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PubMed1997

Prevalence of activated protein C resistance in acute myocardial infarction in Japan.

To investigate the possibility that activated protein C (APC) resistance due to the factor V could be an important predisposing factor in acute myocardial infarction (AMI), we have retrospectively examined the prevalence of APC resistance with protein C, protein S and antithrombin III deficiency and antiphospholipid antibody syndrome in AMI patients (< or = 50 years) admitted to our hospital over the past 7 years. Forty-seven patients were enrolled in the study. We divided the patients into two groups, warfarin group (group A) and a non-warfarin group (group B). APC resistance is defined as when the APC ratio is below or equal to the cut-off value 2. APC resistance was not detected in either group. The prevalence of an APC ratio below or equal to 2.5 was 16.7% (1 case) in group A and 24.4% (10 cases) in group B. The prevalence of protein C deficiency was 5.0% (2 cases) in group B. Two cases (5.0%) in group B had protein S deficiency. Antithrombin III deficiency was not detected in either group. The prevalence of antiphospholipid antibody syndrome measured by APTT was 40.4% (19 cases). We compared the AMI patients with 97 healthy volunteers (< or = 50 years old) without any thromboembolic events or bleeding tendency in their past history. No significant difference were found between these groups and the volunteers. APC resistance is a major cause of venous thromboembolism in Europe and the United States, while in Japan it is believed to be a minor cause of arterial thromboembolism.

Adult↗
PubMed1984

Familial deficiency of antithrombin III: evidence for heterogeneity existing within the family.

An Australian family with familial antithrombin III (AT III) deficiency is described. The deficiency inherited in an autosomal co-dominant manner is characterised by proportionate reduction in antigenically and biologically measured AT III. Some members with AT III deficiency have had major venous thromboses, and the deficiency has possibly been the cause of death in two individuals in the family. Heterogeneity was observed in laboratory and clinical findings in this family.

Adult↗
PubMed1985

A functional abnormal antithrombin III (AT III) deficiency: AT III Charleville.

An antithrombin III (AT III) functional defect (AT III Charleville) was discovered in a patient presenting with recurrent venous thrombosis. Both anti-activated factor X (anti Xa) and antithrombin activity were decreased, in the absence and in the presence of heparin, while protein concentration was normal in an immunological assay. The abnormal AT III copurified with functional AT III using insolubilized heparin affinity chromatography. Polyacrylamide gel electrophoresis (PAGE) and high pressure liquid chromatography (HPLC) on a TSK column suggest that AT III Charleville forms unstable complexes with thrombin from which a modified protein is rapidly released.

Adult↗
PubMed1984

Prophylaxis of thrombosis in antithrombin III-deficient women during pregnancy and delivery.

Prophylactic treatment of two asymptomatic antithrombin III (AT III) -deficient women with oral anticoagulants and heparin during pregnancy and after delivery appeared to be feasible. Oral anticoagulants caused no change in plasma AT III levels in either woman. A high dose of heparin intravenously in one of them caused a strong reduction in the AT III level which was corrected by infusion of AT III concentrate during delivery. A low dose of heparin subcutaneously in the other caused no significant change in plasma AT III levels. There is probably no need for AT III substitution during an uncomplicated pregnancy.

Adult↗
PubMed2002

[Thrombophilias associated with cerebral venous thrombosis].

Many coagulation disorders have been associated with cerebral venous thrombosis. These disorders may be primary like protein C and S deficiency, antithrombine III deficiency and activated protein C resistance. Antiphospholipid antibodies represent an acquired disorders of coagulation. A prothrombotic state induced by more common factor including oral contraceptive, pregnancy and puerperium increases the venous thrombosis risk.

3' Untranslated Regions↗
PubMed1988

Changes of antithrombin III (AT III) in AT III deficient patients during long-term anticoagulant treatment.

Antithrombin III deficient patients with manifest thromboembolic diseases need long term coumarin treatment. There are contradictory data on the change of AT III during this therapy. The authors observed 5 patients with severe AT III decrease type I, 3 with functional abnormality and 2 with a pathological heparin binding. AT III function was determined by the Gerendás-Rák method and with chromogenic substrate. AT III antigen was measured with Behring M-Partigen and Laurell rocket electrophoresis. Crossed immunoelectrophoresis was carried out in all patients. In patients with type I AT III decrease, AT III hasn't changed even in a long period of more than 10 years. In the other types AT III became normal. The pathological heparin binding wasn't changed.

Anticoagulants↗
PubMed1988

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.

Adult↗
PubMed2005

The relationship of the factor V Leiden mutation and pregnancy outcomes for mother and fetus.

