Value of Prothrombin Fragment 1.2 (F 1.2) in the Diagnosis of Stroke in Young Patients With Antiphospholipid Antibodies
Autor: | Yehudit Radnai, Edna Kott, Ziva Friedman, Anat Kesler, Martin Ellis, Ilana Drucker |
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Rok vydání: | 2000 |
Předmět: |
Adult
Male medicine.medical_specialty Ischemia 030204 cardiovascular system & hematology 03 medical and health sciences 0302 clinical medicine Thrombin immune system diseases Internal medicine medicine Humans 030212 general & internal medicine neoplasms Stroke Retrospective Studies biology business.industry Case-control study Retrospective cohort study Hematology General Medicine Middle Aged medicine.disease Thrombosis Peptide Fragments Surgery Ischemic Attack Transient Case-Control Studies Antibodies Antiphospholipid biology.protein Cardiology Etiology Female Prothrombin Antibody business Biomarkers medicine.drug |
Zdroj: | Clinical and Applied Thrombosis/Hemostasis. 6:61-64 |
ISSN: | 1938-2723 1076-0296 |
DOI: | 10.1177/107602960000600201 |
Popis: | The presence in the serum of antiphospholipid an tibodies (aPL) is associated with venous and arterial thrombo sis. This observation has led to the search for these antibodies in young patients with ischemic neurologic syndromes. How ever, 1% to 5% of healthy people may be found to have cir culating aPL without necessarily being at increased risk of thromboembolism. Thus, the finding of APLA in a patient with cerebral ischemia does not necessarily provide an explanation for the etiology of the clinical syndrome. The aim of this study was to determine whether the presence of aPL in young patients with stroke or transient ischemic attacks represents a possible cause of hypercoagulability as defined by ongoing thrombin formation with resultant elevation of prothrombin fragment 1.2 (F1.2) levels. This was a retrospective, case-control study involving 57 subjects. Twenty-seven patients had a recent cerebrovascular ischemic event—either TIA or a stroke. Fifteen were positive for aPL, and 12 were aPL-negative. Thirty subjects, matched for age and sex with no history of cerebrovascular disease, served as controls. Of this group, 20 were aPL-positive and 10 were aPL-negative. Causes of hy percoagulability other than aPL were excluded by laboratory testing. A positive test for aPL was repeated after a 6-week interval and two positive tests were required for a patient to be regarded as being aPL-positive. Levels of F1.2 were measured by an ELISA technique. There was a significant difference ( p < 0.05) in the mean F1.2 levels between the aPL-positive group with a history of cerebrovascular disease (mean F1.2 = 2.3733) and each of the other study groups. There was no statistically significant dif ference between any of the other study groups. Our findings suggest that F1.2 levels are elevated in young patients with cerebrovascular syndromes who have aPL and in whom other causes of hypercoagulability and atherosclerotic vascular disease are absent. Elevated F1.2 in these patients may be a potential marker of the hypercoagulable state associated with aPL. |
Databáze: | OpenAIRE |
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