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PubMed1998

Inherited thrombophilia and pregnancy.

Inherited thrombophilia is associated with an increased risk of thrombosis. Classically it consists of protein C and protein S deficiency, activated protein C resistance and antithrombin III deficiency. In pregnancy, in addition to thrombosis, inherited thrombophilia is associated with poor obstetric outcome, including recurrent miscarriage, late fetal loss, abruption and pre-eclampsia. Hyperhomocysteinaemia is a newly recognized cause of familial thrombophilia. It is likely that further causes such as prothrombin gene mutations will be added to the rapidly expanding list. The diagnosis of some forms of genetic thrombophilia must, however, be approached with caution during pregnancy, particularly protein S deficiency and activated protein C resistance.

Biomarkers↗

PubMed1990

[Perioperative blood coagulation therapy and diagnosis].

The risks and adverse reactions of fresh frozen plasma (FFP) and coagulation components have changed considerably in the last few years because of the spread of HIV on the one hand, and the advances in preparation and sterilisation of the coagulation components on the other hand. Therefore, the indication for FFP and the various coagulation components deserves permanent consideration. FFP is still the therapeutical means of choice for the treatment of acquired (complex) plasmatic coagulation disorders, even though the (still) small risk of virus transmission in Middle Europe has to be taken into account. Coagulation components are primarily indicated in congenital (isolated) plasmatic coagulation disorders. Only in gross or very acute acquired coagulation disorders are coagulation components needed in addition to FFP. The same regimen is recommended for the use of antithrombin III (AT III) concentrates. In cases of acquired antithrombin deficiency, antithrombin III substitution is indicated only when the anticoagulation by heparin alone or in combination with FFP is insufficient or when the heparin dose required might cause an unacceptable bleeding risk, e.g. in simultaneous thrombocytopenia. Then AT III becomes an important therapeutic agent, especially in DIC. In addition, information regarding a rational and economic substitution of FFP and coagulation components is given, and other substitutes are mentioned which could possibly be used with less risk. Finally, the necessity of accurate diagnosing is emphasized. Close cooperation between the physicians in the clinics and in the department of transfusion medicine/hemostaseology reduces unnecessary and inadequate application of coagulation components. This also means an improvement in the patient's therapy.

Antithrombin III↗

PubMed1989

[The status of blood coagulation preparations within the scope of modern hemotherapy in surgical patients].

The risks and adverse reactions of fresh frozen plasma (FFP) and coagulation components have changed considerably in the last few years because of the spread of HIV on the one hand, and advances in the preparation and sterilization of coagulation components on the other. Therefore, the indication for FFP and the various coagulation components deserves constant consideration; this is the intention of this paper. FFP is still the therapeutic choice for the treatment of acquired (complex) plasmatic coagulation disorders, even though the (still) small risk of virus transmission in Middle Europe has to be taken into account. Coagulation components are primarily indicated in congenital (isolated) plasmatic coagulation disorders. Only in gross or very acute acquired coagulation disorders are coagulation components needed in addition to FFP. The same regimen is recommended for the use of antithrombin III (AT III) concentrates. In cases of acquired antithrombin deficiency, antithrombin III substitution is indicated only when the anticoagulation by heparin alone or in combination with FFP is insufficient or when the heparin doses required might entail an unexceptable bleeding risk, e.g. in simultaneous thrombocytopenia. Then AT III becomes an important therapeutic factor, especially in DIC. In addition, information regarding a rational and economic substitution of FFP and coagulation components is given, and other substitutes are mentioned which could possibly be used with less risk. Finally, the necessity for an adequate diagnostic procedure is emphasized. Close cooperation between the physicians in the clinics and in the department of transfusion medicine/hemostaseology reduces unnecessary and inadequate application of coagulation components. This also means an improvement of the patient's therapy.

Blood Coagulation Disorders↗

PubMed1994

Adjunctive intracoronary infusion of antithrombin III during percutaneous transluminal coronary angioplasty. Results of a prospective, randomized trial.

