Thrombin-activatable fibrinolysis inhibitor in human abdominal aortic aneurysm disease
| Autor: | M. Hesketh, Anne Johnson, Robert A.S. Ariёns, Jim Zhong, Helen Philippou, Fraser L. Macrae, Katherine I Bridge, Annick Van Gils, L. Bollen, David J. Scott |
|---|---|
| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Male medicine.medical_specialty Carboxypeptidase B2 medicine.medical_treatment Thrombin-Activatable Fibrinolysis Inhibitor Enzyme-Linked Immunosorbent Assay Disease 030204 cardiovascular system & hematology Gastroenterology Pathogenesis 03 medical and health sciences 0302 clinical medicine Internal medicine Fibrinolysis medicine Humans Fibrinolysin Prospective cohort study Aged Aged 80 and over alpha-2-Antiplasmin business.industry Hematology Middle Aged medicine.disease Thrombosis Abdominal aortic aneurysm Enzyme Activation 030104 developmental biology Case-Control Studies Immunology Female business Peptides Biomarkers Aortic Aneurysm Abdominal |
| Zdroj: | Journal of thrombosis and haemostasis : JTH. 15(11) |
| ISSN: | 1538-7836 |
| Popis: | Background: Intra-luminal thrombosis is a key factor in Abdominal Aortic Aneurysms (AAA) growth. Patients with AAA form dense clots that are resistant to fibrinolysis. Thrombin-activatable fibrinolysis inhibitor (TAFI) has been shown to influence AAA development in murine models. Objective: The aim of this study is to characterise the role of TAFI in human AAA. Methods: Plasma levels of TAFI, TAFI activation peptide (TAFI-AP), activated/inactivated TAFI (TAFIa/ai) and plasmin-α2-antiplasmin complex were measured by ELISAs in patients with AAA (n=202) and controls (n=188). Results: TAFIa/ai and TAFI-AP levels were higher in patients than controls (median (IQR): 20.3 (14.6-32.8) vs. 14.2 (11.2-19.3) and 355.0 (232.4-528.1) vs. 248.6 (197.1-328.1) ng/ml). TAFIa/ai was positively correlated with TAFI-AP (r=0.164). Intact TAFI levels were not different between patients and controls (13.4 (11.2-16.1) vs. 12.8 (10.6-15.4) μg/ml). Plasmin-α2-antiplasmin was higher in AAA patients than controls (690.0 (489.1-924.3) vs. 480.7 (392.6-555.3) ng/ml). Conclusions: The increase in TAFIa/ai and TAFI-AP suggest an increased TAFI activation in patients with AAA. Prospective studies are required to further elucidate the role of TAFI and fibrinolysis in AAA pathogenesis. |
| Databáze: | OpenAIRE |
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