PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Antithrombin III Deficiency”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources
PubMed1992

The prevalence of factor XII deficiency in 103 orally anticoagulated outpatients suffering from recurrent venous and/or arterial thromboembolism.

One hundred and three patients suffering from recurrent venous thrombosis, recurrent arterial thromboembolism and/or recurrent myocardial infarction and 50 healthy subjects were tested for Hageman factor (FXII) coagulant activity and antigen. Among the 103 patients we identified 15 subjects with FXII deficiency (15%), 3 with protein C deficiency (3%) and 3 with protein S deficiency (3%). Combined FXII and protein C, protein S or antithrombin III deficiency was not observed. The 103 patients were divided into subgroups according to the type of thrombotic complication. Among patients with exclusively recurrent venous thromboembolism 8% (p = 0.153) were deficient in FXII. Among patients suffering from recurrent arterial thromboembolism and/or myocardial infarction, the incidence of FXII deficiency was significantly higher (20%, p less than 0.003). In 67% of the patients with FXII deficiency a positive family history of thrombosis could be established. In contrast, only 32% of all venous and 28% of all arterial thrombosis patients had a positive family history. We believe that reduced levels of FXII should be considered as a risk factor in the development of thromboembolism. Consequently, more attention should be payed to the measurement of FXII when evaluating thromboembolic risk factors especially in cases of recurrent arterial thromboembolism and/or myocardial infarction.

Acenocoumarol↗
PubMed1988

Unexplained thromboembolism. When to suspect antithrombin III, protein C, or protein S deficiency.

Patients with recurrent or unusual thromboembolic events may have abnormalities in regulation of hemostasis because of inherited or acquired deficiencies of antithrombin III, protein C, or protein S. A working knowledge of the clotting process and a high degree of suspicion are needed to guide the clinician in this difficult diagnosis. Prompt and appropriate anticoagulant therapy can be lifesaving in these patients.

Antithrombin III Deficiency↗
PubMed1984

Congenital anti-thrombin III deficiency with mesenteric venous thrombosis--functional and immunological estimations.

Familial antithrombin III (AT III) deficiency, with mesenteric venous thrombosis, is reported in an Australian family. Antithrombin III was assayed chromogenically, fluorometrically, and immunologically. The deficiency was further analysed using crossed-immunoelectrophoresis. It is suggested that when AT III deficiency is suspected, both a functional and an immunological assay should be performed.

Adolescent↗
PubMed1991

Antithrombin III: a database of mutations.

Elucidation of the molecular defects responsible for antithrombin III deficiency is proceeding rapidly. In order that a record is kept of the new and duplicated mutations that are found, we have compiled a database that we plan to update annually. In this, the first report of the database, we list 6 antithrombin III locus sequence polymorphisms and 94 recorded mutations causing functional deficiency of the protein, 38 of which are novel. As is the case with mutations affecting other protein genes, most mutations of antithrombin III involve a CG to TG or CA change.

Antithrombin III↗
PubMed1988

[Rapid determination of protein C activity].

The diagnosis of Protein C (PC) congenital deficiency is of first importance because it leads, more frequently than Antithrombin III deficiency, to serious thromboembolic accidents in young patients, even when PC levels are slightly decreased (40 p. cent up to 60 p. cent). In order to measure PC activity, the authors developed a new method using the activator from Agkistrodon C. Contortrix snake venom and the synthetic chromogenic substrate CBS 65-25. Results obtained on plasma from normal individuals, congenital and acquired deficiencies, are comparable on the one hand, to those found with an ELISA method, and on the other hand with the clotting method, except for patients under anticoagulant therapy. This new rapid and sensitive method can be performed manually and is easily adapted on instruments used in clinical chemistry laboratories. This method is potentially available for routine use.

Adult↗
PubMed1993

[Factor XII (Hageman factor) deficiency: a risk factor for development of thromboembolism. Incidence of factor XII deficiency in patients after recurrent venous or arterial thromboembolism and myocardial infarction].