OBJECTIVE: We sought to estimate the frequency of pregnancy-related thromboembolic events among carriers of the factor V Leiden (FVL) mutation without a personal history of thromboembolism, and to evaluate the impact of maternal and fetal FVL mutation carriage or other thrombophilias on the risk of adverse outcomes. METHODS: Women with a singleton pregnancy and no history of thromboembolism were recruited at 13 clinical centers before 14 weeks of gestation from April 2000 to August 2001. Each was tested for the FVL mutation, as was the resultant conceptus after delivery or after miscarriage, when available. The incidence of thromboembolism (primary outcome), and of other adverse outcomes, was compared between FVL mutation carriers and noncarriers. We also compared adverse outcomes in a secondary nested carrier-control analysis of FVL mutation and other coagulation abnormalities. In this secondary analysis, we defined carriers as women having one or more of the following traits: carrier for FVL mutation, protein C deficiency, protein S deficiency, antithrombin III deficiency, activated protein C resistance, or lupus anticoagulant-positive, heterozygous for prothrombin G20210A or homozygous for the 5,10 methylenetetrahydrofolate reductase mutations. Carriers of the FVL mutation alone (with or without activated protein C resistance) were compared with those having one or more other coagulation abnormalities and with controls with no coagulation abnormality. RESULTS: One hundred thirty-four FVL mutation carriers were identified among 4,885 gravidas (2.7%), with both FVL mutation status and pregnancy outcomes available. No thromboembolic events occurred among the FVL mutation carriers (0%, 95% confidence interval 0-2.7%). Three pulmonary emboli and one deep venous thrombosis occurred (0.08%, 95% confidence interval 0.02-0.21%), all occurring in FVL mutation noncarriers. In the nested carrier-control analysis (n = 339), no differences in adverse pregnancy outcomes were observed between FVL mutation carriers, carriers of other coagulation disorders, and controls. Maternal FVL mutation carriage was not associated with increased pregnancy loss, preeclampsia, placental abruption, or small for gestational age births. However, fetal FVL mutation carriage was associated with more frequent preeclampsia among African-American (15.0%) and Hispanic (12.5%) women than white women (2.6%, P = .04), adjusted odds ratio 2.4 (95% confidence interval 1.0-5.2, P = .05). CONCLUSION: Among women with no history of thromboembolism, maternal heterozygous carriage of the FVL mutation is associated with a low risk of venous thromboembolism in pregnancy. Neither universal screening for the FVL mutation, nor treatment of low-risk carriers during pregnancy is indicated. LEVEL OF EVIDENCE: II-2.

Adult↗
PubMed2006

Preconception counseling for women with thrombophilia.

Inherited thrombophilias are a heterogeneous group of coagulation disorders that predispose individuals to thromboembolic events. This group of conditions is the major risk factor for thromboembolism during pregnancy and the puerperium. In addition, thrombophilias have been associated with several adverse obstetric events, including pregnancy loss, preeclampsia, placental abruption, and intrauterine growth restriction. An increased risk for these obstetric complications has prompted many authorities to recommend screening and treating pregnant women for thrombophilias. Optimal obstetric management, however, is controversial as thrombophilias are common and many affected individuals are asymptomatic. Indeed, pregnancy outcome in most women with thrombophilias is normal. The most commonly identified inherited thrombophilias are the factor V Leiden and prothrombin G20210A gene mutations. More rare thrombophilias include protein C and S deficiencies, antithrombin III deficiency. Although relatively common, the association between hyperhomocysteinemia and associated mutations (such as the C677 T methylenetetrahydro-folate reductase) and obstetric complications is controversial.

Factor V↗
PubMed1995

Livedo reticularis associated with hereditary protein C deficiency and recurrent thromboembolism.

We report the occurrence of livedo reticularis in a patient with symptomatic hereditary type 1 protein C deficiency. Antithrombin III deficiency and the antiphospholipid syndrome may also be associated with livedo reticularis, and we suggest that a thrombophilia screen may be a useful investigation in a patient with otherwise unexplained livedo, particularly if there is a personal or family history of thromboembolism.

Adult↗
PubMed1997

[Cerebral sinus thrombosis in a patient with protein S deficiency: a case report].

Cerebral sinus thrombosis associated with protein S deficiency is rare to the best of our knowledge. We report here a 22-year-old female who presented sudden onset of headache, vomiting and disturbance of consciousness. Neuroradiological studies including computed tomography scan, magnetic resonance imaging and cerebral angiography disclosed a huge cerebral sinus thrombosis in the territory of the superior sagittal sinus, torcular herophili, lateral sinus and straight sinus. Hematological studies confirmed the diagnosis of protein S deficiency. We summarize the reported cases of cerebral sinus thrombosis associated with protein S deficiency. For young patients presenting occlusive cerebrovascular disease, we stressed the importance of doing extensive hematological investigation to detect possible etiological factors, such as protein S deficiency, protein C deficiency, antithrombin III deficiency. Once we discover the etiology of a disease, we may be able to designate the precise treatment or regimen for each patient.

