NDLI: In vitro inhibition of factor XIII retards clot formation, reduces clot firmness, and increases fibrinolytic effects in whole blood.

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In vitro inhibition of factor XIII retards clot formation, reduces clot firmness, and increases fibrinolytic effects in whole blood.

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In vitro inhibition of factor XIII retards clot formation, reduces clot firmness, and increases fibrinolytic effects in whole blood.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Jámbor, Csilla Reul, Viviane Schnider, Thomas W. Degiacomi, Priska Metzner, Hubert Korte, Wolfgang C.
Description	Author Affiliation: Jámbor C ( Institute for Clinical Chemistry and Hematology, Kantonsspital, St. Gallen, 9007 Switzerland.)
Abstract	BACKGROUND: Thrombelastography has received renewed interest in the perioperative setting. The main determinants of thrombelastographic results are coagulation factor concentrations (various zymogens and fibrinogen) and platelet count; thus, platelet inhibition renders these assays mainly coagulation factor dependent. Assays with and without platelet inhibition are thus increasingly used to trigger and monitor replacement therapy with blood products. In this study, we evaluated the effect of factor XIII inhibition and additional glycoprotein (GP) IIb/IIIa blockade on (platelet-inhibited) whole blood thrombelastography and whether a modified routine assay (using factor XIII antibody) can be used to detect factor XIII deficiency. METHODS: Normal whole blood was incubated with increasing amounts of a nonspecific antibody, an anti-GPIIb/IIIa antibody, or a neutralizing anti-factor XIII antibody; samples were analyzed with a tissue factor-activated and platelet-inhibited whole blood thrombelastographic assay. Clotting time, clot formation time, maximum clot firmness, and clot lysis at 60 min were evaluated in triplicate. Also, 25 whole blood routine samples were evaluated for factor XIII deficiency using a new thrombelastographic assay incorporating a factor XIII antibody and using a standard factor XIII assay for comparison. RESULTS: Although GPIIb/IIIa inhibition did not alter the results of the platelet-inhibited whole blood thrombelastography, factor XIII inhibition significantly reduced maximum clot firmness (P = 0.020) and increased clot formation time (P = 0.025) and clot lysis (P = 0.007), leaving clotting time unchanged; a ceiling effect seemed to be present with increasing antibody concentrations in whole blood (but not plasma). The thrombelastographic assay for factor XIII deficiency (<70% activity) had a 90% sensitivity and negative predictive value (area under receiver operating characteristic curve 0.803, P = 0.0015); for a deficiency <60%, sensitivity and negative predictive value were 100% (area under receiver operating characteristic curve 0.84, P = 0.0037). CONCLUSION: Factor XIII has significant impact on platelet-inhibited activated whole blood thrombelastography. This phenomenon should be considered when interpreting thrombelastographic results in the bleeding patient, especially when the results trigger procoagulant therapy. Antibody-mediated factor XIII inhibition can be used to establish thrombelastography-based assays to detect factor XIII deficiency.
File Format	HTM / HTML
ISSN	00032999
Issue Number	4
Volume Number	109
e-ISSN	15267598
Journal	Anesthesia & Analgesia
Language	English
Publisher	Lippincott Williams & Wilkins
Publisher Date	2009-10-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Anesthesiology Antibodies Pharmacology Blood Coagulation Drug Effects Factor Xiii Deficiency Diagnosis Factor Xiii Antagonists & Inhibitors Fibrinolysis Thrombelastography Antibodies, Monoclonal Metabolism Blood Humans Immunoglobulin Fab Fragments Platelet Aggregation Inhibitors Platelet Glycoprotein Gpiib-iiia Complex Predictive Value Of Tests Roc Curve Sensitivity And Specificity Thromboplastin Time Factors Journal Article
Content Type	Text
Resource Type	Article
Subject	Anesthesiology and Pain Medicine

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