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P.55 Primary coagulopathic massive obstetrical haemorrhage
S142
Abstracts / Thrombosis Research 127 (2011) S123–S150
P.52 Associations between anemia and coagulation abnormalities in women with menorrhagia
P.54 Pathogenetic prophylaxis in women with history of stroke and thrombophilia during pregnancy
S. Djukic1 *, N. Andjelkovic1 , A. Djukic1 , J.P. Antovic2 . 1 Department of Hematology, Clinic of Internal Medicine, Clinical Center & Faculty of Medicine, Kragujevac, Serbia, 2 Coagulation Research, Karolinska University Hospital & Institute, Stockholm, Sweden
A.D. Makatsaria *, S.V. Akinshina, V.O. Bitsadze. Department of obstetrics and gynecology, I.M. Sechenov First Moscow State Medical University, Russia
Introduction: Menorrhagia is common cause of anemia in women in reproductive period. Although substantial number of women with menorrhagia have mild hemostatic defects there is no data about characteristics of anemia in this population. Objective: To investigate anemia in women with menorrhagia with or without cogulation abnormalities. Materials and Methods: We have investigated coagulation status and anemia indices in 115 women (36.2±9.4 years) with symptoms of menorrhagia. Results: 64 (55.7%) women have had objectively verified menorrhagia (PBAC 226.8±143.2). Anemia was diagnosed in 61 (53.0%) of totally 115 women: 36 with verified menorrhagia and 25 without. Coagulation defects (decreased FIX in 4, decreased FVII in 1, decreased FX in 1, mild VWD type 1 in 5 and 1 hemophilia C carrier) have been found in 12 women. Most of those patients had menorrhagia (11 of 12 or 91.7%) and anemia (10 of 12 or 83.3%). Patients with anemia of non-menorrhagic origin (PBAC 55.1±12.0) were older (40.3±9.5 years, p = 0.03), RBC was significantly higher in patients with anemia as a consequence of menorrhagia (4.2±0.5 vs 3.9±0.7×1012 /L, p = 0.01) while other anemia indices showed no difference. Both D-dimer (250.1±79.7 vs. 162.6±112.3 ng/mL, p = 0.001) and fibrinogen (3.7±0.6 vs 3.3±0.9 g/L, p = 0.05) were significantly higher in women with non-menorrhagic anemia Conclusions: Nearly 60% patients with menorrhagia developed anemia. One third had coagulation abnormalities while almost all of them developed anemia. Anemia of non-hemorrhagic origin was characteristic of older women and was associated with inflammation. In spite of limited data our results may suggest that younger women with objectively verified menorraghia and anemia which is not associated with inflammation should be tested for coagulation abnormalities. P.53 Use of low molecular-weight heparin and natural progesterone for the prevention of recurrent pregnancy complications (pre-eclampsia, pregnancy loss, placental abruption) in women with metabolic syndrome T.B. Radulovich *, E.B. Perederyaeva, A.D. Makatsaria. I.M. Sechenov First Moscow State Medical University Objective: The study of obstetric and perinatal outcomes in women with metabolic syndrome and complicated pregnancy history. Methods: 52 patients aged 22 to 43 years with metabolic syndrome who had the fetal loss syndrome, severe pre-eclampsia, placental abruption in previous pregnancies. Testing for hereditary and acquired forms of thrombophilia. Results: In the study group the multigenic defects were verified in 100% of cases; the feature of multigenic defects is that the 4G/5G polymorphism of plasminogen activator inhibitor-1 gene was found in 92.3% of cases, the 4G/4G phenotype of the gene PAI-1 was verified in 61.5% of cases. The polymorphism in the tissue-type plasminogen activator I/D gene, in the angiotensin-converting enzyme I/D gene, in the fibrinogen 455G/A gene, mutations of methylenetetrahydrofolate reductase C677T were found in 65.4%, 48.1%, 55.8%, 55.8% respectively. Acquired antiphospholid antibodies were verified in 15.4% of cases. All women received antithrombotic therapy from the fertile cycle involved low molecular-weight heparin (Enoxaparin sodium, daily dose 0.4–0.8 ml), vitamins B, folic acid and natural progesterone for indications. Antithrombotic therapy was controlled by thrombophilia markers (D-Dimer) and the anti-Xa test. Pregnancy was achieved in 100%. There were not recurrent fetal loss, severe pre-eclampsia, placental abruption in the study group. Live births was in all cases. Conclusions: There is genetic hypofibrinolysis and acquired form of thrombophilia in patients with metabolic syndrome and complicated pregnancy history. It may play an important part in impaired invasion cytotrophoblast and impaired placental development. Timely antithrombotic prophylaxis may be a key of successful outcome of pregnancy.