103 patients suffering from recurrent venous thrombosis, recurrent arterial thromboembolism and/or recurrent myocardial infarction and 50 healthy subjects were tested for Hageman factor (F XII) coagulant activity and antigen. Among the 103 patients we identified 15 subjects with F XII deficiency (15%), 3 with protein C deficiency (3%) and 3 with protein S deficiency (3%). Combined F XII and protein C, protein S or antithrombin III deficiency was not observed. The 103 patients were divided into subgroups according to the type of thrombotic complication. Among patients with exclusively recurrent venous thromboembolism 8% (p = 0.153) were deficient in F XII. Among patients suffering from recurrent arterial thromboembolism and/or myocardial infarction, the incidence of F XII deficiency was significantly higher (20%, p < 0.003). In 67% of the patients with F XII deficiency a positive family history of thrombosis could be established. In contrast, only 32% (p = 0.043) of all venous and 28% (p = 0.019) of all arterial thrombosis patients had a positive family history. We believe that reduced levels of F XII should be considered as a risk factor in the development of thromboembolism. Consequently, more attention should be payed to the measurement of F XII when evaluating thromboembolic risk factors especially in cases of recurrent arterial thromboembolism and/or myocardial infarction.

Adult↗
PubMed1985

A Swedish family with abnormal antithrombin III.

An abnormal variant of antithrombin III is reported in a young male with deep vein thrombosis. The heparin cofactor, progressive thrombin inhibition, and factor Xa inactivation are decreased. The abnormality seems to be a mutation which is transmitted in an autosomaldominant way. The half-life and fractional catabolic rate of 125I antithrombin III concentrate is the same in this patient as in patients with the classic type of antithrombin III deficiency and in a control.

Adult↗
PubMed1989

Blood component therapy. New guidelines for avoiding complications.

Transfusion medicine is an expanding subspecialty that continues to be reshaped and redefined. The current indications for red blood cell (RBC) transfusion are the presence of tissue hypoxia or a hemoglobin level of less than 7 g/dL. Platelet concentrates should be given prophylactically for severe thrombocytopenia secondary to production defects. In the patient who is in need of an invasive procedure or is bleeding, therapeutic platelet transfusion may be needed if the platelet count is less than 50,000/microL or the bleeding time is twice the upper limit of normal or more. Both RBC and platelet transfusion should be avoided if specific therapy is available for the underlying condition. Transfusion of fresh frozen plasma is indicated for reversal of inherited isolated coagulation factor deficiencies, emergent reversal of the effects of warfarin sodium (Coumadin, Panwarfin, Sofarin), antithrombin III deficiency, and thrombotic thrombocytopenic purpura. No blood transfusion is without risk to the recipient. Two of the major transfusion-related complications are alloimmunization and graft-versus-host disease. Techniques for preventing these conditions are available.

Blood Transfusion↗
PubMed1993

Peripheral arterial thrombosis in the nephrotic syndrome.

Peripheral arterial thrombosis is a rare complication of nephrotic syndrome that occurs in conjunction with a hypercoagulable state and results in a high rate of limb loss and death. We report a case of brachial artery thrombosis in a pediatric patient with nephrotic syndrome, antithrombin III deficiency, and antecedent vessel trauma. An extensive review of the literature is presented. We conclude that management of arterial thrombosis requires aggressive replenishment of antithrombin III and adequate heparinization in addition to the traditional surgical management. Moreover, arterial puncture should be avoided because of the high risk of thrombosis in these patients.

Adolescent↗
PubMed2003

Venous thrombosis: prevalence of prothrombotic defects in north Indian population.

431 patients with thrombosis of different venous system were evaluated for underlying acquired and inherited prothrombotic states. Associated acquired risk factors were observed to be present in 28.7% patients and possible inherited in 32.3%, in the rest, no cause could be identified. Major acquired risk factors included coexistence of liver disease (12.2%), oral contraceptives (4.1%), puerperium (2.5%), malignancy (2.3%) and lupus anticoagulant (2%). Low levels of protein C were detected in 21.1% and of which 11.3% were attributed to acquired factors. Protein S deficiency was found in 19.0% and of these 10.4% cases were associated with acquired risk factors. Antithrombin III (AT III) deficiency was detected in 6.4% of patients, of which 4.8% were secondary to acquired factors. In the rest, deficiency of protein C, protein S and AT III were attributed to inherited factors as no associated acquired risk factor was present. Activated protein C resistance (APC-R) was present in 12.5% cases.

Adolescent↗
PubMed2003

Mesenteric ischemia affects young adults with predisposition.