BACKGROUND: Heparin needs the plasma protein antithrombin III to function as an inhibitor of thrombin, and local antithrombin III deficiency might therefore limit the antithrombotic effectiveness of heparin during percutaneous transluminal coronary angioplasty. METHODS AND RESULTS: In the present double-blind study, 615 consecutive patients undergoing percutaneous transluminal coronary angioplasty (PTCA), of a total of 713 stenoses, were prospectively randomized to receive a bolus injection of 15,000 U heparin followed by a continuous intracoronary infusion via the guiding catheter of either 250 U heparin per minute or 250 U heparin plus 25 U antithrombin III per minute during the procedure. Four clinical variables, 19 lesion-specific characteristics, and 16 procedure-related variables were evaluated. Procedural success was assessed by quantitative angiography; procedure-related ischemic complications were analyzed during in-hospital follow-up. Procedural success rates (< 50% final diameter stenosis and no major ischemic complication) were similar, with 85% in the heparin group (n = 324 patients) and 83% in the heparin+antithrombin III group (n = 291 patients). Percent diameter stenosis after PTCA was 39 +/- 18% in the heparin group and 40 +/- 20% in the heparin+antithrombin III group (NS). There were no differences between the two groups with respect to PTCA-related acute vessel occlusion, angiographic evidence of intracoronary thrombus formation, post-procedure creatine kinase increase, Q-wave myocardial infarction, or emergency coronary artery bypass surgery. High-risk subgroup analysis revealed no beneficial effect of adjunctive intracoronary antithrombin III in any of the analyzed subgroups. In addition, although risk stratification according to the criteria of the American College of Cardiology/American Heart Association Task Force classification proved to be very useful for the entire study population, no beneficial effect of intracoronary antithrombin III infusion was observed in any of the different risk groups. CONCLUSIONS: Compared with heparin alone, adjunctive intracoronary antithrombin III therapy does not appear to have any beneficial effect on procedural outcome as well as type and frequency of acute complications during PTCA even in subgroups of patients with a high risk for thrombotic complications. Thus, a local deficiency of antithrombin III does not play a major role for the failure of heparin to abolish thrombotic complications during PTCA.

Aged↗

PubMed1981

Dural sinus thrombosis in children with acute lymphoblastic leukemia.

Dural sinus thrombosis developed in two children with acute lymphoblastic leukemia during induction treatment with vincristine sulfate, prednisone, and asparaginase. Headache, nausea, emesis, and lethargy were the presenting signs. The diagnosis was confirmed by arteriography. The cause is presumed to be secondary to hypercoagulability due to asparaginase-induced antithrombin III deficiency. The patients received anticoagulation therapy and recovered completely. Only two of the six reported patients without heparinization survived.

Age Factors↗

PubMed2005

The John Charnley Award: heritable thrombophilia and development of thromboembolic disease after total hip arthroplasty.

UNLABELLED: We retrospectively assessed whether heritable thrombophilia-hypofibrinolysis was more common in patients developing venous thromboembolism after total hip replacement than among control patients who did not develop venous thromboembolism, as an approach to better identify causes of venous thromboembolism after total hip arthroplasty. Twenty patients with proximal deep venous thrombosis after THA and 23 patients with symptomatic pulmonary embolism were compared with 43 control patients who did not have postoperative venous thromboembolism. Five of 42 patients with venous thromboembolism (12%) and 0 of 43 control patients (0%) had antithrombin III deficiency (< 75%). Nine of 42 patients with venous thromboembolism (21%) and 2 of 43 control patients (4.7%) had protein C deficiency (< 70%). Ten of 43 patients with venous thromboembolism (9 heterozygous, 1 homozygous; 23%) and 1 of 43 control patients (heterozygous; 2%) had the prothrombin gene mutation. Patients who had venous thromboembolism after total hip arthroplasty were more likely than matched control patients to have heritable thrombophilia with antithrombin III or protein C deficiency, or homo-heterozygosity for the prothrombin gene mutation. Screening for these three tests of heritable thrombophilia before total hip arthroplasty should improve the identification of patients with a reduced risk of venous thromboembolism who may need only mild thromboprophylaxis, and of those patients with heritable thrombophilia in whom prophylaxis should be more aggressive. LEVEL OF EVIDENCE: Prognostic study, Level II-1 (lesser-quality RCT). See the Guidelines for Authors for a complete description of levels of evidence.

