Activated protein C resistance was measured as a ratio: ETP+aPC/ETP-aPC 100

Activated protein C resistance was measured as a ratio: ETP+aPC/ETP-aPC 100. (52.7 16.4%), oAPS (64.1 14.6%) as compared to the control group (27.2 13.8%). Conclusion: Our data suggest an increase of thrombin generation in thrombotic and obstetrical APS and no hypercoagulable states in patients with biological APS. The study of a prospective and a larger controlled cohort could determine the TGA useful for APS monitoring and could confirm an aPCR evaluation in PPP. = 0.08) and a significant increase in oAPS (= 0.02), compared to bAPS. A significant thrombin peak increase was observed in tAPS ( 0.05), oAPS (= 0.001), compared to bAPS. No association was observed between thrombin generation and the type or number of aPL in tAPS and oAPS. One tAPS developed a recurrent thrombosis two years after TGA (ETP: 2538 nM.min; peak: 333 nM). Two oAPS patients developed a first thrombosis during three years after test (ETP: 2067 nM.min and 1867 nM.min; peak: 254.4 nM and 232 nM). The activated protein C resistance was evaluated in the Sydney criteria APS group. An increased aPCR was observed in tAPS (52.7 16.4%), oAPS (64.1 14.6%) as compared to the control group (27.2 13.8%) (Figure 1C). 4. Discussion In this study, we showed a TG increase in tAPS and oAPS (consistent with the Sydney criteria for diagnosis of APS), compared to the control and bAPL. The assessment of TG in a patient with tAPS was safe in our study after transient discontinuation of Mercaptopurine anticoagulant. Moreover, TG seems to be higher in oAPS, compared to tAPS. The first thrombotic event risk has been demonstrated in oAPS recently, in a retrospective study with 63% of deep vein thrombosis development at 7.6 years after postpartum [5]. Our results support the literature data, with a hypercoagulability increase in oAPS and a susceptibility risk to develop thrombo-embolic disease. Primary prevention in APS is still controversial. The absolute risk of a first thrombosis is probably less than 1% per year, without connected comorbidity [17], and 5.3% if a triple positivity is associated, with male sex and additional risk factors for deep vein thrombosis [6]. The results of our study suggest that bAPS did not possess a hypercoagulable state with an equal TG to the control group. Only an increased lag time was observed, as the same mechanism of delayed triggered partial thrombin time. Thrombin generation could be used to confirm no prothrombotic claims in bAPS. In a secondary bAPS without thrombotic event, only a longer lag time was observed, whereas Pereira et al. showed a TG increase in SLE [18]. In their study, six individuals had secondary APS. Profiles of TG were the same between SLE and secondary APS. However, Pereira et al. evaluated the TG secondary Mouse monoclonal to CD48.COB48 reacts with blast-1, a 45 kDa GPI linked cell surface molecule. CD48 is expressed on peripheral blood lymphocytes, monocytes, or macrophages, but not on granulocytes and platelets nor on non-hematopoietic cells. CD48 binds to CD2 and plays a role as an accessory molecule in g/d T cell recognition and a/b T cell antigen recognition to pro-coagulant microparticles. Our results showed a nonsignificant increase of TG in secondary bAPS. Our SLE individuals were treated with HCQ. Rand et al. showed a tissue element decrease in APS individuals Mercaptopurine under HCQ [19]. An endothelial cell model of APS showed a hypercoagulable state with TG increase [12]. Preliminary results showed the prothrombotic state decreased when a mouse and endothelial cell model of APS were treated with HCQ [13]. The hydroxychloroquine treatment could clarify the absence of difference between secondary bAPS and the control group in thrombin generation profiles. Activated Mercaptopurine protein C resistance is known to increase venous thrombotic risk in.