Spuriously Low Levels of Protein C with a Protac® Activation Clotting Assay

Moerloose, Philippe de; Reber, Guido; Bouvier, C A

doi:10.1055/s-0038-1647532

Cited by 27 publications

(14 citation statements)

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“…APTT‐based assays may underestimate the PC level in samples with high FVIII, while FV Leiden impairs the destruction of both FVa and FVIIIa and may reduce PC levels measured in coagulation assays . Predilution of patient plasma in PC‐depleted plasma may reduce or remove the influence of FV Leiden , although this increases costs and may reduce sensitivity to low levels of PC.…”

Section: Assays Of Natural Anticoagulantsmentioning

confidence: 99%

Guidelines on the laboratory aspects of assays used in haemostasis and thrombosis

Mackie

Cooper

Lawrie

et al. 2012

Int J Lab Hematology

142

238

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Section: Assays Of Natural Anticoagulantsmentioning

confidence: 99%

Guidelines on the laboratory aspects of assays used in haemostasis and thrombosis

Mackie

Cooper

Lawrie

et al. 2012

Int J Lab Hematology

142

238

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“…Prolongation of clotting time is proportional to PC concentration, and patient’s PC is determined from a calibration curve, which is tested alongside the test samples. Type of assay can influence the specificity of the assay, for example, with APTT‐based assay, and high levels of FVIII can cause underestimation of PC (de Moerloose, Reber & Bouvier, 1988; Flanders & Rodgers, 2004). Lupus anticoagulant (LA) can also cause inaccuracy in PC assay, either by adding to the anticoagulant effect of APC and causing overestimation or by interfering with the activity of PC and causing underestimation of PC.…”

Section: Clotting‐based Protein C Assaysmentioning

confidence: 99%

The phenotypic and genetic assessment of protein C deficiency

Cooper¹,

Hill

Maclean³

2012

Int J Lab Hematology

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Summary This paper outlines the methods and approaches used for the laboratory detection and investigation of protein C (PC) deficiency. It does not make recommendations as to which patients should have thrombophilia testing performed; this should be done in line with local guidance. Interpretation of PC level is complicated because level varies with age, and many conditions can cause acquired deficiency. Protein C is most usually measured by chromogenic assay as a part of the thrombophilia screen. There exists, however, a very small group of individuals with significant PC deficiency, in whom the chromogenic PC assay is normal. The coagulometric assay of PC is more sensitive to these rare defects, but these assays may lack specificity. Genetic analysis allows definitive diagnosis and may be useful in confirming that deficiency is inherited and not acquired and is particularly valuable in families with severe PC deficiency.

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“…The interference caused by lupus anticoagulant is more pronounced in tests using APTT as activator (90). In the case of increased Factor VIII, the opposite effect might be seen; shortening the clotting time (APTT) will lead to falsely decreased PC activity (91). The most important problem with the clotting method is the influence of the FV Leiden mutation.…”

Section: Laboratory Tests Of Protein C Deficiencymentioning

confidence: 99%

Protein C and protein S deficiencies: similarities and differences between two brothers playing in the same game

Bereczky

Kovács

Muszbek

2010

Clinical Chemistry and Laboratory Medicine

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Protein C (PC) and protein S (PS) are vitamin K-dependent glycoproteins that play an important role in the regulation of blood coagulation as natural anticoagulants. PC is activated by thrombin and the resulting activated PC (APC) inactivates membrane-bound activated factor VIII and factor V. The free form of PS is an important cofactor of APC. Deficiencies in these proteins lead to an increased risk of venous thromboembolism; a few reports have also associated these deficiencies with arterial diseases. The degree of risk and the prevalence of PC and PS deficiency among patients with thrombosis and in those in the general population have been examined by several population studies with conflicting results, primarily due to methodological variability. The molecular genetic background of PC and PS deficiencies is heterogeneous. Most of the mutations cause type I deficiency (quantitative disorder). Type II deficiency (dysfunctional molecule) is diagnosed in approximately 5%-15% of cases. The diagnosis of PC and PS deficiencies is challenging; functional tests are influenced by several pre-analytical and analytical factors, and the diagnosis using molecular genetics also has special difficulties. Large gene segment deletions often remain undetected by DNA sequencing methods. The presence of the PS pseudogene makes genetic diagnosis even more complicated. Clin Chem Lab Med 2010;48:S53-66.

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Spuriously Low Levels of Protein C with a Protac® Activation Clotting Assay

Cited by 27 publications

References 0 publications

Guidelines on the laboratory aspects of assays used in haemostasis and thrombosis

Guidelines on the laboratory aspects of assays used in haemostasis and thrombosis

The phenotypic and genetic assessment of protein C deficiency

Protein C and protein S deficiencies: similarities and differences between two brothers playing in the same game

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