Adult↗

PubMed2006

The relationship between pregnancy induced hypertension and congenital thrombophilia.

OBJECTIVE: To investigate the relationship between some thrombophilic parameters and pregnancy induced hypertension (PIH). METHODS: The study took place at the Department of Obstetrics and Gynecology, Perinatology Unit, Faculty of Medicine, Cukurova University, Turkey, between January 2002 and December 2002. We evaluated 202 patients. Patients were divided into 2 groups: control group comprised 102 normotensive patients >20 weeks of pregnancy without any medical or pregnancy related pathologies and the study group comprised 100 patients over 20 weeks of pregnancy with PIH. These hypertensive patients were divided into 6 sub-groups as follows: eclampsia, severe preeclampsia, preeclampsia, chronic hypertension plus superimposed preeclampsia, eclampsia, and hemolysis elevated liver enzymes and thrombocytopenia (HELLP) syndrome. RESULTS: In all cases, complete blood count, antithrombin III, protein S levels, factor V Leiden mutation, prothrombin 20210 mutation, methylenetetrahydrofolate reductase (MTHFR) 677 mutation and homocysteine levels were studied. Statistical analysis of the data was carried out using SPSS version 11.0 program. In comparing the 2 groups we used Mann-Whitney U tests. In comparing the PIH subgroups we used Kruskal-Wallis tests. The levels of p<0.05 were accepted as statistically significant. CONCLUSION: Antithrombin III deficiency, protein C deficiency, hyperhomocysteinanemia were found to be associated with PIH groups. But protein S deficiency, and homozygote factor V Leiden mutation, prothrombin 20210, MTHFR 677 mutation were not found to be related with PIH.

Antithrombin III Deficiency↗

PubMed1989

Primary hypercoagulable states in general and vascular surgery.

Primary hypercoagulable states are increasingly recognized as causes of venous and arterial thromboembolism in surgical patients. Herein, we describe 10 patients with this syndrome who were diagnosed during a recent 1-year period. A family history and past medical history of thromboembolism and an unusual site of thrombosis are emphasized for accurate diagnosis. Although antithrombin III deficiencies were the most common abnormality found, we describe three patients with hypofibrinolytic syndromes and increased levels of tissue plasminogen activator inhibitor. The effectiveness of anticoagulation therapy in preventing recurrent thromboembolism is stressed.

Adolescent↗

PubMed1996

Resistance to activated protein C, the FV:Q506 allele, and venous thrombosis.

Vitamin K-dependent protein C is an important regulator of blood coagulation. After its activation on the endothelial cell surface by thrombin bound to thrombomodulin, it cleaves and inactivates procoagulant cofactors Va and VIIIa, protein S and intact factor V working as cofactors. Until recently, genetic defects of protein C or protein S were, together with antithrombin III deficiency, the established major causes of familial venous thromboembolism, but they were found in fewer than 5-10% of patients with thrombosis. In 1993, inherited resistance to activated protein C (APC) was described as a major risk factor for venous thrombosis. It is found in up to 60% of patients with venous thrombosis. In more than 90% of cases, the molecular background for the APC resistance is a single point mutation in the factor V gene, which predicts substitution of an arginine (R) at position 506 by a glutamine (Q). Mutated factor V (FV:Q506) is activated by thrombin or factor Xa in normal way, but impaired inactivation of mutated factor Va by APC results in life-long hypercoagulability. The prevalence of the FV:Q506 allele in the general population of Western countries varies between 2 and 15%, whereas it is not found in several other populations with different ethnic backgrounds. Owing to the high prevalence of FV:Q506 in Western populations, it occasionally occurs in patients with deficiency of protein S, protein C, or antithrombin III. Individuals with combined defects suffer more severely from thrombosis, and often at a younger age, than those with single defects, suggesting severe thrombophilia to be a multigenetic disease.

Alleles↗

PubMed1995

Activated protein C resistance: from phenotype to genotype and clinical practice.

