U. Nowak-Göttl , H. Vielhaber , R. Schneppenheim , H.G. Koch
{"title":"Coagulation and fibrinolysis in children with APC-resistance: a population study","authors":"U. Nowak-Göttl , H. Vielhaber , R. Schneppenheim , H.G. Koch","doi":"10.1016/S0268-9499(96)80040-3","DOIUrl":null,"url":null,"abstract":"<div><p><u>Objective</u>: resistance to activated protein C (APCR) has emerged as the most important hereditary cause of venous thromboembolism. To determine to what extent this relatively common gene mutation influences the overall haemostatic balance, coagulation and fibrinolysis were investigated in a population of APC resistant children (n=46) in comparison to an age-matched healthy control group (n=80).</p><p><u>Results</u>: compared to the sex- and age-matched healthy control thrombomodulin (TM), F1+2, D-Dimer formation, t-PA, u-PA, PAP and PAI 1 were significantly increased in the APCR children. In addition, TM, D-Dimer, t-PA, u-PA, PAI 1 and PAP showed a significantly positive correlation to the amount of thrombin generated. No difference was found between children and patients who had suffered from vascular insults before this study was conducted.</p><p><u>Conclusions</u>: children with APCR showed a combination of activated coagulation and fibrinolysis.</p></div>","PeriodicalId":84750,"journal":{"name":"Fibrinolysis","volume":"10 ","pages":"Pages 25-27"},"PeriodicalIF":0.0000,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S0268-9499(96)80040-3","citationCount":"6","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Fibrinolysis","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0268949996800403","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 6
Abstract
Objective: resistance to activated protein C (APCR) has emerged as the most important hereditary cause of venous thromboembolism. To determine to what extent this relatively common gene mutation influences the overall haemostatic balance, coagulation and fibrinolysis were investigated in a population of APC resistant children (n=46) in comparison to an age-matched healthy control group (n=80).
Results: compared to the sex- and age-matched healthy control thrombomodulin (TM), F1+2, D-Dimer formation, t-PA, u-PA, PAP and PAI 1 were significantly increased in the APCR children. In addition, TM, D-Dimer, t-PA, u-PA, PAI 1 and PAP showed a significantly positive correlation to the amount of thrombin generated. No difference was found between children and patients who had suffered from vascular insults before this study was conducted.
Conclusions: children with APCR showed a combination of activated coagulation and fibrinolysis.
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