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Complement AssaysComplement is a collective term for a system of at least 15 serum proteins designed to destroy foreign cells and help remove foreign materials. Complement deficiency can increase susceptibility to infection and predispose to other diseases. Complement assays are indicated in patients with known or suspected immunomediated disease or repeatedly abnormal response to infection. Various laboratory methods are used to evaluate and measure total complement and its components; hemolytic assay, laser nephelometry, and radial immunodiffusion are the most common. Although complement assays provide valuable information about the patient's immune system, the results must be considered in light of serum immunoglobulin and autoantibody tests for a definitive diagnosis of immunomediated disease or abnormal response to infection. Purpose
Patient preparation
Procedure and posttest care
Precautions
Reference values Normal values for complement range as follows:
Abnormal findingsComplement abnormalities may be genetic or acquired; acquired abnormalities are most common. Depressed total complement levels (which are clinically more significant than elevations) may result from excessive formation of antigen-antibody complexes, insufficient synthesis of complement, inhibitor formation, or increased complement catabolism and are characteristicin such conditions as systemic lupus erythematosus (SLE), acute poststreptococcal glomerulonephritis, and acute serum sickness. Low levels may also occur in some patients with advanced cirrhosis of the liver, multiple myeloma, hypogammaglobulinemia, or rapidly rejecting allografts. Elevated total complement may occur in obstructive jaundice, thyroiditis, acute rheumatic fever, rheumatoid arthritis, acute myocardial infarction, ulcerative colitis, and diabetes. C1 esterase inhibitor deficiency is characteristic in hereditary angioedema, the most common genetic abnormality associated with complement; C3 deficiency is characteristic in recurrent pyogenic infection and disease activation in SLE; C4 deficiency is characteristic in SLE and rheumatoid arthritis. C4 is increased in autoimmune hemolytic anemia. Interfering factors
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