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At least 163 records · Page 9Linked to original sources
PubMed1999

[Heparin cofactor II, a thrombin inhibitor with a still not clarified physiologic role].

Heparin Cofactor II (HCII) is a glycoprotein in human plasma which inactivates thrombin rapidly in the presence of dermatan sulfate. Inhibition occurs by formation of a stable equimolar complex between HCII and thrombin. HCII association with thrombotic events has not always been observed, thus decreased HCII does not appear to be a strong risk factor for thromboembolic events. Reduced HCII levels have been detected in different clinical conditions, such as hepatic failure, disseminated intravascular coagulation, thalasemina, sickle cell anemia. Increased physiological levels have been found in pregnant women and oral contraception. In our laboratory, we measured HCII plasmatic levels in the normal Buenos Aires city population and in patients under different clinical conditions, such as sepsis, diabetis, burns, oral anticoagulation and in patients treated with heparin, hyperhomcysteinemia in whom septic and diabetic patients showed decreased values. HCII thrombin inhibition possibly takes place in extravascular sites where dermatan sulfate is present. HCII activity would be important in the regulation of wound healing, inflammation, or neuronal development.

Coagulation Protein Disorders↗
PubMed1999

[Test for detection of activated partial thromboplastin time using ellagic acid].

A simple and sensitive method for estimation of activated partial thromboplastin time (APTT) is developed, making use a complex reagent containing the activator (plant phospholipids) and contact factor (ellagic acid). The test requires additionally only 0.025 M CaCl2. The test is more sensitive to the presence of heparin in the blood and to insufficiency of blood clotting factors VIII and IX than the reagents containing insoluble substances (kaolin and animal phosphatides). Addition of soluble ellagic acid into reagent for APTT estimation allows studies on optic coagulometers.

Blood Coagulation↗
PubMed1999

Applying risk assessment models in orthopaedic surgery: effective risk stratification.

Deep vein thrombosis (DVT) and pulmonary embolism remain important causes of morbidity and mortality. Without prophylaxis, at least 60% of patients undergoing orthopaedic or trauma surgery develop DVT, and the rate may still be as high as 20-45% even with the best prophylaxis available. The rate of thrombosis may be reduced by wider use of established prophylactic measures and targeting more intense prophylaxis to very-high-risk patients. Novel agents such as pentasaccharides and recombinant hirudins may provide more effective prophylaxis in very-high-risk settings, but their optimal use requires accurate assessment of thromboembolic risk. Risk levels are influenced both by the clinical setting and patient factors, such as obesity and malignancy. There is now growing interest in the influence of molecular risk factors, including acquired thrombophilias and congenital coagulation disorders. Activated protein C resistance and hyperhomocysteinaemia have been recently identified as potential risk factors. Further investigations are needed to clarify the individual contribution of different clinical and molecular factors to overall thromboembolic risk, and the effects of interactions between them. Screening for clotting disorders and other additional risk factors may assist identification of very-high-risk patients and allow appropriate targeting of intensive prophylactic therapy.

Humans↗
PubMed1999

Increased operative bleeding during orthopaedic surgery in patients with type I Gaucher disease and bone involvement.

To aid clinicians in identifying patients with type I Gaucher disease who are at risk of excessive bleeding, we reviewed the coagulation parameters of six affected patients with bone involvement who underwent orthopaedic surgery at two centers, and of 22 patients under treatment at another, seven of whom had total splenectomy. All patients were of Jewish Ashkenazi origin. Among the latter group, prolonged prothrombin time was noted in 81%. Incidence of clotting factor deficiency were as follows: factor XI, 36.3%; V, 31.8%; VIII, 27.2%; IX, 13.6%; and XII, 27.2%. Most of the abnormalities occurred in the non-splenectomized patients. Two of the six orthopaedic surgery patients had excessive intraoperative and postoperative bleeding. One, who underwent spinal decompression had prolonged prothrombin time, and the other, who had total hip replacement, showed a deficiency of factor XI. The second patient's hemoglobin level was maintained with transfusion of fresh frozen plasma during contralateral hip arthroplasty five months later. We suggest that preoperative evaluation of clotting factors and replacement therapy may prevent excessive bleeding in patients with type I Gaucher disease.

Adolescent↗
PubMed2001

[Effects of second and third generation oral contraceptives on hemostasis].

Use of oral contraceptives induce changes in haemostatic parameters: changes occur in the procoagulant, anticoagulant, and fibrinolytic systems. The increased risk of venous thromboembolism with use of third, as compared with second generation oral contraceptives, found in epidemiological studies, has stimulated new research in haemostatic changes induced by both generations of oral contraceptives. A randomized crossover study showed that use of the third generation pill caused a greater increase of factor VII and prothrombin and a more pronounced decrease of factor V than the second generation pill. Acquired resistance to activated protein C (APC) was induced more strongly by preparations of the third than by those of the second generation. The concentration of protein S decreased markedly exclusively during use of the third generation pill, while it did not change during use of the second generation pill. The oral contraception-related effects on the anticoagulant system strongly resemble those of some forms of hereditary thrombophilia. If a woman with hereditary APC resistance (caused by factor V Leiden) uses oral contraceptives as well, and especially when she uses those of the third generation, she is subject to a considerable increase of the risk of venous thrombosis and becomes even more resistant to the anticoagulant action of protein C. In view of the epidemiological backgrounds of the difference in risk of thrombosis between second and third generation contraceptives, the second generation pill is recommended as the first choice for oral contraception.

