Objectives: Our study was undertaken to evaluate the levels of thrombin-activatable fibrinolysis inhibitor (TAFI) antigen and also its relationship with other hemostasis markers in a group of patients affected with polycystic ovary syndrome (PCOS)-under Diane-35 (ethinyl estradiol 0.035 mg/cyproterone acetate 2 mg) treatment or not-as compared with a group of healthy controls.
Methods: Forty-two women with PCOS and 30 age-matched healthy controls were involved in the study. Group A were on Diane-35 for at least 6 months; group B did not take any drug; group C served as a control group.
Results: TAFI antigen levels of groups A and B were significantly higher than in controls, but no difference was observed between them. All of the other coagulation and fibrinolysis parameters (including prothrombin time, activated partial thromboplastin time, fibrinogen and D-dimer) were comparable between the three groups.
Conclusion: The evidence presented herein suggests that women with PCOS have impaired fibrinolysis, as reflected by increased TAFI. This impairment can contribute to the risk of cardiovascular disease in PCOS. Elucidation of the modifiable mechanisms in PCOS can represent an opportunity for preventive therapy of the cardiovascular risks associated with PCOS.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1080/09513590802291824 | DOI Listing |
J Thromb Haemost
January 2025
Department of Medicine, McMaster University; Department of Biochemistry and Biomedical Sciences, McMaster University; Thrombosis and Atherosclerosis Research Institute, McMaster University and Hamilton Health Sciences.
Thrombin is the central mediator of hemostasis, where it converts fibrinogen to fibrin, activates upstream factors to promote coagulation, activates factor XIII and thrombin-activatable fibrinolysis inhibitor to stabilize fibrin, mediates anticoagulation, and modulates cellular activity via cell surface receptors. Thus, regulation of thrombin activity is essential to the hemostatic balance. Thrombin is regulated by positively charged surface domains that surround the active site.
View Article and Find Full Text PDFThromb Haemost
January 2025
Department of Medical Physiology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Background: Fibrinolysis is spatiotemporally well-regulated and greatly influenced by activated platelets and coagulation activity. Our previous real-time imaging analyses revealed that clotting commences on activated platelet surfaces, resulting in uneven-density fibrin structures, and that fibrinolysis initiates in dense fibrin regions and extends to the periphery. Despite the widespread clinical use of direct oral anticoagulants (DOACs), their impact on thrombin-dependent activation of thrombin-activatable fibrinolysis inhibitor (TAFI) and fibrinolysis remains unclear.
View Article and Find Full Text PDFRMD Open
December 2024
Rheumatology, Amsterdam UMC Locatie VUmc, Amsterdam, The Netherlands
Objectives: To assess the effect of treatment on haemostatic parameters in patients with early rheumatoid arthritis (RA).
Methods: Patients with newly diagnosed RA started methotrexate and were randomised to additional conventional treatment, certolizumab pegol, abatacept or tocilizumab. Several biomarkers for haemostasis were analysed including parameters of the two global haemostatic assays-overall haemostatic potential (OHP) and endogenous thrombin potential (ETP), as well as single haemostatic factors-fibrinogen, prothrombin fragment 1+2 (F1+2), D-dimer, thrombin activatable fibrinolysis inhibitor (TAFI) and clot lysis time (CLT) in 24 patients at baseline, 12 and 24 weeks after the start of the treatment.
Res Pract Thromb Haemost
November 2024
Department of Biomedical Engineering, Rutgers University, Piscataway, New Jersey, USA.
Background: Anticoagulants prevent the formation of potentially fatal blood clots. Apixaban is a direct oral anticoagulant that inhibits factor (F)Xa, thereby impeding the conversion of prothrombin into thrombin and the formation of blood clots. Blood clots are held together by fibrin networks that must be broken down (fibrinolysis) to restore blood flow.
View Article and Find Full Text PDFPharmaceuticals (Basel)
October 2024
Department of Marine Bio-Pharmacology, College of Food Science and Technology, Shanghai Ocean University, Shanghai 201306, China.
Background: The thrombin-activatable fibrinolysis inhibitor (TAFI) is an important regulator in the balance between blood clot formation (coagulation) and dissolution (fibrinolysis), which is mainly activated by thrombin bonded with thrombomodulin (TM).
Methods: In this study, the investigation focused on the unique target TAFI of fungi fibrinolytic compound 1 (FGFC1), a novel fibrinolytic compound sourced from the deep sea. In this sense, the regulation of TAFI by FGFC1, in comparison to established TAFI inhibitors such as DS-1040 and PCTI in hPPP, was investigated, which was validated through the molecular docking of FGFC1 to TAFI.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!