithrombin, protein S and protein C, antiphospholipid antibodies, the factor V Leiden mutation, and 677T polymorphism in the 5,10 methyltetrahydrofolate reductase (MTHFR 677T) gene. RESULT(S): Seventeen of 20 patients with severe OHSS (85%) and 11 of 41 controls (26.8%) had one or more positive markers of thrombophilia. Of the women with severe OHSS, 6 had a decreased antithrombin level, 8 had decreased levels of protein S, 7 were homozygous for the MTHFR 677T mutation, 1 was heterozygous for the factor V Leiden mutation, and 5 had antiphospholipid antibodies. Eight women with OHSS and no controls had more than one positive marker of thrombophilia. CONCLUSION(S): The prevalence of thrombophilia is increased in women with severe OHSS. These findings suggest that prophylactic screening for this disorder and possible use of heparin prophylaxis for thromboembolic phenomena should be considered in these patients.     

The investigation of hereditary and acquired thrombophilia risk factors in the development of complications in pregnancy in Croatian women

Objectives: To investigate the genetic and acquired thrombophilic risk factors in pregnancy-associated complications and venous thromboembolism (VTE) and evaluate the association between particular thrombophilic risk factors and thromboembolic complications.

Methods: In this study, pregnant women with pregnancy complications and VTE (N?=?101) were the study group, and the control group were women with normal pregnancy (N?=?102). All women underwent testing for factor V Leiden mutation (FVL), mutation of the coagulation factors II (FII20210), methylenetetrahydrofolate reductase (MTHFR), plasminogen activator inhibitor-1, antithrombin III (ATIII), protein C (PC) and protein S, lupus anticoagulant (LAC) antibodies, anticardiolipin antibodies and anti-beta-2-glycoprotein-1.

Results: In this study group, mutations of the FVL was 15.8% (16/101), FII20210 5.9% (6/101) and the MTHFR at locus 677 was TT in 19.8% (20/101). Deficiency of ATIII and PC were rare: 3.0% and 1.0%, respectively. LAC were significantly higher in the study group than in the control group: 32.7% versus 3.9%; p?<?0.0005. Pregnant women with VTE have been more frequent for FVL (41.7%; p?<?0.005), PC deficiency (25.0%; p?<?0.005) and LAC (33.3%; p?<?0.005). Combination of FVL and MTHFR mutation was related to the risk of recurrent fetal death and habitual abortion.

Conclusion: The inherited and the acquired thrombophilic risk factors were found to be up to 10 times more common in the study group than in the control group.     

Second-trimester maternal serum alpha-fetoprotein (MSAFP) is elevated in women with adverse pregnancy outcome associated with inherited thrombophilias

Obstetric complications, such as severe pre-eclampsia, fetal growth restriction, abruptio placentae, or stillbirth are associated with abnormally elevated second-trimester maternal serum alpha-fetoprotein (MSAFP) and beta subunit of human chorionic gonadotrophin (betahCG). This has been attributed to placental abnormalities. Women with thrombophilias have been shown to have abnormalities of the placenta resulting in adverse pregnancy outcome in these patients. The purpose of the present study was to evaluate whether women with pregnancy complications and inherited thrombophilias have abnormally elevated second-trimester MSAFP or betahCG. Sixty-two women with pregnancy complications were tested for inherited thrombophilias several months after delivery. The thrombophilia group included 29 women with pregnancy complications and an inherited thrombophilia and the control group included 33 other patients without thrombophilia. Patients in the thrombophilia group had a higher median MoM MSAFP compared to the controls (1.337 vs. 1.086, p=0.0516). The incidence of abnormally elevated MSAFP (>2.5 MoM) was also significantly higher in the thrombophilia group compared to controls (21% vs. 3%, p=0.04). Neither the median MoM betahCG nor the incidence of abnormally elevated betahCG were significantly different between the groups. We conclude that second trimester MSAFP, but not betahCG, is abnormally elevated in patients with thrombophilia and obstetric complications.     

