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PubMed1984

Substitution of antithrombin III.

AT III substitution is indicated in patients with inherited antithrombin III deficiency if these patients suffer acute thrombosis, if they have to be treated surgically and in the case of pregnancy in women with AT III deficiency who have an abortion or thrombosis, as well as during and after delivery. In acquired antithrombin III deficiency such as in patients with liver cirrhosis or the nephrotic syndrome, AT III substitution may be necessary if thrombotic complications occur. AT III substitution has been propagated especially in patients with polytrauma, septicaemia, DIC, acute liver failure and in toxaemia. In AT III substitution initial doses of 1 U/kg body weight are used to reach a 1,5% rise in plasma AT III level. If AT III turnover is normal a rise above 80% of normal should be achieved. If AT III turnover is increased, much higher initial and maintenance doses may be needed to normalize plasma AT III levels and to block DIC.

Antithrombin III↗
PubMed1986

Management of anti-thrombin III deficiency during pregnancy without administration of anti-thrombin III.

We report a patient with hereditary antithrombin III deficiency who was successfully treated with heparin throughout pregnancy. Functional antithrombin III levels fell to 0.32 U/ml during heparin treatment, but it was possible to achieve a heparin effect, measured by the activated partial thromboplastin time, thrombin clotting time and heparin assay with subcutaneous heparin in doses of 30,000 U to 35,000 U/24 hours. This achieve an long term heparin effect was obtained without the need for antithrombin III infusions.

Adolescent↗
PubMed1995

[Hemorrhagic cerebral infarction at the old age in a case with familial antithrombin III (ATIII) deficiency].

An old woman had stroke at age 67. Cerebral CT scan disclosed the low-density lesion with high-density area in the left temporal lobe, but no empty delta sign in the superior sagittal sinus. Thereafter, she had sometimes panic attacks. At the age of 70, she was admitted because of loss of consciousness probably caused by the same attack. On admission, Brain CT scan showed no fresh lesions. During the stay in the hospital, she had an episode of deep vein thrombosis of her left leg. The patient was found to have not only reduced biochemical activity but also low immunological level of AT III. Her nephew had also the low plasma AT III antigen concentration. Transesophageal echocardiography showed no abnormality, but atherosclerotic change at the aortic arch. We speculated that hemorrhagic cerebral infarction in the territory of the branch of middle cerebral artery could be induced by the arterial thrombus which was related to the hypercoagulable state associated with familial AT III deficiency, although the possibility of cardiogenic embolic infarction or of cerebral vein thrombosis could not be ruled out. Familial AT III deficiency is one of the causes of cerebral infarction even in the elderly.

Aged↗
PubMed2002

Hereditary deficiencies of antithrombin III, protein S, and the protein C pathway in Jordanian thrombosis patients.

Hereditary thrombophilia is caused by various inherited disorders. Most lead to a familial tendency to recurrent venous, not arterial, thrombosis, usually at a young age, and with spontaneous onset. Most of the genetic defects known today affect the function of natural anticoagulant pathways, in particular, the protein C system. In this study, 602 (265 female, 337 male) patients with suspected thrombosis, arterial or venous, were referred to King Hussein Medical Center in Amman, Jordan. The prevalence of hereditary deficiencies of antithrombin (AT), protein S (PS), and protein C (PC) were studied over a seven-year period (1993-2000). Activated protein C (APC-R) resistance subjects were studied over four years (1996-2000). The mean age was 30 years in females and 42 years in males. A diagnosis was established in 22.4% (n = 135) of the subjects (20.3% venous, 2.1% arterial). Protein C deficiency was found in 3.8%, protein S deficiency in 2.3% and antithrombin deficiency in 1.4% of our sample group. An APC-R problem was seen in 23.0% (n = 89) of the surveyed population. Out of the APC-R patients, 75.0% had the DNA analysis of a factor V Leiden mutation present. Of the subjects found to have the mutation 87.0% were heterozygous and 13.0% were homozygous. These results confirm that APC-R, as a result of factor V Leiden mutation, is the most prevalent cause of thrombosis, and thrombophilia is related to venous, not arterial, thrombosis.

Adolescent↗
PubMed1981

Transfusion studies in patients with familial antithrombin III (ATIII) deficiency: half-disappearance time of infused ATIII and influence of such infusion on platelet life-span.

Two patients with familial ATIII deficiency received infusions of a concentrate of ATIII prepared from human plasma. Serial plasma samples were assayed for their functional and immunological content of ATIII. The rates of disappearance of ATIII activity found in this study suggest that, initially, frequent infusions are necessary to maintain normal levels of ATIII activity in patients with a severe deficiency. In one patient platelet survival did not appear to be influenced by ATIII infusions.

Adult↗
PubMed1997

Application of argatroban, direct thrombin inhibitor, in heparin-intolerant patients requiring extracorporeal circulation.

