CASE REPORTSHemeoxygenase-1 mediated hypercoagulability in a patient with thyroid cancerNielsen, Vance G.; Garol, Benjamin D.; Zelman, Eric A.; Guerrero, Marlon A.Author Information aDepartment of Anesthesiology bDepartment of Surgery, The University of Arizona College of Medicine, Tucson, Arizona, USA Correspondence to Vance G. Nielsen, MD, Department of Anesthesiology, The University of Arizona College of Medicine, P.O. Box 245114, 1501 North Campbell Avenue, Tucson, AZ 85724-5114, USA Tel: +1 520 626 7999; fax: +1 520 626 6943; e-mail: email@example.com Received 19 March, 2013 Accepted 4 May, 2013 Blood Coagulation & Fibrinolysis: September 2013 - Volume 24 - Issue 6 - p 663-665 doi: 10.1097/MBC.0b013e328363ab86 Buy Metrics Abstract Thyroid cancers can cause significant regional thrombotic morbidity and mortality. Of interest, thyroid cancer cell lines can have upregulation of the carbon monoxide-producing enzyme, hemeoxygenase-1. Carbon monoxide has been demonstrated to markedly enhance plasmatic coagulation in vitro and in vivo via enhancement of fibrinogen's substrate properties by binding to a fibrinogen-associated heme group(s). We present a patient undergoing removal of a malignant thyroid tumour who was serendipitously found to have abnormally increased carboxyhaemoglobin concentration (2.4%) and plasmatic hypercoagulability with a carbon monoxide-mediated clot strength as determined by a thrombelastographic method. This initial observation serves as a rationale to further investigate the role played by hemeoxygenase-1 upregulation in the setting of cancers associated with increased endogenous carbon monoxide production. Copyright © 2013 YEAR Wolters Kluwer Health, Inc. All rights reserved.