Objectives: Our objective was to evaluate the role of thrombophilia in pathogenesis of stoke, the effectiveness of our prophylactic strategy during pregnancy and outcomes for mother and fetus. Material and Methods: We studied 59 women with history of stroke (32±5.5 years). In 7 pts pregnancy was interrupted in I-II trimester. 25 pts were followed prospectively (group I) in preconception period and during pregnancy (low molecular weight heparin (LMWH) guided by D-dimer, aspirin, antioxidants, vitamins of B group, folic acid). In 27 pts (group II) therapy was started in II-III trimester. Results: Thrombophilia was detected in 100%: defects of homocystein metabolism (72.9%), fibrinolysis defects (fibrinogen −455G/A, PAI-1 4G/5G, t-PA I/D) (61%), FV Leiden (16.9%), APA (50.8%). Stroke was associated with severe medical conditions (hypertension, rheumatic diseases, SLE, prosthetic valves, thrombosis) and obstetric complications. In group I mildto-moderate obstetrics complications were detected in 9 pts (36%). All pts were delivered at term and all babies were alive. In group II 62.9% of pts had moderate to severe obstetrics complications, which required preterm delivery in 18.5% (p < 0.05). Conclusions: Thrombophilia might be the main pathogenic mechanism of stroke and obstetrics complications. Hypergomocysteinemia and APA were detected in most cases. Preconception treatment with LMWH allows preventing pregnancy complications, adverse fetal outcomes and recurrent thrombosis. The mode of delivery in pts with history of stroke is ultimately cesarean section. P.55 Primary coagulopathic massive obstetrical haemorrhage A.D. Makatsaria *, V.O. Bizadze, V.V. Smurygina, S.V. Akinshina, D.H. Khizroeva. Department of obstetrics and gynecology, I.M. Sechenov First Moscow State Medical University, Russia Aim: to evaluate pathogenetic factors of massive blood loss in women with history of obstetrical haemorrhage. Materials and Methods: From year 2000 were have evaluated 57 women with history of massive obstetrical haemorrhage accounting for 1.5% to 5% of the body weight. All women were screened for genetic thrombophilia, antiphospholipid antibodies and platelet disorders. Results: Thrombocytopathy was diagnosed in 31.6%, different forms of von Willebrand disease in 14%. Thrombophilia was detected in 59.6%: genetic (54.4%), acquired (7%) and combined (15.8%). In 38.6% thrombophilic disorders went together with platelet defects. All women with thrombophilic disorders had placental pregnancy complication, including preeclampsia, abruptio placentae, fetal growth restriction. Conclusion: Clinical analysis revealed the following mechanisms of massive obstetrical haemorrhage: acute disseminated intravascular coagulation (abruptio placentae, amniotic fluid embolism); transition from subacute to acute DIC (preeclampsia); hidden haemostatic disorders (thrombocytopathy, undiagnosed Willebrand disease); drug-related haemorrhage and inhibitory forms of coagulopathy. Accounting for this factors and timely detection of occult haemostatic disorders might play the key in prevention severe hemorrhagic obstetrical and maternal mortality. P.56 Tissue factor (TF) and tissue factor pathway inhibitor (TFPI) plasma levels in severe reeclampsia L.C. Godoi1 *, P.N. Alpoim1 , H. Madeira2 , J. Petterson3 , A.P. Fernandes1 , M.G. Carvalho1 , K.B. Gomes1 , L.M.S. Dusse1 . 1 Department of Clinical and Toxicological Analysis, Faculty of Pharmacy of Federal University of Minas ublico Gerais, 2 Maternidade Odete Valadares – Belo Horizonte, 3 Hospital P´ Regional de Betim, Brazil Background and Aims: Preeclampsia (PEc) is a major cause of maternal death and is associated with a higher hypercoagulability state. The aim of this study was to assess TF and TFPI plasma levels in women with severe PEc and normotensive pregnant. Methods: Three groups were evaluated – group I: Pregnant women with severe PE, systolic/diastolic measure ≥160/110mmHg and/or proteinuria ≥2 g/L and gestational age (GA) ≥30 weeks; group II: Normotensive pregnant, systolic/diastolic measure ≤120/80 mmHg, with no history of hypertension and no proteinuria and GA ≥30 weeks; and group III: Non pregnant healthy women. TF and TFPI plasma levels were measured by ELISA.
