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PubMed2004

Frequency of hereditary thrombophilia: an AKUH experience.

OBJECTIVE: To determine the frequency of various causes of hereditary thrombophilia at a referral laboratory and the age and gender distribution. METHODS: This is a descriptive study incorporating a retrospective analysis of requests for thrombophilia screening sent to Clinical laboratory, Aga Khan University Hospital from November 1995 to May 2002. Patients were screened for hereditary causes of thrombophilia including Protein C, Protein S, antithrombin III, Factor V Leiden and homocysteine. Frequency of each disorder; and age and sex distribution was determined. RESULTS: All the patients suspected clinically for thrombophilia were screened. Of the 2825 patients, 70 were diagnosed to have inheritance as a cause of thrombophilia with a frequency of 2.3% for protein C deficiency, 1.4% for protein S deficiency, 1.5% for antithrombin III deficiency, 14.2% for factor V leiden mutation and 2.0% for homocystenemia. CONCLUSION: All the causes of hereditary thrombophilia can be diagnosed by relatively simple laboratory methods, however because of the low frequency of these disorders the screening of general population is not indicated in the absence of clinical symptoms. More prospective studies are required to define the occurrence of these disorders and other causes of thrombosis.

Adolescent↗
PubMed2000

Antithrombin III concentrate in the acute phase of thermal injury.

BACKGROUND: Thermal injury disrupts homeostasis by inducing subclinical disseminated intravascular coagulation, fibrinolysis. and an acquired deficiency of Antithrombin III (ATIII), a natural anticoagulant. As a result, thermally injured patients have a high incidence of hypercoagulability and thrombosis. OBJECTIVE: ATIII (Human) concentrate was given to a thermally injured patient to evaluate safety, and dosage requirements in this setting. DESIGN: The patient was a 40 yr old male with a 68% total burn surface area, right femoral comminuted fracture, and C5-C6 subluxation sustained in a vehicular crash. He received nine infusions of AT III (H) concentrate (100-50 u/kg) within the first four days of injury. RESULT: The ATIII plasma level increased from 45% on admission (normal = 100+/-20%) to 120+/-25% in the next four days. During the 64 day hospitalization, there were 11 grafting procedures with an estimated blood loss (EBL)/procedure: 1140 cc; and EBL/grafted surface area ratio: 0.6 cc cm2. The average time to healing of the meshed autograft was 6.4 days. CONCLUSION: ATIII (H) concentrate can be safely utilized in the acute phase of thermal injury: no excessive bleeding or prolongation of wound healing was documented.

Acute Disease↗
PubMed1996

Hereditary deficiency of protein C, protein S and antithrombin III.

It is estimated that 5% of patients with deep vein thrombosis and 50% of those with recurrent thrombosis have an inherited abnormality of coagulation, most commonly deficiency of protein C, protein S or antithrombin III. These disorders should be suspected when venous thrombosis occurs in a young person, if there is a family history of thrombosis, if thrombosis occurs at an unusual site or if there is recurrent thrombosis with no predisposing factors. Affected patients are treated with lifelong anticoagulation therapy. Thromboembolism and its sequelae often produce abnormal findings on radiologic examinations, and therefore the radiologist who is familiar with these abnormalities is in a position to be the first to suggest the diagnosis.

Adult↗
PubMedDate not supplied

Circadian rhythms of fibrinogen and antithrombin III in liver cirrhosis.

BACKGROUND: Since acquired deficiencies of fibrinogen and antithrombin III are reported in liver cirrhosis and it is known that their plasma levels fluctuate during the day, the circadian rhythms of plasma fibrinogen and plasma antithrombin III were investigated in patients with compensated and decompensated cirrhosis, compared to healthy controls. METHODS: Three groups of subject were considered: (A) 10 healthy controls; (B) 10 patients with compensated liver cirrhosis; (C) 10 patients with decompensated liver cirrhosis. The fibrinogen and antithrombin III levels were determined in blood samples drawn in each studied subject during the span of a whole day and every three hours starting from midnight. The time-related data were analyzed by means of the "mean-group cosinor" method. RESULTS: Significant (p < 0.05) circadian rhythms were detected for the two variables in groups A and B, with peaks in the afternoon hours. No significant (p > 0.05) rhythms were found for group C. A significant (p < 0.05) difference was found between the three groups regarding the circadian rhythm of fibrinogen, and between controls and patients with compensated cirrhosis and between compensated and decompensated patients regarding the circadian rhythm of antithrombin III. CONCLUSIONS: These data suggest that in healthy subjects the plasma levels of fibrinogen and antithrombin III present daily variations with own circadian rhythms, and that liver cirrhosis is associated with chronobiological circadian changes in the coagulation system, related to the stage of the disease. This progressive derangement could be considered as an index of evolution in the natural history of cirrhosis of the liver.

