Carbon monoxide (CO), a colorless and odorless gas, has antiapoptotic properties (second link). It can also enhance plasma coagulation. Patients with brain tumors have a high incidence of deep vein thrombosis and venous thromboembolism.
Dr. Vance G. Nielsen and colleagues from the departments of Anesthesiology, and Surgery, The University of Arizona, Tucson, Arizona, hypothesized that patients with brain tumors had increased hemeoxygenase-1 (HO-1) activity, responsible for endogenous production of CO during the catabolism of heme, increased CO production, increased plasmatic hypercoagulability, and formation of carboxyhemefibrinogen (COHF), through which CO has been shown to enhance coagulation. Their work will be published in the article titled “Brain Tumors Enhance Plasmatic Coagulation: The Role of Hemeoxygenase-1” and appeared in the May 2014 issue of Anesthesia & Analgesia.
The authors studied the blood coagulation profile of 20 non-smoking patients, average age 50 years, with brain tumors who were scheduled to undergo craniotomy. Compared to normal coagulation profiles, in patients with brain tumors the time to maximum rate of thrombus formation was faster and maximum velocities of clot growth and final clot strengths significantly greater. In other words, they were hypercoagulable. In the authors’ laboratory, normal carboxyhemoglobin (COHb) levels are 0% to 1.5%. For the brain tumor patients, the average was 1.5%. In 10 patients the COHb levels were greater than 1.5%. Twelve patients had COHF formation; of these, 5 were also hypercoagulable. Eleven patients with COHF formation had COHb values >0.91%.
As the authors note, these results are preliminary. More patients need to be studied to better understand the relationship between CO formation, hypercoagulability, deep vein thrombosis, and venous thromboembolism. At the very least, however, the results of this study highlight the association between hypercoagulation and brain tumors.