ORIGINAL ARTICLESThrombelastographic method to quantify the contribution of factor XIII to coagulation kineticsNielsen, Vance Ga; Kirklin, James Kb; Hoogendoorn, Hughc; Ellis, Truitt Ca; Holman, William LbAuthor Information aDepartment of Anesthesiology bDepartment of Surgery, The University of Alabama at Birmingham, Birmingham, Alabama, USA cAffinity Biologicals, Ancaster, Ontario, Canada Inc. Received 13 July, 2006 Revised 17 November, 2006 Accepted 20 November, 2006 Correspondence and requests for reprints to Vance G. Nielsen, MD, Department of Anesthesiology, The University of Alabama at Birmingham, 901 South 19th Street, Basic Medical Research II, Room 206, Birmingham, AL 35249-6810, USA Tel: +1 205 934 4696; fax: +1 205 934 7437; e-mail: [email protected] Blood Coagulation & Fibrinolysis: March 2007 - Volume 18 - Issue 2 - p 145-150 doi: 10.1097/MBC.0b013e32802f7d91 Buy Metrics Abstract Factor XIII (FXIII) plays a critical role in clot strength, and FXIII deficiency or excess is associated with hemorrhage or thrombosis, respectively. Our goal was to design a thrombelastography-based method to characterize the effects of FXIII on plasma clot strength. Normal human plasma was exposed to 0 or 200 μg/ml anti-FXIII antibodies for 20 min prior to celite activation and calcium addition. Other plasma had addition of fibrinogen (625 mg/dl)/FXIII (2 U/ml) or 30% dilution with hydroxyethyl starch before exposure to 0 or 200 μg/ml anti-FXIII antibodies. Thromboelastography was performed and data were collected until stable clot strength was observed. The exposure of normal plasma to anti-FXIII antibodies resulted in a significant (P < 0.05) decrease in clot strength (63%) compared with plasma without antibodies. Further samples exposed to anti-FXIII antibodies had clot strength no different from FXIII-deficient plasma. The FXIII-mediated clot strength varied between 44 and 50% in hypercoagulable and hypocoagulable plasma, respectively. In conclusion, the present investigation successfully demonstrated a novel method to detect the impact of FXIII activity in plasma samples. Further actuarial investigation will be required to determine the utility of this approach in the diagnosis and treatment of patients with either acquired FXIII deficiency or excess and concordant coagulopathy. © 2007 Lippincott Williams & Wilkins, Inc.