Adult↗
PubMedDate not supplied

[Familial deficiency of antithrombin III].

The systematic search for a deficiency in antithrombin III must be considered in case of: venous thrombosis in a young patient, recurrent venous thrombosis especially if these occurred under Heparin, venous mesenteric infarction since this type of thrombosis is rare and seems relatively frequent in case of congenital deficiency in antithrombin III, familial past history of venous thrombosis in a woman desiring to undergo estrogen-progesterone therapy. The most often used techniques are: study of antithrombin III activity by amidolytic method and titration by immunodiffusion. Anti-vitamin K treatment is the only effective therapy proposed to patients suffering from a hereditary deficiency in antithrombin III.

Anticoagulants↗
PubMed1991

Two cases of inherited triple deficiency in a large kindred with thrombotic diathesis and deficiencies of antithrombin III, heparin cofactor II, protein C and protein S.

Thirty-three subjects, belonging to a large family with functional antithrombin III (ATIII) deficiency (type IIa) and recurrent thromboembolism, were investigated for ATIII, heparin cofactor II (HCII), protein C (PC) and protein S (PS). We report the exceptional finding of two cases of triple deficiency: ATIII combined with HCII and PC in the first case aged 15 and ATIII combined with HCII and PS in the second case aged 27. Interestingly, both are asymptomatic thus far. Twenty-five other deficient members were found, among which seven are affected with a double deficiency. Totally, the results of our study show 38 deficiencies of four distinct antithrombotic protein: ATIII (n = 9), HCII (n = 9), PC (n = 7) or PS (n = 13). Two types of HCII deficiency were observed and type I PC deficiency was found. Functional PS deficiency was characterized by reduced levels of cofactor activity for activated PC. Our report demonstrates that combined deficiencies should be sought in a family already known to be deficient in one antithrombotic protein.

Adolescent↗
PubMed1988

Quantitative and qualitative congenital deficiency of antithrombin III: a new molecular variant called ATIII-Barcelona 2.

A Spanish family with a quantitative-qualitative antithrombin III (ATIII) deficiency and thrombotic tendency is reported. The qualitative defect was suggested by the crossed immunoelectrophoresis (CIE) in the presence of heparin in plasma of all those affected. However, the crossed immunoelectrofocusing (CIEF) showed the same ATIII pattern in controls and affected members. Two populations of ATIII were detected by affinity chromatography on heparin-sepharose from affected members' plasma. The ATIII unbound to sepharose beads was devoid of heparin cofactor activity and showed a lack of anodal migration in CIE in the presence of heparin. The ATIII eluted corresponded to normal ATIII. Our data supports the view that an abnormal ATIII molecule is present in all affected family members in the heterozygous state. This is the first reported ATIII variant in which a molecular abnormality produces a lack of affinity for heparin but no changes in its isoelectric point. This familial ATIII deficiency was named ATIII- Barcelona 2.

Antithrombin III↗
PubMed1994

Different incidence of venous thrombosis in patients with inherited deficiencies of antithrombin III, protein C and protein S.

A cohort study was undertaken to compare the incidence of thrombosis in patients with inherited deficiency of Antithrombin III (n = 9), Protein C (n = 36) and Protein S (n = 36). The patients were stratified for schedule of antithrombotic prophylaxis and followed for a total period of 160 patient-years. Seven venous thrombosis were observed for a total incidence of 4.3% pts.-ys. The incidence of thrombosis was not significantly different in patients of different age, sex and schedule of prophylaxis, although there was a trend to a lower incidence in young individuals and in those receiving long-term oral anticoagulation. Patients with AT III deficiency had an higher incidence of thrombosis than patients with Protein C or Protein S deficiency (12 vs. 2.8 vs. 3.3% pts.-ys, p < 0.05), despite the fact that they were, on average, younger and more prophylaxed. This study suggests that congenital Antithrombin III deficiency constitutes a greater risk of thrombosis than congenital deficiencies of Protein C and Protein S.

Administration, Oral↗
PubMed1984

Deficiency of antithrombin III in children with hemolytic-uremic syndrome.

In nine patients with hemolytic-uremic syndrome, the plasma activity and plasma concentrations of antithrombin III were determined on admission to the hospital and during the clinical course of the disease. Hemodialysis was necessary in six of the patients. In seven children the plasma AT III activity was moderately to markedly below the lower limit of normal at 75%, and did not rise after plasmapheresis with fresh frozen plasma. Replacement therapy with AT III concentrate was started in these patients. During the first 2 days an average dose of AT III concentrate of 2.1 U/kg in 24 h was necessary to raise plasma AT III activity by 1%. No side effects were observed. An already pre-existing procoagulant status and the administration of heparin may lead to AT III deficiency in hemolytic-uremic syndrome.

Antithrombin III Deficiency↗