Thoracic tumor effects on plasmatic coagulation: role of hemeoxygenase-1.

TitleThoracic tumor effects on plasmatic coagulation: role of hemeoxygenase-1.
Publication TypeJournal Article
Year of Publication2014
AuthorsNielsen VG, Gharagozloo F, Matika RW, Kim S, Zelman EA, Steinbrenner EB
JournalLung cancer (Amsterdam, Netherlands)
Volume83
Issue2
Pagination288-91
Date Published2014 Feb
ISSN1872-8332
KeywordsAdolescent, Adult, Aged, Aged, 80 and over, Blood Coagulation, Carbon Monoxide, Carboxyhemoglobin, Female, Gene Expression Regulation, Neoplastic, Heme Oxygenase-1, Humans, Male, Middle Aged, Thoracic Neoplasms, Thrombelastography, Thrombophilia, Up-Regulation, Young Adult
Abstract

OBJECTIVES: Lung cancer is an important health threat worldwide, and is associated with a 3.8-13.9% incidence of thrombophilia. Of interest, patients with lung tumors have been noted to have an increase in endogenous carbon monoxide production via upregulation of hemeoxygenase-1 activity. Given that it has been demonstrated that carbon monoxide enhances plasmatic coagulation in vitro and in vivo via formation of carboxyhemefibrinogen, we sought to determine if patients with thoracic tumors undergoing lung resection/pneumonectomy had an increase in endogenous carbon monoxide and concurrent plasmatic hypercoagulability.

MATERIALS AND METHODS: Nonsmoking patients with thoracic tumors (n=19) had preoperative carboxyhemoglobin (a measure of carbon monoxide production) determined, and a thromboelastometric method to assess citrated plasma coagulation kinetics and the formation of carboxyhemefibrinogen was utilized. Thoracic tumor patient coagulation kinetics was compared with normal subject (n=30) plasma samples.

RESULTS AND CONCLUSION: Patients with thoracic tumors were determined to have an abnormally increased carboxyhemoglobin concentration of 2.1±0.6%, indicative of hemeoxygenase-1 upregulation. It was found that 84% of thoracic tumor patients had plasma clot strength that exceeded the 95% confidence interval value observed in normal subjects, and 44% of this hypercoagulable subgroup had carboxyhemefibrinogen formation. Future investigation of the role played by plasmatic hypercoagulability and hemeoxygenase-1 derived carboxyhemefibrinogen in the pathogenesis of thoracic tumor related thrombophilia is warranted.

DOI10.1016/j.lungcan.2013.11.012
Alternate JournalLung Cancer