1/22. Intracranial venous thrombosis associated with severe antithrombin-III deficiency in pregnancy.We report a patient with intracranial venous thrombosis in the third trimester of pregnancy associated with severe antithrombin-III deficiency. The evaluation of protein c, protein s and antithrombin-III levels in patients with thrombotic events during pregnancy may reveal the specific cause of the thrombotic event and thereby influence patient management- - - - - - - - - - ranking = 1keywords = pregnancy (Clic here for more details about this article) |
2/22. Severe preeclampsia in antithrombin iii deficiency with no history of venous thromboembolism.Complications of pregnancy, such as preeclampsia, placental abruption, fetal growth retardation, still-birth and fetal death are associated with an increased frequency of pro-thrombotic abnormalities. We describe a case of severe preeclampsia and multiple placental infarctions in a 28-year-old woman at 31 weeks' gestation. Despite a negative personal history for venous thromboembolism, coagulation screening for thrombophilia detected an isolated antithrombin iii deficiency. In view of the high prevalence of pro-thrombotic complications, laboratory screening for thrombophilia would be advantageous in women with complicated pregnancies, to ensure adequate management in high-risk situations, as suggested by larger-scale clinical investigations.- - - - - - - - - - ranking = 0.1965727307754keywords = pregnancy, gestation (Clic here for more details about this article) |
3/22. Management of pregnancy with congenital antithrombin iii deficiency: two case reports and a review of the literature.Women with antithrombin (AT) III deficiency are prone to pregnancy-associated venous thromboembolism. We report 2 cases with genetically confirmed ATIII deficiency, one with a mutation in exon 3A and the other with an exon 4 deletion, in whom the pregnancies were successfully managed with prophylactic therapies for thrombosis. A 35-year-old pregnant woman was treated with intravenous infusions of ATIII concentrate alone, and the other 22-year-old pregnant woman was mainly treated with subcutaneous injections of heparin and oral low-dose aspirin therapy. Both pregnancies resulted in vaginal deliveries of healthy neonates. The literature concerning prophylactic therapies for thrombosis in ATIII deficiency-complicated pregnancy is reviewed, and the clinical problems, including the adverse effects of the therapies, are discussed.- - - - - - - - - - ranking = 1keywords = pregnancy (Clic here for more details about this article) |
4/22. Prophylactic antithrombin III administration during pregnancy immediately reduces the thrombin hyperactivity of congenital antithrombin iii deficiency by forming thrombin-antithrombin III complexes.We examined the changes of haemostatic molecular markers after antithrombin III (AT III) administration in a 22-year-old woman with congenital AT III deficiency in the third trimester of pregnancy who did not have thrombosis. Various markers including fibrinopeptide a (FPA), thrombin-antithrombin III complex (TAT), prothrombin fragment F1 2 (F1 2), plasmin-alpha 2antiplasmin, D-dimer, beta-thromboglobulin, and platelet factor 4 were measured before and just after 3,000 U of AT III concentrate, which was given three times per week from the 34 week of pregnancy until delivery. Just after AT III administration, F1 2 and FPA levels decreased on most occasions, while TAT sometimes increased. plasma FPA levels were markedly decreased on all 8 occasions when the plasma FPA levels was above 2.0 ng/ml before AT III administration. plasma FPA levels were always greater than or equal to 6.4 ng/ml before AT III administration on the 4 occasions when TAT increased to above 115%. The changes of plasma F1 2 levels were significantly correlated with the AT III level. These results suggest that prophylactic AT III administration in the third trimester immediately inactivates intravascular thrombin to form TAT and reduce the plasma FPA level. Thus, the transient TAT elevation following AT III administration may not only be due to extraction of thrombin from the fibrin clots of thrombi but also to intravascular thrombin which is not attached to thrombi. FPA is the best molecular marker for thrombin hyperactivity and it should be monitored in AT III-deficient pregnant women in the third trimester.- - - - - - - - - - ranking = 1keywords = pregnancy (Clic here for more details about this article) |
