医学
胃肠病学
抗凝血酶
川地31
内科学
纤溶酶原激活物抑制剂-1
血小板
单中心
纤溶酶原激活剂
肝素
免疫组织化学
作者
Andrea Piccin,Maria Teresa Sartori,Gianni Bisogno,Muriel van Schilfgaarde,Graziella Saggiorato,Angela Maria Di Pierro,Daisy Corvetta,Luigi Marcheselli,Mega Andrea,Günther Gastl,Simone Cesaro
摘要
Abstract Background Entry criteria included patients who developed sinusoidal obstruction syndrome ( SOS ) at a single centre from January 2000 to December 2011. Patients who underwent haemopoietic stem cell transplantation or actinomicyn‐based chemotherapy for nephroblastoma were selected. The study group comprised five patients with SOS who were compared with a control group of seven patients without SOS . Aim To study the relationships between endothelial extracellular vesicles ( EV ) and plasminogen‐activator inhibitor type 1( PAI ‐1) to assess their modification in the early phase of SOS . Methods Consecutive blood samples were tested for cell‐derived EV , PAI ‐1 and coagulation parameters. Any statistically significant correlation between all datasets was searched. Results Antithrombin level and platelet count were statistically significantly reduced in SOS patients, suggesting a consumption status. PAI ‐1:Ag and PAI ‐1:act showed an inverse relationship with platelet counts (coef. −0.034, SE = 0.016; P = 0.041 and −0.052, SE = 0.019; P = 0.011 respectively). During follow up, PAI ‐1:Ag was inversely related to EV CD144 + (coef. −0.261, SE = 0.094; P = 0.007) and antithrombin (coef −0.509, SE = 0.175; P = 0.005). PAI ‐1:act showed an inverse association with EV CD144 + (coef.−0.251, SE = 0.121; P = 0.043), EV CD31 +/ CD41 + (coef. −0.004, SE = 0.002; P = 0.026) and antithrombin (coef. −0.470, SE = 0.220; P = 0.038). EV generated by rupture of gap junctions ( EV CD144 +) were increased in SOS patients and also showed a change over time. Conclusion This study demonstrates the existence of an ongoing procoagulant and hypofibrinolytic status in SOS , indicating a possible role for anticoagulant therapy. Moreover, these findings suggest a role for EV CD 144+, either alone or in combination with PAI ‐1, as a new biomarker for SOS .
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