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Thrombophilia · Thrombosis risk

When activated protein C can't switch off the clot.

In normal plasma, activated protein C (APC) dampens further thrombin generation by inactivating Factor Va. The Factor V Leiden mutation — R506Q — abolishes one of the three APC cleavage sites on Factor Va (Arg506), so the activated cofactor resists inactivation and keeps driving the clot, leaving the plasma APC-resistant. A functional APC-resistance assay flags that phenotype before PCR genotyping confirms the mutation, and the protein C, protein S and antithrombin panel covers the other heritable deficiencies a single test would miss. As UK partner we represent Technoclone's APC Resistance Kit, the chromogenic Technochrom Protein C activity assay and an Antithrombin assay; protein S, which the panel also needs, runs on a complementary assay we advise on from outside the Technoclone line.

Clinical area  Venous thrombosis risk Anchor  Functional APC resistance Confirms with  FV Leiden PCR genotyping
The APC-sensitivity ratio, against the abnormal cut-off

A normal sample sits well above the threshold; APC-resistant plasma — the Factor V Leiden phenotype — falls below it.

0 1 2 3 4 cut-off 2.0 below = abnormal (lab-specific) normal Factor V Leiden (R506Q) APC-resistant abnormal ← → APC-sensitive APC-sensitivity ratio
Illustrative — schematic, not data.

On the APC-sensitivity-ratio scale (0–4, abnormal at the low end, APC-sensitive at the high end), normal plasma reads APC-SR 3.1 and Factor V Leiden (R506Q) plasma reads APC-SR 1.6. Abnormal sits below the lab-specific cut-off of APC-SR < 2.0 — the resistant ratio drops into the abnormal region.

The evidence

A phenotypic screen, then a genotype — and the rest of the panel.

APC resistance is the most common heritable risk factor for venous thrombosis, and it is almost always Factor V Leiden (BSH thrombophilia-testing guideline, Arachchillage et al. 2022). The functional screen and the genotype answer different questions; the figures below set out how each performs, and where the protein C, protein S and antithrombin assays fit.

First-generation aPTT screen
50% sens · 98% spec

A first-generation aPTT-based APC-resistance assay detected Factor V Leiden with 50% sensitivity and 98% specificity. Specific, but it misses half of carriers — the reason a clotting-based screen is read alongside, not instead of, the genotype.

Zehnder 1996 · Am J Clin Pathol 106(1):107–11 peer-reviewed
Caveat

The APC-sensitivity-ratio cut-off (around <2.0) is lab-specific, and first-generation ratios overlap between carriers and non-carriers near the threshold.

Modified / TF-dependent assay class

Modified Factor V-based APC-resistance methods — Factor V-deficient-plasma predilution, or tissue-factor-dependent Factor V assays — approach near-complete sensitivity and specificity for Factor V Leiden as a method class. That class-level performance is not a benchmark we attach to the APC Resistance Kit.

de Ronde 1999 · PMID 10070830 Liebman 1996 · PMID 8943900 peer-reviewed
Caveat

Class-level performance is not the same as kit-level performance, and phenotypic resistance is not the same as the genotype — DNA testing remains the confirmatory step.

What the genotype confirms

Factor V Leiden is the point mutation R506Q (the G1691A substitution in F5, in legacy numbering). It removes one of the APC cleavage sites on Factor Va, so the activated cofactor resists inactivation and keeps supporting prothrombinase — the molecular basis of the resistant ratio on the scale above. A functional screen identifies the phenotype; PCR genotyping confirms the mutation and distinguishes heterozygous from homozygous carriers.

A panel, not a single test

APC resistance is only one route to heritable thrombophilia. The chromogenic Technochrom Protein C activity assay — a chromogenic activity assay of the kind guidelines recommend first-line for protein C, detecting Type 1 and most Type 2 deficiency, though an amidolytic method can miss the rare Type 2 defects that impair protein C's non-catalytic anticoagulant function while sparing active-site activity, where a clot-based assay is needed — and an Antithrombin assay cover two of the natural anticoagulants; the Technozym Protein C antigen ELISA subtypes a low activity result, and protein S completes the panel on a complementary assay we advise on. As a chromogenic method, the activity assay sidesteps the direct-oral-anticoagulant and heparin interference that clot-based functional protein C assays are prone to. They read together — a phenotypic deficiency in one rarely settles the picture alone.

Caveat

This is a panel, not one test. Results are affected by pre-analytical handling, the acute-phase response, warfarin (which lowers protein C and protein S) and DOAC interference — so timing and treatment status must be known before a deficiency is called. Protein S testing in particular must distinguish free from total protein S, and free protein S is lowered by oestrogen (combined hormonal contraception, HRT) and by pregnancy — so hormonal and pregnancy status must be known before a protein S deficiency is called.

How it's run · what we do

The assays, the method, and where our judgement sits.

The functional screen

The APC Resistance Kit is a clotting-based APC-resistance assay: a clotting time is measured with and without added activated protein C, and the ratio of the two — the APC-sensitivity ratio — is reported against a lab-validated cut-off. A ratio below the cut-off flags the resistant phenotype for genotype confirmation.

The anticoagulant panel

The chromogenic Technochrom Protein C activity assay and an Antithrombin assay quantify two of the natural anticoagulants — with the Technozym Protein C antigen ELISA to subtype a low result, and protein S covered on a complementary assay we advise on. Read alongside the APC-resistance result and the clinical picture, they build the heritable-thrombophilia panel rather than standing alone.

elixir represents the Technoclone range as its UK partner and advises on where each assay earns its place — including when a clotting-based screen should give way to genotyping, and how warfarin, DOACs or an acute event change what a single value means. Where modelling or computational work helps interpret an unusual pattern, that is a human-led service we provide, reported with its assumptions stated — never an off-the-shelf product.

References

Every figure on this page, traceable to source.

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Pricing the thrombophilia panel, or scoping a screen.

Tell us which assays you are running or considering — APC resistance, protein C, protein S, antithrombin — and the question in front of you. We will reply with how we would approach it, what it would involve, and an honest quote, usually within two working days.