The anticoagulant protein C system is an important regulator of the blood coagulation process. Its targets are the procoagulant cofactors factor Va and factor VIIIa, which are cleaved and inactivated by activated protein C, protein S and intact factor V working as cofactors. Genetic defects of protein C or protein S were, together with antithrombin III deficiency, the previously established major causes of familial venous thromboembolism. However, these abnormalities are found in less than 5-10% of patients with thrombosis. Inherited resistance to activated protein C was recently identified as a major risk factor for venous thromboembolism. The activated protein C-resistance phenotype is found in 20-60% of the patients with venous thrombosis, depending on selection criteria and on the prevalence of activated protein C-resistance in the population. The frequency of activated protein C-resistance is 2-10% in the normal populations studied so far. In more than 90% of cases, the molecular background for the activated protein C-resistance is a single point mutation in the factor V gene, which predicts substitution of an arginine at position 506 by a glutamine. Mutated factor V is activated by thrombin or factor Xa in the normal way, but impaired inactivation of mutated factor Va by activated protein C results in a life-long hypercoagulability. Owing to the high prevalence of activated protein C-resistance in the population, it occasionally occurs in patients with deficiency of protein S, protein C or antithrombin III. Individuals with combined defects suffer more severely from thrombosis, and often at a younger age, than those with single defects, suggesting thrombophilia to be a multigenetic disease.

Anticoagulants↗

PubMed1993

[Pulmonary embolism in adolescents].

BACKGROUND: Pulmonary embolism is rare in children, but its incidence is probably underestimated. While its causes are the same as in adults, the role of clotting factor deficiency and oral contraceptive agents has recently been stressed. CASE REPORTS: Case n. 1: A 15 year-old girl was immobilized for an ankle strain. She developed thrombophlebitis of the deep veins of the right leg. The condition was confirmed by Doppler. A phlebogram showed a clot floating in the inferior vena cava. This required the insertion of a clip around it and further thrombectomy. Despite immediate intravenous heparin therapy, the adolescent died of a massive pulmonary embolization. The girl had a congenital antithrombin III deficiency; she was also taking an oral contraceptive. Case n. 2: A 15 year-old suffered from left thoracic pain radiating to the shoulder. Perfusion scintiphotography showed evidence of pulmonary embolism of the left inferior lobe and a phlebogram showed thrombosis of the hypogastric veins. This adolescent was 4 months pregnant. A filter was placed inside the inferior vena cava to permit therapeutic interruption of the pregnancy. The girl was treated with intravenous heparin, followed by antivitamin K with an uneventful course. She suffered from no clotting factor deficiency. CONCLUSION: Pulmonary embolism remains a severe complication of thrombi in the femoral and pelvic veins. It can occur in adolescents, especially those with a congenital clotting factor deficiency, those on oral contraceptives or those who are pregnant.

Adolescent↗

PubMed1999

Primary antiphospholipid syndrome: a cause of catastrophic shunt thrombosis in the newborn.

This is a unique report of systemic-to-pulmonary artery shunt thromboses secondary to primary antiphospholipid syndrome and antithrombin III deficiency in a neonate with cyanotic congenital heart disease. This infant with tricuspid atresia experienced thromboses of two modified Blalock-Taussig shunts en route to a bidirectional cavo-pulmonary shunt and potential future Fontan operation. Chronic warfarin anticoagulation has prevented additional thrombo-embolic events.

Antiphospholipid Syndrome↗

PubMed1990

Fibrinolytic therapy for renal vein thrombosis in the child.

Renal vein thrombosis may lead to significant renal impairment, even death, yet therapy remains controversial. Thrombolytic therapy in general may be attended by significant hemorrhagic complications and has not been used widely in children. We treated a 9-year-old boy with antithrombin III deficiency and acute renal vein thrombosis in a solitary kidney with a selective 48-hour infusion of low dose urokinase with return of renal function. Minor bleeding from a fresh surgical incision was the only morbidity. Such use of fibrinolytic agents in children with acute renal vein thrombosis may prevent significant renal impairment and deserves further clinical trials.