Abstracts / Thrombosis Research 127 (2011) S123–S150
P.52 Associations between anemia and coagulation abnormalities in women with menorrhagia
P.54 Pathogenetic prophylaxis in women with history of stroke and thrombophilia during pregnancy
S. Djukic1 *, N. Andjelkovic1 , A. Djukic1 , J.P. Antovic2 . 1 Department of Hematology, Clinic of Internal Medicine, Clinical Center & Faculty of Medicine, Kragujevac, Serbia, 2 Coagulation Research, Karolinska University Hospital & Institute, Stockholm, Sweden
A.D. Makatsaria *, S.V. Akinshina, V.O. Bitsadze. Department of obstetrics and gynecology, I.M. Sechenov First Moscow State Medical University, Russia
Introduction: Menorrhagia is common cause of anemia in women in reproductive period. Although substantial number of women with menorrhagia have mild hemostatic defects there is no data about characteristics of anemia in this population. Objective: To investigate anemia in women with menorrhagia with or without cogulation abnormalities. Materials and Methods: We have investigated coagulation status and anemia indices in 115 women (36.2±9.4 years) with symptoms of menorrhagia. Results: 64 (55.7%) women have had objectively verified menorrhagia (PBAC 226.8±143.2). Anemia was diagnosed in 61 (53.0%) of totally 115 women: 36 with verified menorrhagia and 25 without. Coagulation defects (decreased FIX in 4, decreased FVII in 1, decreased FX in 1, mild VWD type 1 in 5 and 1 hemophilia C carrier) have been found in 12 women. Most of those patients had menorrhagia (11 of 12 or 91.7%) and anemia (10 of 12 or 83.3%). Patients with anemia of non-menorrhagic origin (PBAC 55.1±12.0) were older (40.3±9.5 years, p = 0.03), RBC was significantly higher in patients with anemia as a consequence of menorrhagia (4.2±0.5 vs 3.9±0.7×1012 /L, p = 0.01) while other anemia indices showed no difference. Both D-dimer (250.1±79.7 vs. 162.6±112.3 ng/mL, p = 0.001) and fibrinogen (3.7±0.6 vs 3.3±0.9 g/L, p = 0.05) were significantly higher in women with non-menorrhagic anemia Conclusions: Nearly 60% patients with menorrhagia developed anemia. One third had coagulation abnormalities while almost all of them developed anemia. Anemia of non-hemorrhagic origin was characteristic of older women and was associated with inflammation. In spite of limited data our results may suggest that younger women with objectively verified menorraghia and anemia which is not associated with inflammation should be tested for coagulation abnormalities. P.53 Use of low molecular-weight heparin and natural progesterone for the prevention of recurrent pregnancy complications (pre-eclampsia, pregnancy loss, placental abruption) in women with metabolic syndrome T.B. Radulovich *, E.B. Perederyaeva, A.D. Makatsaria. I.M. Sechenov First Moscow State Medical University Objective: The study of obstetric and perinatal outcomes in women with metabolic syndrome and complicated pregnancy history. Methods: 52 patients aged 22 to 43 years with metabolic syndrome who had the fetal loss syndrome, severe pre-eclampsia, placental abruption in previous pregnancies. Testing for hereditary and acquired forms of thrombophilia. Results: In the study group the multigenic defects were verified in 100% of cases; the feature of multigenic defects is that the 4G/5G polymorphism of plasminogen activator inhibitor-1 gene was found in 92.3% of cases, the 4G/4G phenotype of the gene PAI-1 was verified in 61.5% of cases. The polymorphism in the tissue-type plasminogen activator I/D gene, in the angiotensin-converting enzyme I/D gene, in the fibrinogen 455G/A gene, mutations of methylenetetrahydrofolate reductase C677T were found in 65.4%, 48.1%, 55.8%, 55.8% respectively. Acquired antiphospholid antibodies were verified in 15.4% of cases. All women received antithrombotic therapy from the fertile cycle involved low molecular-weight heparin (Enoxaparin sodium, daily dose 0.4–0.8 ml), vitamins B, folic acid and natural progesterone for indications. Antithrombotic therapy was controlled by thrombophilia markers (D-Dimer) and the anti-Xa test. Pregnancy was achieved in 100%. There were not recurrent fetal loss, severe pre-eclampsia, placental abruption in the study group. Live births was in all cases. Conclusions: There is genetic hypofibrinolysis and acquired form of thrombophilia in patients with metabolic syndrome and complicated pregnancy history. It may play an important part in impaired invasion cytotrophoblast and impaired placental development. Timely antithrombotic prophylaxis may be a key of successful outcome of pregnancy.