Activated Protein C Resistance↗
PubMed2001

Genetic interactions between the coagulation and fibrinolytic systems.

Nearly all of the genes encoding the established coagulation and fibrinolytic factors have been successfully altered or disrupted in transgenic mice. Although comprehensive studies of each of these gene-targeted mouse lines are still ongoing, the initial findings have significantly refined our understanding of the roles of selected hemostatic factors in vivo, and occasionally altered long-standing concepts. This review summarizes some of the progress that has been made in the generation and phenotypic characterization of mice lacking key hemostatic factors, including coagulation, fibrinolytic, platelet and endothelial cell-associated factors. New insights regarding the role(s) and interplay of hemostatic factors that have emerged from detailed studies of mice carrying multiple deficits in coagulation and fibrinolytic system components are highlighted.

Afibrinogenemia↗
PubMed2001

[Oto- and rhinosinusogenic sepsis in children].

Clinical characteristics of 25 cases of otogenic and 26 cases of rhinosinusogenic sepsis have been analysed. The main diagnostic criteria of the sepsis were the following: fever, leukocytosis, micro- and macrovascular abnormalities, respiratory and coagulation disorders, abnormal protein levels in plasma, etc. Oto- and rhinosinusogenic sepsis in 45(88.2%) examinees was associated with intracranial complications. Early diagnosis of sepsis, timely operation after adequate preparation, administration of antimicrobial drugs and infusions, stay of patients in intensive care unit with permanent monitoring provided a good outcome in 94% patients.

Adolescent↗
PubMed2002

[Hypercoagulability in atrial fibrillation and its relationship with risk factors for systemic embolism].

BACKGROUND: Atrial fibrillation is associated to a high risk of systemic embolism and to hypercoagulability. AIM: To evaluate the activation of the coagulation cascade through determinations of the thrombin-antithrombin complex in patients with atrial fibrillation and to correlate this data with the clinical and echocardiographic risk factors for systemic embolism. PATIENTS AND METHODS: In 53 patients with atrial fibrillation plasma levels of the thrombin-antithrombin complex were determined on admission to a coronary care unit and 30 days later. Using a univariate and multiple regression analysis, the association basal thrombin-antithrombin with the duration of the arrhythmia, age over 70 years, previous use of antiplatelet agents, history of hypertension, mitral valve disease, diabetes, heart failure, previous systemic embolism, left atrial diameter and the presence of spontaneous contrast echo or thrombus in the left atrial appendage, was studied. RESULTS: Basal thrombin-antithrombin values were 40.1 +/- 69 mg/L (Median 8.34 [3.0-47.5]) compared to 2.7 +/- 3.3 mg/L in healthy controls (p < 0.001). No significant correlation was found between activation of the coagulation cascade and risk factors for systemic embolism. There were no significant differences in thrombin-antithrombin values between patients with chronic or paroxysmal atrial fibrillation (29.5 +/- 43 mg/L and 49.4 +/- 83 mg/L respectively). Mean thrombin-antithrombin values in patients under antiplatelet agents were lower than in those without treatment (17.3 +/- 43 vs 66.8 +/- 127 mg/L; p = 0.018). CONCLUSIONS: The activation of the coagulation cascade in patients with atrial fibrillation was confirmed. However, no association of this activation with well known clinical and echocardiographic risk factors for systemic embolism, was found. Previous antiplatelet treatment prevented a higher activation of the coagulation cascade.

Aged↗
PubMed2003

Axillary vein thrombosis and congenital dysfibrinogenemia in a commercial pilot: a case report.

A 34-yr-old male commercial pilot developed a painful swollen right upper arm following an episode of trauma. Venography confirmed the clinical diagnosis of a right axillary deep venous thrombosis. Magnetic resonance imaging suggested the presence of a fibrous tissue band overlying the junction of the right subclavian and innominate veins, potentially creating a thoracic outlet syndrome. A thrombophilia screen revealed an abnormal fibrinogen variant consistent with a diagnosis of congenital dysfibrinogenemia. The pilot was treated with anticoagulant therapy for 4 mo. There were diagnostic difficulties in determining the definitive etiology of the axillary vein thrombosis. Congenital dysfibrinogenemia is a rare condition, which is asymptomatic in the majority, but may manifest with hemorrhage or thrombosis in up to 45% of cases. The clinical management of the pilot and the aeromedical implications of the diagnosis are discussed.

Adult↗
PubMedDate not supplied

DNA-based lab tests.

Explore the source record for details and available documents.

Blood Coagulation↗