Acute Disease↗

PubMed1987

[Thrombophlebitis of the superior longitudinal sinus in the surgical stage. Apropos of a case. Value of low-molecular weight heparin].

A case of superior sagittal sinus thrombosis is reported. The patient was a 27 years women and thrombosis occurred at 5 weeks pregnancy. This patient had one antithrombin III deficiency. Neurological feature associated hemiplegia and comatose with signs of severe intracranial hypertension (intracranial pressure greater than 50 mmHg). CT scan showed hemorrhagic infarct with man effect (real intracranial hematoma). This case was successful treated by surgical removal and low molecular weight heparin as anticoagulant. The patient recovered rapidly and kept only a slight focal deficit.

Adult↗

PubMed2003

[Obstetric aspects of hereditary thrombophilias: epidemiology, complications and prophylaxis].

The study gives a survey of literature on obstetric aspects of hereditary thrombophilias e.i. factor V Leiden, prothrombin gene 20210A mutation, antithrombin III deficiency, protein C/protein S deficiency, and hyperhomocysteinemia. All types of thrombophilia cause similar pathomorphological changes in placenta and decidua (high number of infarcts and microclots, decidual vasculopathia) as well as insufficient invasion of cytotrophoblast in spiral arteries. The study also discusses prophylactic rules: application of low molecular weight heparin and non-fractionated heparin in prophylaxis and in hyperhomocysteinemia application of folic acid.

Abortion, Habitual↗

PubMed1993

Ischemic stroke in congenital (type II C) defective antithrombin III.

Type II C is a subtype of defective antithrombin III deficiency in which there is a molecular defect in the heparin binding site. Usually, heterozygous patients with this defect have little or no thrombotic symptoms. Ischemic stroke has never been described. We report the case of a young woman who had an episode of right-sided hemiparesis. The computed tomographic scan showed an ischemic lesion in the left hemisphere. There were no previous thrombotic episodes in the patient's history and the sole risk factor for thrombosis was taking of an oral contraceptive. Her family history was midly positive for thrombosis (superficial thrombophlebitis in two relatives). Laboratory tests showed normal antithrombin III antigen, low heparin cofactor activity and an increased slow-moving peak in crossed-immunoelectrophoresis with heparin. The same pattern was found in 7 of 20 relatives. Thus, a diagnosis of congenital type II C defective antithrombin III was made. This report suggests that young patients with ischemic stroke should be screened for defective antithrombin III.

Adult↗

PubMed1995

Involvement of dysplasminogenemia in occurrence of deep vein thrombosis.

Although various hematological disorders have been considered to be etiologic factors in deep vein thrombosis (DVT), the involvement of dysplasminogenemia (DPG) in DVT has not been studied in detail. In 72 consecutive DVT patients, the presence of DVT was suspected based on a history of lower limb swelling and tenderness with acute onset, and was confirmed by duplex scanning, radioisotope venography, or contrast venography. DPG was identified by the observation of dissociation between the activity and antigenicity of plasminogen. Of the 72 patients, 9 (12.5%) were diagnosed as having DPG, and several antithrombin-III deficiency and protein C and S deficiency were identified. The mean age of the genetically normal and DPG patients was 52 +/- 15 and 40 +/- 15 years, respectively (p < 0.05). Thus, these findings suggest that DPG is deeply related to the development of DVT, and that abnormality of the fibrinolytic system is one of the major etiologic factors in DVT.

Adult↗

PubMed2003

A case of cortical vein thrombosis with the cord sign.

BACKGROUND: Computed tomography is performed in suspicious cases of cerebral venous thrombosis. Although an empty delta sign is not uncommonly reported, a cord sign is rarely reported. But this is, if present, pathognomonic, especially in the case of cortical vein thrombosis. CASE DESCRIPTION: A young man with antithrombin III deficiency sought emergency treatment for headache and seizure. Noncontrast computed tomography showed a typical cord sign in multiple sections. It seemed to be independent from the adjacent pathologic findings in most sections. Brain magnetic resonance imaging verified it as a thrombosed vein in conjunction with acute venous infarction. CONCLUSION: The cord sign should be considered for early and accurate diagnosis of cortical vein thrombosis.

Adult↗