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Acute CO Poisoning is Associated with Impaired Fibrinolysis and Increased Thrombin Generation
Author(s) -
Gawlikowski Tomasz,
Gomolka Ewa,
Piekoszewski Wojciech,
Jawień Wojciech,
Undas Anetta
Publication year - 2013
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/bcpt.12042
Subject(s) - fibrinolysis , fibrin , tissue plasminogen activator , ex vivo , thrombin , medicine , plasminogen activator , carbon monoxide poisoning , in vivo , factor xii , whole blood , immunology , pharmacology , coagulation , chemistry , in vitro , poison control , biochemistry , platelet , biology , microbiology and biotechnology , environmental health
Abstract 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.