Laboratory Testing for Activated Protein C Resistance (APCR): An Update.

Autor:	Favaloro EJ; School of Medical Sciences, Faculty of Medicine and Health University of Sydney, Westmead Hospital, Westmead, NSW, Australia. emmanuel.favaloro@health.nsw.gov.au.; School of Dentistry and Medical Sciences, Faculty of Science and Health, Charles Sturt University, Wagga, Wagga, NSW, Australia. emmanuel.favaloro@health.nsw.gov.au., Mohammed S; Haematology Department, Institute of Clinical Pathology and Medical Research (ICPMR), NSW Health Pathology, Westmead Hospital, Westmead, NSW, Australia., Vong R; Haematology Department, Institute of Clinical Pathology and Medical Research (ICPMR), NSW Health Pathology, Westmead Hospital, Westmead, NSW, Australia., Pasalic L; Haematology Department, Institute of Clinical Pathology and Medical Research (ICPMR), NSW Health Pathology, Westmead Hospital, Westmead, NSW, Australia.; Sydney Centres for Thrombosis and Haemostasis, Westmead, NSW, Australia.; Westmead Clinical School, Sydney University, Westmead, NSW, Australia.
Jazyk:	angličtina
Zdroj:	Methods in molecular biology (Clifton, N.J.) [Methods Mol Biol] 2023; Vol. 2663, pp. 203-210.
DOI:	10.1007/978-1-0716-3175-1_11
Abstrakt:	Activated protein C resistance (APCR) reflects a hemostatic state defined by a reduced ability of activated protein C (APC) to affect an anticoagulant response. This state of hemostatic imbalance is characterized by a heightened risk of venous thromboembolism. Protein C is an endogenous anticoagulant that is produced by the hepatocytes and undergoes proteolysis-mediated activation to APC. APC in turn degrades activated Factors V and VIII. APCR describes a state of resistance by activated Factors V and VIII to APC-mediated cleavage of these factors, thereby promoting amplified thrombin production and a potentially procoagulant state. This resistance of APC may be inherited or acquired. Mutations in Factor V are responsible for the most frequent form hereditary APCR. The predominant mutation, a G1691A missense mutation at Arginine 506, the so-called Factor V Leiden [FVL], causes a deletion of an APC-targeted cleavage site in Factor Va, thereby rendering it resistant to inactivation by APC. There are a variety of laboratory assays for APCR, but this chapter focuses on a procedure using a commercially available clotting assay that utilizes a snake venom and ACL TOP analyzers. (© 2023. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)
Databáze:	MEDLINE
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