An 8-year retrospective review of Indiana University Hospital records consisting of any patient age 18 to 40 years old who presented with arterial mesenteric ischemia was performed. Three patients were identified that met our criteria. The first patient was discovered to have a protein C deficiency. The second patient was afflicted with afibrinoginemia, a protein C and an antithrombin III deficiency. The third patient had been previously diagnosed with Takayasu's arteritis and had an elevated ESR. Each patient had a protracted course of symptoms before mesenteric disease was considered, confirmed by angiography, and treated by arterial bypass with/without bowel resection. All patients survived and are currently asymptomatic at an average of 2 years postoperatively. Mesenteric ischemia in patients under the age of 40, especially in the absence of cocaine use, is rare and often causes a delay in diagnosis and appropriate treatment. The high incidence of hypercoagulable states in our study cases suggests the need for a search for such disorders and the possible need for long-term anticoagulation therapy as a deterrent to recurrence.

Adult↗
PubMed1989

Mesenteric venous thrombosis.

Sixteen patients with mesenteric venous thrombosis were reviewed retrospectively during a period from 1983 to 1987. Twelve patients had progressive abdominal pain, three had gastrointestinal bleeding, and one had general malaise. Seven of these 16 patients had previous deep-vein thrombosis. After negative routine gastrointestinal and hepatobiliary evaluation, 11 patients underwent an infusion computerized tomographic scan. Of these, 10 had superior mesenteric vein thrombosis; three of these 10 patients had portal vein thrombosis. Selective arteriography was done in two patients because of gastrointestinal bleeding, and a diagnosis of mesenteric vein thrombosis was made on the venous phase of the examination. The remaining four patients developed acute abdominal symptoms requiring surgical exploration, at which time mesenteric venous thrombosis was discovered. An identifiable coagulopathy was detected in nine patients (protein C deficiency in six, protein S deficiency in two, and factor IX deficiency treated with factor IX concentrate in one). No case of congenital antithrombin-III deficiency was identified. Six of these nine patients had a past history of deep venous thrombosis. Of five patients who underwent surgical exploration, all required bowel resection. In follow-up, two patients died of intestinal necrosis and a third died of associated pancreatic cancer. Thirteen patients were discharged from the hospital. Treatment of coagulopathy was by heparin in three patients and sodium warfarin (Coumadin) in four patients. Long-term anticoagulation was not instituted because of gastrointestinal bleeding in three and cirrhosis in three patients. Mesenteric venous thrombosis can occur without gangrenous bowel. Diagnosis should be suspected when acute abdominal symptoms develop in patients with prior thrombotic episodes and a coagulopathy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Free protein S deficiency in a family with venous thrombosis.

Inherited deficiencies of protein S, an inhibitor of the coagulation system, are now recognized as occurring at least twice as frequently as antithrombin III deficiency in patients with venous thrombosis. Protein S is present in plasma in a complexed form, which is inactive, and in a free or functional form. Free protein S combines with activated protein C to inhibit factors V and VIII. This report describes the evaluation of a family with recurrent deep venous thrombosis and superficial thrombophlebitis. Levels of antithrombin III and protein C as well as plasminogen were normal. The levels of total protein S, which includes the value for the free and complexed forms of protein S, were also normal. However, the free protein S levels were greatly reduced in all symptomatic members who were studied. This report illustrates the importance of obtaining measurement of free protein S levels in patients who are suspected of having inherited venous thrombotic disorders.

Adult↗
PubMed1995

Cerebral venous thrombosis in adults. A study of 40 cases from Saudi Arabia.

BACKGROUND AND PURPOSE: We undertook this study to determine the frequency, clinical patterns, and etiologies of cerebral venous thrombosis in a Middle Eastern country. METHODS: Records of all adults patients admitted with an angiographically documented diagnosis of cerebral venous thrombosis from 1985 through 1994 in two major hospitals of Riyadh, Saudi Arabia, were reviewed. RESULTS: Forty patients (20 men, 20 women) aged 16 to 40 years were identified. Hospital frequency was 7 per 100,000 patients, and the relative frequency against arterial strokes was 1:62.5. Nineteen cases (47%) had a clinical picture of pseudotumor cerebri. Behçet's disease was the cause in 10 cases (25%). Other causes included antiphospholipid antibodies in 4, protein S deficiency in 3, intracranial tumors in 3, systemic lupus erythematosus in 3, infections in 3, antithrombin III deficiency in 2, postpartum in 1, and oral contraceptives in 1. CONCLUSIONS: Cerebral venous thrombosis in adults is not uncommon in Saudi Arabia. Behçet's disease is the single most common etiology. Infection is no longer an important cause, whereas "new" coagulation disorders are common. Patients with a pseudotumor cerebri syndrome should undergo angiography or brain MRI before being labeled idiopathic.