Antithrombin III↗
PubMed1982

[Antithrombin III in infantile nephrotic syndrome].

In the Nephrotic Syndrome an hypercoagulable state can cause an increased incidence of thromboembolic phenomena and the course of the syndrome. The deficiency of Antithrombin III has been suggested to explain the hypercoagulability. We measured plasma antithrombin concentration (as percentage) in 24 children suffering from N.S. and the values were correlated with serum albumin, proteinuria and Partial Thromboplastin Time (PTT). The results of this study show that plasma Antithrombin III (AT-III) is significantly correlated with serum albumin, with proteinuria and PTT. Moreover plasma AT-III concentration was found to be low particularly when patients relapsed and in 2 children who developed thombophlebitis of the safena vein.

Adolescent↗
PubMed2001

Hemostatic effects of antithrombin III supplementation during cardiac surgery: results of a prospective randomized investigation.

Failure to suppress thrombin generation during cardiac surgery promotes fibrin generation, fibrinolysis, and a consumptive coagulopathy. Acquired deficiencies of antithrombin III may play a contributory role. We hypothesized that antithrombin III supplementation to normal physiologic concentrations would decrease thrombin generation and potentially reduce peri-operative bleeding. Twenty patients undergoing coronary artery bypass graft surgery were randomized for this prospective, double-blind, placebo-controlled study. Ten patients received antithrombin III supplementation (50 U/kg) by intravenous infusion prior to incision, and 10 patients received a placebo. Blood samples were obtained pre-operatively, at 1 and 2 h following initiation of cardiopulmonary bypass (CPB), and at 1, 3, and 24 h after completion of CPB. Samples were analyzed for antithrombin III, thrombin-antithrombin III (TAT) complex, and D-dimer concentrations. Cumulative blood loss was recorded at 6 and 12 h after CPB. No statistically significant differences in patient demographics or total heparin dose administered were observed between groups. As expected, plasma antithrombin III concentrations were maintained near pre-operative values in the treatment group, but not in the placebo group. Despite this difference, no statistically significant alterations in generation of TAT complex, D-dimer, or blood loss occurred between groups. Antithrombin III supplementation to maintain normal physiologic concentrations during CPB did not alter significantly thrombin generation, fibrinolytic activity, or blood loss in adults undergoing elective cardiac surgery.

Aged↗
PubMed1994

Coagulation abnormalities in ischaemic optic neuropathy.

The aetiology of non-arteritic ischaemic optic neuropathy (ION) is multifactorial with local anatomical and systemic haemodynamic abnormalities both playing a role. A careful search for treatable vascular disease risk factors is required to allow rational therapy, to optimise the visual prognosis and to allow new insights into pathogenesis. We describe 7 cases in which there was an associated thrombophilic (prothrombotic) state; 4 had deficiencies of the physiological anticoagulants proteins C and S and antithrombin III and 2 had anti-phospholipid antibody (lupus anticoagulant) syndromes. A further patient had reduced levels of the physiological fibrinolytic agent tissue plasminogen activator (t-PA). In 5 patients other risk factors for small vessel occlusive disease were also present, and 4 had recurrent episodes of ION in the same eye. The visual prognosis in these patients may be improved by anticoagulation with warfarin.

Adult↗
PubMed2001

Inherited thrombophilia in ischemic stroke and its pathogenic subtypes.

BACKGROUND AND PURPOSE: One or more of the inherited thrombophilias may be causal risk factor for a proportion of ischemic strokes, but few studies have addressed this association or the association between thrombophilia and pathogenic subtypes of stroke. METHODS: We conducted a case-control study of 219 hospital cases with a first-ever ischemic stroke and 205 randomly selected community control subjects stratified by age, sex, and postal code. With the use of established criteria, cases of stroke were classified by pathogenic subtype in a blinded fashion. The prevalence of conventional vascular risk factors; fasting plasma levels of protein C, protein S, antithrombin III; and genetic tests for the factor V Leiden and the prothrombin 20210A mutation were determined in cases and control subjects. RESULTS: The prevalence of any thrombophilia was 14.7% (95% CI, 9.9% to 19.5%) among cases and 11.7% (95% CI, 7.4% to 17.0%) among control subjects (OR, 1.3; 95% CI, 0.7% to 2.3%). The prevalence of individual thrombophilias among cases ranged from 0.9% (95% CI, 0.1% to 3.4%) for protein S deficiency to 5.2% (95% CI, 0.3% to 9.1%) for antithrombin III deficiency; among control subjects, the prevalence ranged from 1.0% (95% CI, 0.1% to 3.6%) for protein S deficiency to 4.1% (95% CI, 0.2% to 7.8%) for antithrombin III deficiency. There were no significant differences in the prevalence of thrombophilia between cases and control subjects or between pathogenic subtypes of ischemic stroke. CONCLUSIONS: One in 7 patients with first-ever acute ischemic stroke will test positive for one of the inherited thrombophilias, but the relation is likely to be coincidental rather than causal in almost all cases, irrespective of the pathogenic subtype of the ischemic stroke. These results suggest that routine testing for thrombophilia in most patients with acute ischemic stroke may be unnecessary. Whether the thrombophilias may still be important in younger patients with ischemic stroke or in predicting complications (eg, venous thrombosis) and stroke outcome remains uncertain.

