Sorted By Test Name - Mayo Medical Laboratories

APCRV
81967
neoepitopes presented by complexes of phospholipid and proteins, such as prothrombin (factor II) or beta
2 glycoprotein I, but these antibodies do not specifically inhibit any of the coagulation factors. Clinically,
lupus anticoagulant represents an important marker of thrombotic tendency. In contrast, patients with
specific coagulation inhibitors, such as factor VIII inhibitor antibodies, have a significant risk of
hemorrhage and often require specific treatment for effective management. Both types of disorders may
have similar prolongation of the APTT.
Useful For: Monitoring heparin therapy (unfractionated heparin [UFH]) Screening for certain
coagulation factor deficiencies Detection of coagulation inhibitors such as lupus anticoagulant, specific
factor inhibitors, and nonspecific inhibitors
Interpretation: Since activated partial thromboplastin time (APTT) reagents can vary greatly in their
sensitivity to unfractionated heparin (UFH), it is important for laboratories to establish a relationship
between APTT response and heparin concentration. The therapeutic APTT range in seconds should
correspond with an UFH concentration of 0.3 to 0.7 U/mL as assessed by heparin assay (inhibition of
factor Xa activity with detection by a chromogenic substrate). In our laboratory, we have found the
therapeutic APTT range to be approximately 70 to 120 seconds. Prolongation of the APTT can occur as a
result of deficiency of 1 or more coagulation factors (acquired or congenital in origin), or the presence of
an inhibitor of coagulation such as heparin, a lupus anticoagulant, a nonspecific inhibitor such as a
monoclonal immunoglobulin, or a specific coagulation factor inhibitor. Shortening of the APTT usually
reflects either elevation of factor VIII activity in vivo that most often occurs in association with acute or
chronic illness or inflammation, or spurious results associated with either difficult venipuncture and
specimen collection or suboptimal specimen processing.
Reference Values:
28-38 seconds
Clinical References: 1. Miletich JP: Activated partial thromboplastin time. In Williams
Hematology. 5th edition. Edited by E Beutler, MA Lichtman, BA Coller, TJ Kipps. New York,
McGraw-Hill, 1995, pp L85-86 2. Greaves M, Preston FE: Approach to the bleeding patient. In
Hemostasis and Thrombosis: Basic Principles and Clinical Practice. 4th edition. Edited by RW Colman, J
Hirsh, VJ Marder, et al. Philadelphia, JB Lippincott Co, 2001, pp 1197-1234 3. Olson JD, Arkin CF,
Brandt JT, et al: College of American Pathologists Conference XXXI on laboratory monitoring of
anticoagulant therapy: laboratory monitoring of unfractionated heparin therapy. Arch Pathol Lab Med
1998;122:782-798
Activated Protein C Resistance V (APCRV), Plasma
Clinical Information: Protein C, a part of the natural anticoagulant system, is a vitamin K-dependent
protein zymogen (molecular weight=62,000 da) that is synthesized in the liver and circulates at a plasma
concentration of approximately 5 mcg/mL. Protein C is activated to activated protein C (APC) via
proteolytic cleavage by thrombin bound to thrombomodulin, an endothelial cell surface membrane
protein. APC downregulates the procoagulant system by proteolytically inactivating procoagulant factors
Va and VIIIa. Protein S, another vitamin K-dependent coagulation protein, catalyzes APC inactivation of
factors Va and VIIIa. APC interacts with and proteolyses factors V/Va and VIII/VIIIa at specific APC
binding and cleavage sites, respectively. Resistance to activated protein C (APC resistance) is a term used
to describe abnormal resistance of human plasma to the anticoagulant effects of human APC. APC
resistance is characterized by a reduced anticoagulant response of patient plasma after adding a standard
amount of APC. For this assay, the activated partial thromboplastin time clotting test fails to prolong
significantly after the addition of APC. The vast majority of individuals with familial APC resistance have
a specific point mutation in the procoagulant factor V gene (1691G-A, factor V Leiden) encoding for a
glutamine (Q) substitution for arginine (R)-506 in the heavy chain of factor V (factor V R506Q). This
amino acid change alters an APC cleavage site on factor V such that factor V/Va is partially resistant to
inactivation by APC. The carrier frequency for the factor V Leiden mutation varies depending on the
population. Approximately 5% of asymptomatic white Americans of non-Hispanic ancestry are
heterozygous carriers, while the carrier frequency among African Americans, Asian Americans, and
Native Americans is