This study describes the present knowledge regarding the clinical application of argatroban, a direct competitive thrombin inhibitor for heparin-intolerant patients, including those with congenital and acquired antithrombin III deficiencies, those with heparin-induced thrombocytopenia, and those with high levels of polymorphonuclear granulocyte elastase. These patients are often associated with intracircuit clot formation with heparin anticoagulation during extracorporeal circulation. Therefore, argatroban may be chosen as one of the alternate anticoagulants. Because the anticoagulant effect of argatroban is reflected in the prolongation of activated thromboplastin time, monitoring is easy, similar to that for heparin. Because argatroban has a fast acting anticoagulant effect without any cofactors such as antithrombin III, this drug is a favorable anticoagulant for heparin-intolerant patients with antithrombin III deficiencies requiring extracorporeal circulation. In adverse reactions to heparin, heparin acts as an antigen after complexing with platelet factor 4, which leads to life-threatening heparin-induced thrombocytopenia. As argatroban prevents heparin-induced platelet aggregation, it is effective for use as a therapeutic anticoagulant. In other clinical applications, heparin decreases antithrombin activity and causes intracircuit clot formation during extracorporeal circulation when the polymorphonuclear granulocyte elastase level is very high. The antithrombin activity shows less decrease when argatroban is substituted for heparin. These findings indicate that argatroban is a useful alternative anticoagulant in these heparin-intolerant patients.

Anticoagulants↗
PubMed1992

[A cases of antithrombin III (ATIII) deficiency associated with extrahepatic portal occlusion undergoing operation for esophgogastric varices].

A 23-year-old woman developed thrombosis of the superior mesenteric vein and underwent an extensive enterectomy. She was diagnosed to have ATIII deficiency with extrahepatic portal vein thrombosis and esophagogastric varices. She was admitted to our department and underwent esophageal mucosal transection and splenectomy. Her activities of ATIII were 46%, but ATIII activities of her family were over 90%. ATIII activities during perioperative period were kept more than 70% following administration of ATIII drug. After splenectomy thrombocythemia which was over 300 x 10(4)/mm3 appeared with severe headache and slight pain of hands. She was discharged on 76th postoperative day with no complications and collapse of esophageal varices.

Adult↗
PubMed1996

[Mesenteric vein infarction associated with congenital antithrombin III (ATIII) deficiency].

A venous mesenteric infarction in a 27-year-old patient is reported. This patient presented a genetic quantitative AT-III deficiency without anticoagulation therapy. Ultrasonography revealed portal vein thrombosis and laparoscopy showed mesenteric vein infarction. Laparotomy was performed mmediately and revealed segmental infarction of 60 cm of the jejunum which was resected; the portal vein was considered to be partially occluded on palpation. No strangulation or mechanical factors were identified. Immediately postoperatively the patient received therapeutic doses of heparin with AT-III concentrates to increase AT-III levels; no recurrent thrombotic episode was observed. A systematic second-look operation 24 hours postoperatively showed good bowel viability. Five days later, long-term anticoagulation with acenocoumarol was decided. Twelve days later, ultrasonography showed complete portal revascularization which was confirmed by a third surgical operation on D60.

Adult↗
PubMed1999

Coagulation abnormalities in idiopathic portal venous thrombosis.

BACKGROUND: Portal vein thrombosis, usually idiopathic, is the cause of portal hypertension in 46% of Indian patients, who present with a variceal bleed. The presence of lupus anticoagulant (LA) and antithrombin III deficiency have been reported to be associated with an increased tendency to venous thrombosis. METHODS AND RESULTS: We studied 30 patients with portal venous thrombosis diagnosed by ultrasound. Two patients were positive for a lupus anticoagulant and both had very prolonged partial thromboplastin time with kaolin. None of the patients had antithrombin III deficiency.

Adolescent↗
PubMed1991

Management of thrombophilia in pregnancy.

Thromboembolism remains a major cause of maternal morbidity and mortality. The incidence of thrombosis associated with pregnancy is stated to be around 0.09%1 but is greater in women with familial or acquired thrombophilia. Around 50% of pregnancies in women with antithrombin III deficiency are complicated by thrombosis. Anticoagulation throughout pregnancy and the puerperium is recommended in women with antithrombin III deficiency. Because thrombosis is less common in women with protein C or protein S deficiency less aggressive management may be appropriate during pregnancy but anticoagulation post partum is generally recommended. The most important acquired thrombophilic abnormality is the development of antiphospholipid antibodies ('lupus anticoagulants'). Women with these antibodies may present major problems but no clear guidelines for their management currently exist. The majority of women with a history of thrombosis have no identifiable haemostatic abnormality. Management of pregnancy in these patients depends on individual circumstances.

Blood Coagulation Disorders↗
PubMed1984

Myocardial infarction and severe thromboembolic complications. As seen in an estrogen-dependent transsexual.

