Laboratory testing for activated protein C resistance (APCR): An update

Emmanuel J Favaloro, Soma Mohammed, Ronny Vong, Leonardo Pasalic

Research output: Book chapter/Published conference paperChapter (peer-reviewed)peer-review

1 Citation (Scopus)

Abstract

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.
Original languageEnglish
Title of host publicationHemostasis and thrombosis
Subtitle of host publicationMethods and protocols
EditorsEmmanuel J. Favaloro , Robert C. Gosselin
Place of PublicationNew York
PublisherHumana Press
Chapter11
Pages203-210
Number of pages8
Edition2nd
ISBN (Electronic)9781071631751
ISBN (Print)9781071631744
DOIs
Publication statusPublished - 2023

Publication series

NameMethods in Molecular Biology
Volume2663
ISSN (Print)1064-3745
ISSN (Electronic)1940-6029

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