Aged↗
PubMed1984

Inhibition of human activated Factor X by antithrombin III and alpha 1-proteinase inhibitor in human plasma.

The inhibition of activated human Factor X by human plasma protease inhibitors was investigated in both purified and plasma systems. In the former, antithrombin III, alpha 1-proteinase inhibitor, and alpha 2-macroglobulin, at normal plasma concentrations, markedly inhibited activated Factor X. Significant inhibition by alpha 2-antiplasmin, however, was only achieved when present at 40 times its plasma concentration. The relative rates of inhibition of activated Factor X coagulant activity in normal human plasma, antithrombin III-deficient plasma, and alpha 1-proteinase inhibitor-deficient plasma were 1.0, 0.63, and 0.75, respectively. From these relative rates of inhibition and their measured concentrations in the 3 plasmas, it was calculated that antithrombin III, alpha 1-proteinase inhibitor, and alpha 2-macroglobulin contribute 53, 35, and 12%, respectively, to the inhibition of activated Factor X in normal human plasma. Using 125I-labeled activated Factor X and a combination of sodium dodecyl sulfate disc gel electrophoresis and immunoadsorption, it was then demonstrated that antithrombin III accounted for 45-55%, alpha 1-proteinase inhibitor, 35-40%, and alpha 2-macroglobulin, 10-15% of the inhibition of the labeled protease in normal human plasma. The values obtained with the deficient plasmas are consistent with the distribution of activated Factor X-inhibitor complexes in normal human plasma. These data show by two independent techniques, one measuring coagulant activity and the other 125I-labeled activated Factor X-inhibitor complexes, that both antithrombin III and alpha 1-proteinase inhibitor are the major inhibitors of activated Factor X in normal human plasma.

Antithrombin III↗
PubMed1991

[A case of congenital antithrombin II deficiency with pulmonary infarction].

A 48-year-old woman was admitted because of increased bloody sputum. Since she had had a history of repeated thrombotic episodes including venous thrombosis in the lower limbs (21 year old) and pulmonary emboli developing into pulmonary infarction (41 years old), the patient was treated with anti-coagulant therapy using Warfarin for 7 years. Warfarin was discontinued after admission and heparin was administered instead at a relatively low dose of 5,000 units daily, resulting in a considerable diminution of hemoptysis. Unfortunately however, it caused a relapse of active thrombosis associated not only with a significant increase of the product of fibrinolysis (FDP), LDH and GOT but with a concomitant decrease of the platelet count. Hematological examinations concerning coagulation and fibrinolysis remained within a normal range except for the serum concentration of antithrombin III (AT III) and its functional property with regard to the heparin cofactor, which were 8.8 mg/dl and 48%, respectively. Since the findings were consistent with congenital deficiency of AT III, some members of her family were also examined. The concentration of AT III and its activity in the patient's son and her daughter deteriorated in a similar manner, indicating that this was a definite case of congenital deficiency of AT III. The clinical manifestations of 87 cases with congenital AT III deficiency, belonging to 24 families reported in Japan were reviewed.

Antithrombin III↗
PubMed1989

[Use of antithrombin III concentrates].

Concentrates of antithrombin III (AT III) have been applied in congenital as well as in acquired AT III deficiency. Congenital defects only require substitution during surgery and in the case of pregnancy. Otherwise prophylaxis of thrombosis can be successfully carried out with oral anticoagulants. In acquired AT III deficiency substitution was found to be useful in cases of advanced DIC. When AT III activity was constantly kept around 100% the duration of DIC could be considerably shortened. No beneficial effect of additional administration of heparin was found. In cases of DIC due to septic shock the survival rate could be increased from an average of 20% without substitution to over 70% with AT III substitution as could be shown by different authors.

Antithrombin III↗