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Acute CO poisoning is associated with impaired fibrinolysis and increased thrombin generation

Acute CO poisoning is associated with impaired ...

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dc.contributor.author Gawlikowski, Tomasz [SAP20001554] pl
dc.contributor.author Gomółka, Ewa [SAP20008191] pl
dc.contributor.author Piekoszewski, Wojciech [SAP11019420] pl
dc.contributor.author Jawień, Wojciech [SAP20000816] pl
dc.contributor.author Undas, Anetta [SAP20001686] pl
dc.date.accessioned 2015-01-23T08:22:08Z
dc.date.available 2015-01-23T08:22:08Z
dc.date.issued 2013 pl
dc.identifier.issn 1742-7835 pl
dc.identifier.uri http://ruj.uj.edu.pl/xmlui/handle/item/2683
dc.language eng pl
dc.title Acute CO poisoning is associated with impaired fibrinolysis and increased thrombin generation pl
dc.type JournalArticle pl
dc.description.physical 352-356 pl
dc.abstract.en Carbon monoxide (CO) poisoning is a leading cause of unintentional poisoning deaths in many countries. In ex vivo studies, CO released from carbon monoxide-releasing molecules has been shown to attenuate fibrinolysis via increased alpha-2-antiplasmin activity. Hypofibrinolysis is associated with coronary ischaemia, which is also commonly observed in CO poisoning. We examined fibrin clot properties in acutely poisoned CO patients. Ex vivo plasma fibrin clot permeability, turbidimetry and efficiency of fibrinolysis were investigated in 48 patients and controls matched for age and sex. CO-poisoned patients had 11.6% longer clot lysis time than the controls (p < 0.0001). No intergroup differences in clot permeability or turbidimetric variables were observed. Plasma tissue-type plasminogen antigen (tPA), plasminogen activator inhibitor-1 (PAI-1) antigen and activity and F1.2 prothrombin fragments were higher in the patients than in the controls (all p < 0.0001). Plasma tPA activity was lower in the CO-poisoned group. Multiple linear regression showed that a thrombin generation marker, F1.2, is the strongest predictor of clot lysis time, followed by PAI-1 activity and carboxyhaemoglobin levels. In conclusion, this report is the first to demonstrate that acute CO poisoning in human beings is linked to increased thrombin generation and impaired fibrinolysis, which might contribute to ischaemic complications. pl
dc.description.volume 112 pl
dc.description.number 5 pl
dc.description.points 25 pl
dc.identifier.doi 10.1111/bcpt.12042 pl
dc.identifier.eissn 1742-7843 pl
dc.title.journal Basic & Clinical Pharmacology & Toxicology pl
dc.language.container eng pl
dc.affiliation Wydział Lekarski : Instytut Kardiologii pl
dc.affiliation Wydział Farmaceutyczny : Zakład Farmakokinetyki i Farmacji Fizycznej pl
dc.affiliation Wydział Chemii : Zakład Chemii Analitycznej pl
dc.affiliation Wydział Lekarski : Katedra Toksykologii i Chorób Środowiskowych pl
dc.affiliation Wydział Lekarski : Klinika Toksykologii i Chorób Środowiskowych pl
dc.subtype Article pl
dc.rights.original bez licencji pl
.pointsMNiSW [2013 A]: 25


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