Lowered values of C3 are indicative of activation, with additional differentiation being made when determining C4 in tandem. If the C4 level is normal, then activation of the alternative route is likely. Depressed values are observed in a number of inflammatory and infectious diseases. Primary causes are systemic lupus erythematosus (SLE), rheumatoid arthritis, subacute bacterial endocarditis, viremia, parasitic infections or bacterial sepsis. A considerable decrease in C3 can be found in patients with partial lipodystrophy or membranoproliferative glomerulonephritis when the C3-nephritis factor is present. Other causes of deficient C3 is a primary Immune deficiency of complement component (although C3 deficiency is extremely rare). More common genetic causes are C2 deficiency (classical) and deficiency of proteins controlling the alternate pathway including factor H, I and x-linked properdin. Further Immunological investigation must be initiated if suspected. As C3 is an acute phase protein, it is produced to an increased extent during inflammatory processes. It is elevated in systemic infections, non-infectious chronic inflammatory conditions (primarily chronic polyarthritis) and physiological states (pregnancy). The elevation rarely exceeds twice the normal value and can mask a reduction in the current consumption.
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