An estrogen-dependent genetic-male transsexual had an extensive anterior wall myocardial infarction, despite insignificant coronary artery disease, a subsequent mural thrombosis, and resultant multiple cardioarterial thromboembolic events, despite heparin therapy. With an otherwise lack of cardiac risk factors, the patient was demonstrated to have an antithrombin III deficiency that resolved when conjugated estrogen therapy was withdrawn. Although congenital, plasminogen-activator dysfunction, or heparin-induced etiologies could not be ruled out, we believe this case demonstrated an estrogen-induced-antithrombin III deficiency culminating in thrombotic diathesis. This identifies a previously unrecognized population at risk. Prophylactic and therapeutic considerations are discussed.

Adult↗
PubMed1997

Protein C, protein S and antithrombin III in children with portal vein obstruction.

BACKGROUND/AIMS: Portal vein obstruction is the most common single cause of portal hypertension in children and its cause is unknown in most instances. The aim of the present study was to evaluate the incidence of protein C, protein S and antithrombin III deficiencies and to screen for possible genetic deficiencies of these proteins. METHODS: A prospective study was undertaken in 20 consecutive children with portal vein obstruction, their parents and 20 matched healthy children. RESULTS: Children with portal vein obstruction displayed a reduction in protein C (p<0.05), protein S (p<0.0001), and antithrombin III (p<0.001) activities as compared with controls. Protein C and protein S activities were below 60% in nine and eleven of the children with portal vein obstruction, respectively, and antithrombin III activities were below or equal to 85% in ten of them. Repeated assay of protein C activity in seven children following a surgical portosystemic shunt showed a decrease as compared with preoperative values. Protein C, protein S and antithrombin III were normal in all parents, except two mothers in whom the levels of protein S activity and protein S antigen were found to be either below or at the lower limit of the normal range. CONCLUSIONS: These results indicate that protein C, protein S and/or antithrombin III deficiencies are frequently found in children with portal vein obstruction but are not likely to be of genetic origin in most cases.

Adolescent↗
PubMed1979

Diagnostic problems in thromboembolism.

Some pathogenetic aspects and diagnostic problems in venous thrombosis are briefly discussed. Emphasis is put on the value of blood tests. It is concluded that the various tests are neither able to detect ongoing thrombosis, nor to identify a prethrombotic state. The necessity of direct demonstration of the thrombus preferably by phlebography is stressed. The tests are valuable as a part of the "coagulation profile", and may aid to discover e.g. antithrombin III deficiency or subnormal fibrinolytic activity.

Antigen-Antibody Complex↗
PubMedDate not supplied

[Multiple thromboembolism associated with anti-thrombin III deficiency].

Congenital deficiency of antithrombin III is considered as one serious primary hypercoagulable state. The authors present a case of deficiency of antithrombin III in a 28 years old young male, with aortic valve disease and several thromboembolic events. When discussing their diagnostical and therapeutical aspects they call the attention to the need for investigation of the situations in which thrombophilia presents with recurrent venous and arterial thrombosis.

Adult↗
PubMed1995

Antithrombin III concentrates--are they clinically useful?

Treatment with AT III concentrates is a good example for the discrepancy between the optimistic expectations based on theoretical considerations or animal experiments and the result of clinical studies. 15 years after the introduction into clinical practice, a benefit for patients treated with AT III concentrates has not been proven. In hereditary antithrombin III deficiency, randomized clinical trials are completely lacking and only few and small sized randomized studies were performed in patients with acquired AT III deficiency. In none of these trials, a significant clinical benefit with regard to reduction of morbidity or mortality was detectable. Based on the published data, one can state that AT III concentrates may be beneficial in some special clinical situations in patients with hereditary antithrombin III deficiency (such as delivery, acute serious thromboembolic complications and postoperative thromboprophylaxis). In acquired AT III deficiency, there is no proven indication for the use of AT III concentrates.

Antithrombin III↗
PubMed1998

Prevalence of the factor V leiden mutation in children and neonates with thromboembolic disease.

OBJECTIVE: Resistance to activated protein C (APC) has been identified as a risk factor for thrombotic disease in adults. In over 90% of cases, the basis for the APC resistance is a mutation in the coagulation factor V gene (factor V Leiden) that renders the protein more resistant to inactivation by APC. We sought to determine the prevalence of the factor V Leiden (FVL) mutation in neonates and children who had experienced an arterial or venous thromboembolic event. STUDY DESIGN: We retrospectively analyzed the clinical records of 33 neonates and 52 children with thromboembolic disease. Screening for the FVL mutation was performed by DNA analysis, allowing for identification of patients as normal, heterozygous, or homozygous. RESULTS: Of the 85 patients studied, 12 (14.1%) were heterozygous for FVL; none were homozygous. Of the 47 patients who had arterial central nervous system events, 8 (17%) were positive for the FVL mutation, including 6 of 22 (27%) neonates. Of those patients who had a venous thrombosis, 4 of 32 (12.5%) were FVL positive. None of the 85 patients had protein C deficiency, 3.5% had protein S deficiency, 1.2% had antithrombin III deficiency, and 16.5% had anti-phospholipid antibodies. CONCLUSION: These data suggest that the FVL mutation plays a role in the development of arterial and venous thrombotic events in neonates and children.

Adolescent↗