Obstetric implications of activated protein C resistance and factor V Leiden mutation

An increasing number of reports have focused on activated protein C resistance (APCR) as it has been shown not only to be the most common genetic factor predisposing patients to thromboembolic disease but the most common identifiable cause overall. More than 90 percent of the cases of APCR are caused by the factor V Leiden mutation, in which a guanine to adenine substitution in the factor V gene at nucleotide position 1691 results in a glutamine to arginine switch at position 506. Recent studies have also pointed to evidence of an association between APCR/factor V Leiden mutation and hypertensive disorders of pregnancy, first and second trimester miscarriage, placental infarction, and placental abruption.     

HELLP syndrome and factor V Leiden

The association of thrombophilia and obstetrical complications is documented and well consistent with the hypothesis of an insufficient placental perfusion due to fibrin deposition as a major underlying pathophysiological mechanism. Factor V Leiden is one of the most frequent thrombophilic mutations. A high prevalence of this mutation has recently been reported in a group of 21 German women with haemolysis, elevated liver enzymes, low platelets (HELLP) syndrome. In this respect, we studied the prevalence of factor V Leiden in 18 women who were consecutively diagnosed at our Department of Obstetrics and Gynaecology as having HELLP syndrome, between 1995 and 1999.Women were tested either at the time of diagnosis or months or years after delivery for coagulation parameters, protein C (PC), protein S (PS), antithrombin III, lupus-like anticoagulant, anticardiolipin antibodies (ACA), activated protein C (APC) resistance and detection of the G1691A mutation (factor V Leiden). In all women, the parameters studied were normal and in none of the investigated cases was the G1691A mutation found. HELLP being a severe form of preeclampsia, we think that the reported association between factor V Leiden and HELLP may reflect the well-known association with preeclampsia.     

Third trimester nonrecurrent fetal loss is associated with factor V Leiden and prothrombin gene mutations.

OBJECTIVE: To determine the role of factor V Leiden and prothrombin gene mutation in the pathogenesis of unexplained second and third trimester nonrecurrent fetal loss. MATERIALS AND METHODS: One hundred and fourteen women with unexplained nonrecurrent late fetal loss made up the study group, and 106 normal pregnant women with a history of delivery of at least one healthy fetus and no history of late fetal loss made up the control group. The study group was further divided into two subgroups: second (n = 36) and third (n = 78) trimester fetal loss. All women were tested for factor V Leiden and G20210A prothrombin gene mutations. RESULTS: Twenty-one (18.4%) of the women in the study group and seven (6.6%) of the women in the control group were heterozygous carriers of factor V Leiden mutation (OR = 3.19). Eleven (9.6%) of the women in the study group and three (2.8%) of the women in the control group were heterozygous carriers of prothrombin gene mutation (OR = 3.66). In assessing with regard to trimesters, 18 (23%) factor V Leiden and 10 (12.8%) prothrombin gene mutations were present in the group of third trimester fetal loss (OR = 4.24 and OR = 5.04, respectively). Three (8.3%) factor V Leiden and one (2.7%) prothrombin gene mutation were detected in women with second trimester fetal loss (OR = 1.28 and OR = 0.40, respectively). CONCLUSION: Factor V Leiden and prothrombin gene mutations were associated with third trimester nonrecurrent fetal loss. These mutations should be screened in women with third trimester but not second trimester unexplained nonrecurrent late fetal loss.     

Inheritance and perinatal consequences of inherited thrombophilia in Greece.

OBJECTIVE: To investigate the impact of inherited thrombophilic factors on the gestational outcome of unselected pregnant women. METHOD: A total of 392 women with spontaneous pregnancy were investigated for Factor V Leiden, prothrombin G20210A, and MTHFR C677T mutations. Adverse pregnancy outcomes were recorded. RESULTS: Thrombophilic genotypes were significantly higher in women with placental abruption. Heterozygocity for Factor V Leiden increased the risk for placental abruption 9.1 times. The MTHFR T677T genotype increased the risk for placental abruption 4.8 times despite folate supplements, and normal serum folate and B(12) levels. Women with inherited thrombophilia and previous obstetric complications were at significant risk for complications in a subsequent pregnancy (P<0.05). CONCLUSION: Women with placental abruption should be screened for thrombophilic factors and plasma homocysteine should be measured. Subgroups of women with inherited thrombophilia and obstetric complications might benefit from prophylactic anticoagulation in subsequent pregnancies.     

How strong is the association between maternal thrombophilia and adverse pregnancy outcome? A systematic review.