5/22. The pregnant antithrombin III deficient patient: management without antithrombin III concentrate.Pregnant patients with antithrombin III (AT III) deficiency have an unacceptably high risk of venous thromboembolism (VTE). Antithrombotic therapy is therefore recommended. The reported clinical experience of such prophylaxis is limited. Some authors have recommended the use of AT III concentrate in addition to heparin in the management of these patients. We report successful management with heparin alone during pregnancy and the postpartum period in two patients with AT III deficiency. Both patients had experienced VTE during a prior pregnancy; one also experienced VTE during the reported pregnancy. Both patients were therefore at particularly high risk of further VTE. Based on the good results in these two patients, and a review of previously reported cases, we propose that heparin alone, in a dose to maintain the APTT in a therapeutic range, provides adequate prophylaxis and treatment for VTE during pregnancy and delivery in many AT III deficient subjects.- - - - - - - - - - ranking = 0.66666666666667keywords = pregnancy (Clic here for more details about this article) |
6/22. Antithrombin Nagasaki (Ser 116 to Pro): a rare antithrombin variant with abnormal heparin binding presenting during pregnancy.Quantitative antithrombin deficiency constitutes an important risk factor for venous thromboembolism, stillbirth, and other complications of pregnancy. Studies suggest, however, that individuals heterozygous for missense mutations involving the heparin-binding site of antithrombin do not have a significantly increased thrombotic risk. Owing to the rarity of such mutations, it remains unclear whether any specific heparin-binding site defects might be associated with thrombotic potential. We report here the case of a pregnant woman with an exceptionally rare Type II heparin-binding site antithrombin variant. This case highlights the difficult issues that are associated with the management of Type II antithrombin deficiency during pregnancy.- - - - - - - - - - ranking = 1keywords = pregnancy (Clic here for more details about this article) |
7/22. emergency treatment with recombinant tissue plasminogen activator of pulmonary embolism in a pregnant woman with antithrombin iii deficiency.Thromboembolic complications during pregnancy are frequent in patients with congenital antithrombin iii deficiency. We report on a 29-year-old patient with congenital antithrombin iii deficiency and severe pulmonary embolism treated with recombinant tissue plasminogen activator. The diagnosis of antithrombin deficiency is retrospective. This case indicates that the risk of thrombolytic therapy in this clinical setting might have been overemphasized.- - - - - - - - - - ranking = 0.16666666666667keywords = pregnancy (Clic here for more details about this article) |
8/22. Management of pregnancy in women with antithrombin III congenital defect: report of four cases.Four pregnant women with antithrombin III congenital deficiency underwent thrombosis prophylaxis including oral anticoagulants administered from the 16-18th week to the 36-37th week of pregnancy, subcutaneous heparin before the 16-18th week and after the 36-37th week, and a single infusion of AT III concentrate in the peripartum period in order to obtain a minimal level of 0.8 U/ml of AT III functional activity. The level of circulating AT III after the concentrate infusion needs to be evaluated by functional methods, because of a consistent amount in the concentrates of inactive AT III immunoreactive material. No thrombotic or haemorrhagic complication occurred after starting prophylaxis in any woman either in any newborn.- - - - - - - - - - ranking = 0.83333333333333keywords = pregnancy (Clic here for more details about this article) |
9/22. Cerebral thrombosis in a newborn with a congenital deficiency of antithrombin III.An Israeli Arab family with type I antithrombin III (AT-III) deficiency with several affected symptomatic members in three generations is reported. The propositus presented with deep vein thrombosis and pulmonary emboli associated with gestation. The propositus infant presented at the age of 2 weeks with superior sagittal and rectus sinus thrombosis. Hereditary AT-III deficiency should be considered in infants with cerebral thrombosis, especially if they have a family history of thromboembolism. The role of prophylactic therapy by AT-III concentrates in these infants should be further assessed.- - - - - - - - - - ranking = 0.029906064108736keywords = gestation (Clic here for more details about this article) |
10/22. Prophylactic use of antithrombin III concentrate following surgery in congenital antithrombin iii deficiency.Antithrombin III is the major physiological inhibitor of thrombin, and congenital deficiency of antithrombin III is associated with increased risk of venous thrombosis either spontaneously or following trauma, surgery or pregnancy. The successful use of antithrombin III concentrate during and following surgery to prevent venous thrombosis is described in a previously asymptomatic man with familial antithrombin iii deficiency.- - - - - - - - - - ranking = 0.16666666666667keywords = pregnancy (Clic here for more details about this article) |
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