Adolescent↗
PubMed1997

Hyperhomocysteinaemia and protein S deficiency in complicated pregnancies.

OBJECTIVE: The aim of our study was to investigate whether women with placental abruption, intrauterine fetal death or small for gestational age infants have metabolic and/or haemostatic abnormalities which are known to be risk factors for intravascular thrombosis. DESIGN: For two years blood tests were performed at > 10 weeks after delivery on all women without hypertensive disorders either before or during pregnancy, who had been consecutively admitted to our hospital with placental abruption, intrauterine fetal death and small for gestational age. SAMPLE: A total of 62 women who had placental abruption (n = 31), intrauterine fetal death (n = 18) and a small for gestational age infant (n = 13). SETTING: Obstetric outpatient clinic in a university hospital (Free University Hospital, Amsterdam). METHODS: Presence of hyperhomocysteinaemia, various coagulation abnormalities and anticardiolipins was investigated. RESULTS: Abnormalities were found in 20 women in the placental abruption group (20/31, 65%), in 10 women in the intrauterine fetal death group (10/18, 56%) and in 11 women in the small for gestational age group (11/13, 85%). Eight out of these 31 women had more than one abnormality. In the group of 62 women protein S deficiency was demonstrated in 26%, hyperhomocysteinaemia in 24%, Protein C deficiency in 6%, anticardiolipin IgG in 11%, anticardiolipin IgM in 5%, Lupus anticoagulant in 2%. An antithrombin III deficiency was not found. Thirty-three women were tested for activated protein C resistance (9% positive) and factor V Leiden mutation (6% positive). Hyperhomocysteinaemia was treated with a daily oral dose of 250 mg pyridoxine and 5 mg folic acid. After six weeks of vitamin supplementation homocysteine levels were tested again. At that time a mean reduction of fasting homocysteine value of 68% (95% CI 57-79) was found and of post-load value of 65% (95% CI 55-76). CONCLUSIONS: Based on the results of our study, it can be concluded that women whose pregnancies are complicated by either placental abruption, intrauterine fetal death or small for gestational age, even if there is no history of thrombo-embolic disorders or hypertension during pregnancy, should be advised to undergo an examination for metabolic and/or haemostatic abnormalities.

Abruptio Placentae↗
PubMed2005

Ischemic stroke subtypes and thrombophilia in young and elderly Brazilian stroke patients admitted to a rehabilitation hospital.

BACKGROUND AND PURPOSE: We sought to examine ischemic stroke subtypes and prevalence of thrombophilia in Brazilian stroke patients. METHOD: A total of 130 consecutive young and 200 elderly stroke patients were studied. RESULTS: Prevalence of thrombophilia was, respectively: protein S deficiency (11.5% versus 5.5%), protein C deficiency (0.76% versus 1%), resistance to activated protein C (2.3% versus 3.5%), mutation in V Leiden factor (1.5% versus 2%), antithrombin III deficiency (0% versus 0%), lupus anticoagulant (0% versus 0.5%), anticardiolipin antibodies (3% versus 10%; P=0.01), hyperhomocysteinemia (31.5% versus 53.5%; P=0.0001), mutation of the MTHFR gene in homocigosis (10% versus 5%), and heterocigosis (27.6% versus 41.9%; P=0.01). CONCLUSIONS: Prothrombotic conditions were more frequent in stroke of undetermined cause.

Activated Protein C Resistance↗
PubMed1997

Preeclampsia is associated with a reduced response to activated protein C.

OBJECTIVE: Resistance to activated protein C is an inherited mutation of the coagulation factor V gene, a major factor predisposing to thromboembolic events. The purpose of this study was to investigate the occurrence of heterozygote and homozygote activated protein C resistance in women with preeclampsia. STUDY DESIGN: Activated protein C resistance and protein C and antithrombin III levels were determined in women (n = 50) with a history of preeclampsia and in controls (50 women with a previous normal pregnancy). The mutation of the factor V gene was analyzed. RESULTS: Activated protein C resistance was found in 22% of women with previous preeclampsia compared with 10% among controls. Two women in the previous preeclampsia group had a homozygote mutation of factor V; the others were heterozygous. There was a significant difference in the activated protein C ratio between women with previous preeclampsia and the control group, 2.6 +/- 0.4 versus 3.1 +/- 0.5 (p = 0.04). None of the women had protein C or antithrombin III deficiency. CONCLUSION: The results indicate that activated protein C resistance may be a contributory factor in the pathogenesis of preeclampsia.

Antithrombin III↗