1/26. antithrombin iii deficiency in a patient with multifocal osteonecrosis.The authors examined a 35-year-old man who had multifocal osteonecrosis on the right and left femoral heads, left humeral head, and right scaphoid. The patient previously had a diagnosis of Type I congenital antithrombin iii deficiency but had no other risk factors for osteonecrosis. This patient was thought to have systemic thromboembolism because of the increased blood coagulability resulting from antithrombin iii deficiency. thrombophilia (increased likelihood of thrombosis) and hypofibrinolysis (reduced ability to lyse thrombi) have been implicated as causative factors for osteonecrosis. This case shows a possible relationship between thrombophilic antithrombin iii deficiency and multifocal osteonecrosis.- - - - - - - - - - ranking = 1keywords = thromboembolism (Clic here for more details about this article) |
2/26. 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 = 5keywords = thromboembolism (Clic here for more details about this article) |
3/26. Homozygous antithrombin deficiency type II (99 Leu to Phe mutation) and childhood thromboembolism.We report 5 children from 3 families with homozygous antithrombin deficiency type II affecting the heparin binding site (99 Leu to Phe mutation). Four children had severe spontaneous thromboembolic events (deep leg or caval vein thrombosis, ischaemic stroke) at one week, 3 months, 13 and 14 years of age. The fifth patient, a 17 year-old boy was asymptomatic. Early manifestation of homozygous deficiency calls for prompt and accurate diagnosis. In doubtful cases genetic analysis is required. Long-term oral anticoagulation should be considered in affected individuals.- - - - - - - - - - ranking = 4keywords = thromboembolism (Clic here for more details about this article) |
4/26. 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 = thromboembolism (Clic here for more details about this article) |
5/26. Pulmonary thromboembolectomy in congenital antithrombin iii deficiency associated with acute pulmonary embolism -report of a case-.Antithrombin III (AT III) deficiency is a rare hereditary disease that predisposes to thromboembolic complications. We report a case of AT III deficiency complicated with acute pulmonary thromboembolism, successfully treated with emergency pulmonary thromboembolectomy after insertion of an inferior vena cava filter. AT III activity before treatment was found to be 44% of normal value and remained less than 50% of normal throughout the postoperative course. In his family line, both the patient's aunt and deceased father had a history of pulmonary infarction. AT III activity of the patient's aunt was 47 to 58% of normal value. The patient was discharged on the 15th day after surgery and has been doing well for four years receiving warfarin as anticoagulant therapy. Careful follow-up is essential for early detection of the recurrent pulmonary thromboembolism resulting in pulmonary hypertension and/or right heart failure.- - - - - - - - - - ranking = 2keywords = thromboembolism (Clic here for more details about this article) |
6/26. Treatment of venous thromboembolism in patients with congenital deficiency of antithrombin III.The treatment course of all thromboembolic events in the patients with congenital deficiency of antithrombin III (AT III) in the national Swedish register was reviewed in order to assess the appropriate medical therapy in this situation. The medical treatment of 70 events of venous thromboembolism was evaluated. There were eight cases with signs of clinical progression. The risk of therapeutic failure with heparin could be as low as 1.5% or as high as 9.2%. It would not be cost-effective to substitute with concentrates of AT III in every case with congenital deficiency thereof in connection with acute venous thromboembolism. "heparin resistance" does not seem to be a problem in the vast majority of these patients.- - - - - - - - - - ranking = 6keywords = thromboembolism (Clic here for more details about this article) |
7/26. 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 = 1keywords = thromboembolism (Clic here for more details about this article) |
8/26. Congenital antithrombin iii deficiency causing mesenteric venous infarction: a lesson to remember--a case history.Congenital antithrombin iii deficiency is an uncommon but important cause of venous thrombosis, usually presenting with recurrent or atypical venous thromboembolism. Its importance lies in the fact that early recognition can lead to treatment in the acute stage, which can prevent propagation of the disease, and further prophylactic treatment may reduce the incidence of further episodes. The authors present a case of mesenteric venous infarction associated with congenital antithrombin iii deficiency and briefly discuss the diagnosis, surgical implications, and treatment of this disorder.- - - - - - - - - - ranking = 1keywords = thromboembolism (Clic here for more details about this article) |
9/26. 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 = thromboembolism (Clic here for more details about this article) |
10/26. Two cases of chronic pulmonary thromboembolism saved by postoperative use of a percutaneous cardiopulmonary support device.We performed pulmonary thromboendarterectomy under deep hypothermic intermittent circulatory arrest in 18 patients with chronic pulmonary thromboembolism from August 2001 to January 2004. In some of these cases, reperfusion pulmonary edema prevented a satisfactory improvement in hemodynamic data soon after the surgery. Here we report two cases of chronic pulmonary thromboembolism in which we successfully prevented postoperative persistent pulmonary hypertension and hypoxia caused by severe reperfusion pulmonary edema by the use of a percutaneous cardiopulmonary support device.- - - - - - - - - - ranking = 6keywords = thromboembolism (Clic here for more details about this article) |
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