Results 91 to 100 of about 203 (142)
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Thrombosis Research, 1987
Antithrombin III (AT III) microheterogeneity was investigated in 12 cases of congenital AT III deficiency and 2 cases of congenital AT III abnormality by isoelectric focusing (IEF) and immunofixation. In congenital AT III deficiency, IEF and immunofixation revealed AT III as 8 bands which was indistinguishable from normal control in terms of the number
N, Sakuragawa +4 more
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Antithrombin III (AT III) microheterogeneity was investigated in 12 cases of congenital AT III deficiency and 2 cases of congenital AT III abnormality by isoelectric focusing (IEF) and immunofixation. In congenital AT III deficiency, IEF and immunofixation revealed AT III as 8 bands which was indistinguishable from normal control in terms of the number
N, Sakuragawa +4 more
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Hereditary antithrombin III deficiency. Effect of antithrombin III deficiency on platelet function
The American Journal of Medicine, 1976Antithrombin III (AT III) is the main physiologic inhibitor of thrombin, and activated factors X and IX as well. Normal levels of AT III appear to be necessary to maintain blood fluidity and to prevent thrombosis. Four families with AT III deficiency and recurrent venous thromboembolism have been reported on. We present an additional family with AT III
A, Carvalho, L, Ellman
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Aortic Thrombosis in Antithrombin III Deficiency
JAMA: The Journal of the American Medical Association, 1982To the Editor.— Although we are told in the article by Michael E. Shapiro, MD, and Edwin W. Salzman, MD (1981;245:1759), that abnormal antithrombin III (AT III) levels were documented in both cases weeks to months after any short-term event or surgery, in case 1 the reduced AT III level was found at a time when resting pain had been present for three ...
J H, Winter, B, Bennett, A S, Douglas
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Blood Reviews, 1988
A moderate reduction of plasma antithrombin activity is an uncommon but clinically important cause of severe thromboembolic disease. In recent years the molecule responsible for the major part of this activity (antithrombin III) has been extensively characterised and the mode of inheritance of familial deficiencies worked out.
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A moderate reduction of plasma antithrombin activity is an uncommon but clinically important cause of severe thromboembolic disease. In recent years the molecule responsible for the major part of this activity (antithrombin III) has been extensively characterised and the mode of inheritance of familial deficiencies worked out.
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Heterogeneity of the "Classical" Antithrombin III Deficiency
Thrombosis and Haemostasis, 1980SummaryWe investigated two thrombophilia families with the "classical" type of antithrombin III deficiency, i.e., with a low antithrombin III level measured both by immunochemical and functional methods.We obtained different antithrombin III patterns in the plasma of the affected members of the two families with the modified two dimensional ...
G, Sas +4 more
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Neonatal antithrombin III deficiency
The American Journal of Medicine, 1989Hemorrhagic and thrombotic complications are common in sick preterm infants and may reflect inadequate regulation of coagulation. All neonates have low levels of the pivotal regulator antithrombin III (ATIII) compared with adults. Plasma levels of ATIII are very low in preterm infants and are further diminished in infants with respiratory distress ...
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Pathophysiology of Antithrombin III Deficiency
Veterinary Clinics of North America: Small Animal Practice, 1988This article focuses on the pathophysiology of thrombosis in patients with acquired antithrombin III deficiency. Antithrombin III is an important natural inhibitor of the hemostatic mechanism, and a hypercoagulable state is often induced in diseases causing antithrombin III deficiency.
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Venous Thrombosis: Antithrombin III Deficiency
Critical Care Nursing Clinics of North America, 1993Antithrombin (ATIII) is believed to be one of the body's most powerful natural anticoagulants, so individuals with a deficiency of this protein exhibit a marked propensity to venous thrombosis. This article will focus on the pathophysiology of this disorder, including clinical presentation, diagnosis, and treatment.
M, Halfman, D E, Berg
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ANTITHROMBIN III DEFICIENCY IN A CHINESE FAMILY
Medical Journal of Australia, 1981Familial antithrombin III deficiency, which is inherited by autosomal dominant transmission, is now well recognized as a cause of recurrent venous thromboembolism. Many such families have now been described, but few came from Asia. This report details a Chinese kindred with three members living in Sydney, two of whom are affected.
A J, Concannon, J, Low
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Inherited Antithrombin III Deficiency in the Neonate
Archives of Pediatrics & Adolescent Medicine, 1994To describe two cases of inherited antithrombin III (AT-III) deficiency presenting at less than or equal to 28 days of age, and to review other neonatal reports.Clinical descriptions of two patients and literature review of known references to the neonatal presentation of this disorder.Academic neonatal intensive care unit.Case reports--two patients ...
J, Seguin, K, Weatherstone, C, Nankervis
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