OBJECTIVE: To determine whether inherited and acquired thrombophilias are associated with adverse obstetric complications. STUDY DESIGN: A systematic review; studies where women with adverse obstetric complications were tested for one or more acquired and inherited thrombophilias were included. MAIN OUTCOME MEASURES: Prevalence of thrombophilia in women with severe pre-eclampsia/eclampsia, severe placental abruption, intrauterine growth restriction or unexplained stillbirth. RESULTS: Compared with controls, placental abruption was more often associated with homozygous and heterozygous factor V Leiden mutation, heterozygous G20210A prothrombin gene mutation, homocysteinaemia, activated protein C resistance or anticardiolipin IgG antibodies. Women with pre-eclampsia/eclampsia were more likely to have heterozygous factor V Leiden mutation, heterozygous G20210A prothrombin gene mutation, homozygous MTHFR C677T mutation, protein C deficiency, protein S deficiency or activated protein C resistance compared with controls. Unexplained stillbirth, when compared with controls, was more often associated with heterozygous factor V Leiden mutation, protein S deficiency, activated protein C resistance, anticardiolipin IgG antibodies or lupus anticoagulant. Women with intrauterine growth restriction had a higher prevalence of heterozygous G20210A prothrombin gene mutation, homozygous MTHFR C677T gene mutation, protein S deficiency or anticardiolipin IgG antibodies than controls. There was wide heterogeneity in the prevalence of thrombophilia between the studies. CONCLUSIONS: Women with adverse pregnancy outcome are more likely to have a positive thrombophilia screen but studies published so far are too small to adequately assess the true size of this association. Screening for thrombophilia should not become standard practice until clear evidence emerges that thromboprophylaxis during pregnancy improves perinatal outcome. Further research into the link between the observed association, causality and heterogeneity is required.     

Factor V Leiden mutation in pregnancy

Normal maternal adaptation to pregnancy significantly increases the risk for thrombus formation. Inherited thrombophilias further increase risk for deep venous thrombosis and adverse outcome in pregnancy. Factor V Leiden mutation is the most common inherited thrombophilia, occurring in approximately 5% of the White and 1% of the Black populations. Nurses should be knowledgeable about screening for and diagnosis of factor V Leiden mutation, risk reduction counseling, recommended care of the affected patient, and implications of anticoagulant therapy during the perinatal period.     

Thrombophilia and fetal growth restriction

OBJECTIVE: Genetic thrombophilia may represent a new risk factor for obstetrical complications. The aim of the study was to determine which subgroups may be associated with genetic thrombophilia for small for gestational age infants (SGA). METHODS: A case-control study was performed in three different maternity wards in Normandy. Cases (n=203) were women who had pregnancies complicated by unexplained SGA infants defined as a birth weight below the 3rd centile and control subjects (n=203) were women who had infants with birth weight > or =10th centile. Patients were tested in the immediate postpartum period and 2 months later for factor V Leiden mutation, and prothrombin 20210A mutation. Frequencies of these mutations were observed in different subgroups of SGA infants depending on pregnancy or neonatal outcomes usually associated with intrauterine growth restriction (IUGR), and were then compared with the overall prevalence for these mutations detected in the control group. RESULTS: Prevalences for factor V Leiden mutation (or=2.58; 95% confidence interval: 0.83-8.04), prothrombin 20210A mutation (or=2.03; 95% confidence interval: 0.51-8.01), were comparable between cases and controls (4.9% versus 1.9% and 2.9% versus 1.4%, respectively). Frequencies for these two polymorphisms significantly increased in subgroups of SGA infants with a normal Pourcelot index (13/133 versus 7/203; P=0.04), a gestational age > or =37 weeks of gestation (15/143 versus 7/203; P=0.01), a vaginal delivery (11/117 versus 7/203; P=0.04), a birth weight > or =2000 g (12/121 versus 7/203; P=0.03), no admission to paediatric ward (11/116 versus 7/203; P=0.01), a low Ponderal index <2.5(e) centile (6/45 versus 7/203; P=0.04), and normal head circumference >10th centile (7/53 versus 7/203; P=0.01) in comparison with the control group. CONCLUSIONS: An association was found between polymorphisms for factor V Leiden and prothrombin, and asymmetrical intrauterine growth restriction with immediate favourable neonatal outcomes.     

