Loredana Salton

Università degli Studi di Torino, Torino, Piedmont, Italy

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Publications (4)13.92 Total impact

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    ABSTRACT: Women with antiphospholipid antibodies (aPL) such as lupus anticoagulant, anticardiolipin antibodies, and anti-β(2) glycoprotein-1 antibodies are at high risk of late pregnancy complications, such as severe pre-eclampsia, placental insufficiency, and fetal loss. It has been observed that aPL consists of a heterogeneous group of antibodies targeting several phospholipid-binding plasma proteins, including also anti-prothrombin (anti-PT), anti-protein S (anti-PS), and anti-protein C (anti-PC) antibodies. Their potential role in late pregnancy complications is not known. The aim of this work was to investigate the association between those autoantibodies and histories for adverse pregnancy outcome. Anti-PT, anti-PS, and anti-PC antibodies were evaluated in 163 patients with previous severe pre-eclampsia, fetal death, and/or placental abruption and in as many women with previous uneventful pregnancies, negative for aPL. The prevalence of anti-PT antibodies was higher in cases than in controls (OR, 95% CI: 10.92, 4.52-26.38). The highest prevalence was observed in subjects with fetal death. Anti-PT antibodies appear to be associated with adverse pregnancy outcome, irrespectively of aPL.
    American Journal Of Reproductive Immunology 06/2011; 66(5):404-9. DOI:10.1111/j.1600-0897.2011.01031.x · 3.32 Impact Factor
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    ABSTRACT: The HELLP syndrome is a serious complication of pregnancy characterized by hemolysis (H), elevated liver (EL) enzymes, and low platelet (LP) count that occurs in 0.2-0.6% of all pregnancies and in 10-20% of cases with severe preeclampsia and frequently leads to adverse maternal and perinatal outcome. The exact pathobiology of HELLP syndrome has not been clearly defined. As it is considered a form or a complication of severe preeclampsia, it likely has its origin in aberrant placental development and function resulting in ischemia-producing oxidative stress. However, there is still a debate on whether HELLP must be considered a severe form of preeclampsia or a separate disease entity. It can be described as a placenta-induced disease, as is preeclampsia itself, but with a more acute and predominant inflammatory process typically targeting the liver and with a greater activation of the coagulation system. This occurs during a disordered immunologic process and may be due to a genetic predisposition. In this review, we discuss the main biochemical characteristics of HELLP syndrome, particularly focusing on molecular aspects of placental involvement and maternal systemic responses.
    Advances in clinical chemistry 01/2011; 53:85-104. DOI:10.1016/B978-0-12-385855-9.00004-7 · 4.30 Impact Factor
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    ABSTRACT: Both acquired and inherited thrombophilias are associated with an increased risk of pregnancy-related venous thromboembolism (VTE) as well as with adverse pregnancy outcome. However, the extension of attributable risk for each thrombophilia and outcome is still a question of debate. Thrombophilias have been investigated in connection with VTE and pregnancy complications such as: recurrent and nonrecurrent early pregnancy loss, late fetal death, placental abruption, fetal growth restriction, and preeclampsia. This review discusses the evidence of association between thrombophilias and pregnancy outcome together with issues as to clinical management and preventive strategies.
    Annals of the New York Academy of Sciences 09/2010; 1205(1):106-17. DOI:10.1111/j.1749-6632.2010.05674.x · 4.31 Impact Factor
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    ABSTRACT: 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. 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. 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%). 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.
    Acta Obstetricia Et Gynecologica Scandinavica 01/2003; 81(12):1095-100. DOI:10.1034/j.1600-0412.2002.811201.x · 1.99 Impact Factor