| Autor: |
Carrillo Torres P; Gynaecology Department, Clinic Institute of Gynaecology, Obstetrics and Neonatology (ICGON), Hospital Clinic of Barcelona, Universitat de Barcelona, 08007 Barcelona, Spain., Martínez-Zamora MÁ; Gynaecology Department, Clinic Institute of Gynaecology, Obstetrics and Neonatology (ICGON), Hospital Clinic of Barcelona, Universitat de Barcelona, 08007 Barcelona, Spain., Tàssies D; Hemotherapy and Hemostasis Department, Clinic Institute of Hemato-Oncological Disease (ICMHO), Hospital Clínic of Barcelona, Universitat de Barcelona, 08007 Barcelona, Spain., Castillo H; Gynaecology Department, Clinic Institute of Gynaecology, Obstetrics and Neonatology (ICGON), Hospital Clinic of Barcelona, Universitat de Barcelona, 08007 Barcelona, Spain., Gracia M; Gynaecology Department, Clinic Institute of Gynaecology, Obstetrics and Neonatology (ICGON), Hospital Clinic of Barcelona, Universitat de Barcelona, 08007 Barcelona, Spain., Feixas G; Gynaecology Department, Clinic Institute of Gynaecology, Obstetrics and Neonatology (ICGON), Hospital Clinic of Barcelona, Universitat de Barcelona, 08007 Barcelona, Spain., Reverter JC; Hemotherapy and Hemostasis Department, Clinic Institute of Hemato-Oncological Disease (ICMHO), Hospital Clínic of Barcelona, Universitat de Barcelona, 08007 Barcelona, Spain., Carmona F; Gynaecology Department, Clinic Institute of Gynaecology, Obstetrics and Neonatology (ICGON), Hospital Clinic of Barcelona, Universitat de Barcelona, 08007 Barcelona, Spain. |
| Abstrakt: |
There has been increasing interest in the study of new pathogenic mechanisms in endometriosis (END), including the coagulation/fibrinolysis system and its link with inflammation and tissue remodeling. It has been suggested that END patients, especially with deep-infiltrating (DE) forms, could present a hypercoagulable state revealing higher levels of proinflammatory and procoagulant markers, such as total circulating microparticles (cMPs) and cMP-TF (tissue factor), released by cells in response to damage, activation, or apoptosis. However, no previous study has assessed the effect of END hormonal treatments on cMP and cMP-TF levels. Therefore, the aim of this study was to evaluate the impact of these treatments on cMP and cMP-TF levels in DE patients. Three groups were compared: DE patients receiving a continuous combined oral contraceptive regimen (CCOCR) (n = 41), DE patients without CCOCR (n = 45), and a control group (n = 43). cMP and cMP-TF levels were evaluated in platelet-free plasma. A significant decrease in the total cMP levels was found in the DE group with CCOCR versus the group without CCOCR, reflecting a higher chronic inflammatory status in DE patients that decreased with the treatment. cMP-TF levels were higher in DE patients receiving CCOCR versus those not receiving CCOCR, suggesting that treatments containing estrogens play a predominant role in suppressing the inhibitory pathway of TF. |