Activated protein C resistance in normal and pre-eclamptic pregnancies

OBJECTIVES: A lower ratio in the classic activated protein C resistance (APC-R) test has been reported during pregnancy, which has been called 'acquired' APC-R. However, little is known about the cause of the lowered ratio, and whether or not there is a correlation with blood coagulation activation. The primary objective of our study was to determine changes in APC-R levels in each of the trimesters of normal pregnancy. The secondary objective was to confirm whether APC-R levels were lower in pregnancies complicated by pre-eclampsia than in a control group. Finally, this prospective study was performed to investigate the prevalence of APC-R among pregnant women and to elucidate its obstetric consequences. METHODS: We enrolled 35 healthy pregnant women and 47 pregnant women affected by pre-eclampsia in our study. The following laboratory tests were performed: prothrombin time, partial thromboplastin time, fibrinogen levels, antithrombin III, plasmatic fibronectin (as a marker of endothelial damage), haptoglobin (as a marker of intravascular haemolysis), a functional test for APC-R and analysis of factor V Leiden mutation by polymerase chain reaction. RESULTS: The activated protein C sensitivity ratio was lower in the pathological group than in the control group (p = 0.008 and p = 0.02, respectively). Plasmatic fibronectin was found to be higher in the pathological group than in the control group (p = 0.05). Finally, the overall prevalence of factor V Leiden mutation was 5.4%, i.e. 2/35 women (5.7%) in the control group and 3/47 women in the pathological group (6.38%). CONCLUSIONS: The APC ratio decreased after 20 weeks of gestation until week 42. This decrease was most pronounced in the third trimester, in which resistance was demonstrated in 34.2% of control group patients. In pre-eclampsia, we found a greater reduction of the APC ratio than in controls. We hypothesise that this is due to a decrease in the plasmatic levels of coagulation inhibitors and an increase in coagulatory factors.     

Factor V Leiden mutation: the most commonly inherited risk factor for venous thromboembolism

Factor V Leiden mutation is a common genetic risk factor for venous thrombosis. It has been documented in up to 65% of patients with unexplained venous thromboembolism. This genetic mutation is now known to be the most common inherited cause of activated protein C (APC) resistance. Recently, FV Leiden mutation has been associated with adverse pregnancy outcomes (including recurrent fetal loss, severe preeclampsia, placental abruption, intrauterine growth restriction and stillbirth), in addition to venous thromboembolic disorders. In this article, we discuss the genetic basis, diagnosis and clinical significance of FV Leiden mutation. Awareness of the clinical manifestations associated with FV Leiden mutation should ensure screening of appropriate populations and prophylaxis against thromboembolic disease when indicated.     

Low plasma levels of oxidized low density lipoprotein in preeclampsia

BACKGROUND: Markers of lipid peroxidation are commonly used to assess oxidative stress in preeclampsia. The aim of this study was to assess the concentration of oxidized low density lipoprotein (oxLDL), a novel marker for lipid peroxidation, and that of the thiobarbituric acid reactive substances (TBARS) in the pathogenesis of severe preeclampsia and to investigate the influence of gestational age on these parameters. METHOD: Plasma levels of oxLDL and TBARS were assayed in women with severe preeclampsia (n = 40), normotensive pregnant controls matched for gestational age (n = 24) and normotensive pregnant controls at full term (n = 16). RESULTS: Women with preeclampsia showed lower oxLDL levels (mean +/- SE) than matched controls (181 +/- 12 vs. 219 +/- 14; p = 0.027), whereas no differences were found for the TBARS concentration (3.8 +/- 0.6 vs. 3.7 +/- 0.4). When women with preeclampsia were compared to control women at full term, TBARS were elevated (3.8 +/- 0.6 vs. 1.5 +/- 0.2; p = 0.01). However, in women with normotensive pregnancy TBARS were also lower in full-term control pregnancy compared to early third-trimester values (p < 0.0001). CONCLUSION: Plasma TBARS decreased during the third trimester of pregnancy, underlining the importance of matching for gestational age when studying markers of lipid peroxidation in pregnant women. Women with preeclampsia had lower plasma levels of oxLDL compared to gestational age-matched controls, indicating that oxLDL could be a marker for preeclampsia.