Discover the benefits of the Svar Complement Assays

Providing the full picture of complement function

In contrast to hemolytic assays, the Svar Complement functional  ELISA is based on quantifying the formation of the Membrane Attack Complex, and will reflect all the different steps in the complement activation pathways and hence provide the full picture of complement function.

Replacing in-house hemolytic assay

Compared to traditional hemolytic assays (CH50, AH50) the Svar Complement functional assays offer increased reagent stability and less analytical variation, thereby strengthening and improving functional assessment of complement in different analytical situations.

The Svar functional assay allow for measurement of the lectin pathway, and properdin deficiency is detectable with our alternative pathway, which is not possible with hemolytic methods. 

The ELISA format used offers superior ease of handling, increased objectivity in interpretation and faster turnaround time. The Svar assays are also optimized for automation resulting in decreased hands-on-time and increased reliability and reproducibility.

Learn more about how the Wieslab® Complement System Screen assay correlates with hemolytic based method.

Assessing the complement system

- more than measuring C3 and C4

Limitations with determination of C3 and C4

In a number of situations, it is assumed that the concentrations of certain complement components (C3 and C4) reflect the overall functionality and activity of the complement system. Only measuring the level of C3 and C4 provides an oversimplified and incomplete view, and is associated with serious limitations such as:

  • A significant variation in the concentration of both C3 and C4 that may overlap the concentration in many disease states
  • Most analytic methods does not discriminate between native C3 and C4 and the activation fragments derived from C3 and C4
  • The liver function is important since the synthesis of a majority of complement proteins takes place in this organ
  • During inflammation the synthesis of C3 and C4 increase which may counter-balance a concurrent consumption 
  • Simple analytic determination may not reflect the functionality of the proteins 
  • Genetic variation may result in primary deficiency which may be interpreted as consumption during disease flares
  • Tissue deposition of immune complexes may lead to local complement activation, not revealed in the circulation
  • Any deficiency downstream from C3/C4 and several other complement deficiencies will go undetected if only C3 and C4 is measured