Objectives: Our objective was to evaluate the role of thrombophilia in pathogenesis of stoke, the effectiveness of our prophylactic strategy during pregnancy and outcomes for mother and fetus. Material and Methods: We studied 59 women with history of stroke (32±5.5 years). In 7 pts pregnancy was interrupted in I-II trimester. 25 pts were followed prospectively (group I) in preconception period and during pregnancy (low molecular weight heparin (LMWH) guided by D-dimer, aspirin, antioxidants, vitamins of B group, folic acid). In 27 pts (group II) therapy was started in II-III trimester. Results: Thrombophilia was detected in 100%: defects of homocystein metabolism (72.9%), fibrinolysis defects (fibrinogen −455G/A, PAI-1 4G/5G, t-PA I/D) (61%), FV Leiden (16.9%), APA (50.8%). Stroke was associated with severe medical conditions (hypertension, rheumatic diseases, SLE, prosthetic valves, thrombosis) and obstetric complications. In group I mildto-moderate obstetrics complications were detected in 9 pts (36%). All pts were delivered at term and all babies were alive. In group II 62.9% of pts had moderate to severe obstetrics complications, which required preterm delivery in 18.5% (p < 0.05). Conclusions: Thrombophilia might be the main pathogenic mechanism of stroke and obstetrics complications. Hypergomocysteinemia and APA were detected in most cases. Preconception treatment with LMWH allows preventing pregnancy complications, adverse fetal outcomes and recurrent thrombosis. The mode of delivery in pts with history of stroke is ultimately cesarean section. P.55 Primary coagulopathic massive obstetrical haemorrhage A.D. Makatsaria *, V.O. Bizadze, V.V. Smurygina, S.V. Akinshina, D.H. Khizroeva. Department of obstetrics and gynecology, I.M. Sechenov First Moscow State Medical University, Russia Aim: to evaluate pathogenetic factors of massive blood loss in women with history of obstetrical haemorrhage. Materials and Methods: From year 2000 were have evaluated 57 women with history of massive obstetrical haemorrhage accounting for 1.5% to 5% of the body weight. All women were screened for genetic thrombophilia, antiphospholipid antibodies and platelet disorders. Results: Thrombocytopathy was diagnosed in 31.6%, different forms of von Willebrand disease in 14%. Thrombophilia was detected in 59.6%: genetic (54.4%), acquired (7%) and combined (15.8%). In 38.6% thrombophilic disorders went together with platelet defects. All women with thrombophilic disorders had placental pregnancy complication, including preeclampsia, abruptio placentae, fetal growth restriction. Conclusion: Clinical analysis revealed the following mechanisms of massive obstetrical haemorrhage: acute disseminated intravascular coagulation (abruptio placentae, amniotic fluid embolism); transition from subacute to acute DIC (preeclampsia); hidden haemostatic disorders (thrombocytopathy, undiagnosed Willebrand disease); drug-related haemorrhage and inhibitory forms of coagulopathy. Accounting for this factors and timely detection of occult haemostatic disorders might play the key in prevention severe hemorrhagic obstetrical and maternal mortality. P.56 Tissue factor (TF) and tissue factor pathway inhibitor (TFPI) plasma levels in severe reeclampsia L.C. Godoi1 *, P.N. Alpoim1 , H. Madeira2 , J. Petterson3 , A.P. Fernandes1 , M.G. Carvalho1 , K.B. Gomes1 , L.M.S. Dusse1 . 1 Department of Clinical and Toxicological Analysis, Faculty of Pharmacy of Federal University of Minas ublico Gerais, 2 Maternidade Odete Valadares – Belo Horizonte, 3 Hospital P´ Regional de Betim, Brazil Background and Aims: Preeclampsia (PEc) is a major cause of maternal death and is associated with a higher hypercoagulability state. The aim of this study was to assess TF and TFPI plasma levels in women with severe PEc and normotensive pregnant. Methods: Three groups were evaluated – group I: Pregnant women with severe PE, systolic/diastolic measure ≥160/110mmHg and/or proteinuria ≥2 g/L and gestational age (GA) ≥30 weeks; group II: Normotensive pregnant, systolic/diastolic measure ≤120/80 mmHg, with no history of hypertension and no proteinuria and GA ≥30 weeks; and group III: Non pregnant healthy women. TF and TFPI plasma levels were measured by ELISA.