SPECIFICATION
In vitro test for the quantitative determination of Complement C3c in human serum and plasma on cobas c systems
Activation of the complement system occurs through a classical and an alternative pathway. The two pathways join together in a joint terminal pathway. Since the complement factor C3 is a factor common to both pathways, the concentration of C3 and its degradation products (including C3c) can be evaluated as a parameter for the activation of the complement system.
Reduced values are indicative of activation. Further differentiation can be made by determining C4. If the C4 level is normal, activation of the alternative pathway is likely. Reduced values are observed in several inflammatory and infectious diseases. The main causes are systemic lupus erythematosus (SLE), rheumatoid arthritis, subacute bacterial endocarditis, viremia, parasitic infections, or bacterial sepsis. A considerable decrease in C3 may be found in patients with partial lipodystrophy or membranoproliferative glomerulonephritis when nephritic factor C3 is present.
As an acute-phase protein, C3 is produced in greater quantities during inflammatory processes. Its levels are elevated in the case of systemic infections, chronic non-infectious inflammatory conditions (mainly chronic polyarthritis) and physiological states (pregnancy). The increase rarely exceeds twice the normal value and may mask a reduction in daily consumption.
Several methods are available for the determination of complement factor C3, including nephelometry, radial immunodiffusion and turbidimetry.