complement C3 in serum
Reference interval
Table
| age | MEAN mg/dL | RANGE mg/dL |
|---|---|---|
| Adult | 125 | 83-177 |
| CORD BLOOD | 83 | 57-116 |
| 1 month | 96 | 53-124 |
| 2 months | 96 | 59-149 |
| 3 months | 94 | 64-131 |
| 4 months | 107 | 62-175 |
| 5 months | 107 | 64-167 |
| 6 months | 115 | 74-171 |
| 7-9 months | 113 | 75-166 |
| 10-12 months | 126 | 73-180 |
| 1 year | 129 | 84-174 |
| 2 years | 120 | 81-170 |
| 3 years | 117 | 77-171 |
| 4-5 years | 121 | 86-166 |
| 6-8 years | 118 | 88-155 |
| 9-10 years | 134 | 89-195 |
Principle
The Beckman Array Protein System, in conjunction with the C3 Reagent Test Kit, is intended for in vitro diagnostic quantitation of C3 of biological fluids by rate nephelometry.
The complement proteins are a group of at least 20 immunologically distinct components in blood & tissue fluids. They are able to interact sequentially with antigen-antibody complexes, with each other, & with cell membranes in a complex but adaptable way to destroy viruses & bacteria &, pathologically, even the host's own cells. Complement proteins are synthesized by the liver & are normally present in the blood as functionally inactive molecules. A sequence of interactions can be activated by antigen-antibody complexes through the 'classical' pathway from C1 to C5, or even by nonantibody initiating factors through the 'alternative' or nonclassical pathway form C3 to C5. C3 is an acute phase reactant & is common to both paths. Either path leads to the final membrane attack sequence (C5 to C9 & lysis). The whole process is controlled by the very short life of many of the intermediates & by the presence of specific inhibitor proteins which are an integral part of the system.
Clinical significance
Abnormal serum levels of complement proteins may be due to either inherited or acquired diseases. Deficiency of C3 results in recurrent infections & impaired leukocyte mobilization. Deficiency of C3b inhibitor has a similar outcome since activation of the alternative pathway is not controlled & C3 & Factor B deficiencies ensue.
Acquired disease in serum complement levels may occur in either direction. Levels increase in acute phase reactions; they decrease in immune complex diseases because the classical pathway is activated so that consumption of complement proteins exceeds their synthesis. C3 & C4 are sometimes called 'subacute phase' proteins because the levels of these proteins rise at a later time than other acute phase proteins. Circulating levels of C3 & C4 reflect a balance between complement consumption due to immune complex formation & increased synthesis due to the acute phase response.
Immune complex diseases are disorders in which antigen-antibody complexes either are formed & deposited in tissues or are formed in the circulation & then become permanently attached to tissue cells. Measurement of complement components can be useful in the diagnosis of these diseases, because the Ag-Ab complexes activate the complement system. Hence, changes in the concentration of the complement components reflect the activity of the deposition process.
Evidence for an active process consists of decreasing levels of C3 & C4 as well as the presence of Laboratory results, however, must be interpreted with caution. For example, inadequate preservation of the specimen will allow dissociation of C3 & C4 polymers. As a result, serum levels of C3 or C4 will be overestimated. A concurrent acute phase reaction in the patient will also affect C3 & C4 levels. In this case, extensive tissue damage releases proteolytic enzymes that cleave complement components that become detectable in the assays. In some cases, <A13275>immune complexes</A13275> are produced intermittently, & clinical symptoms may not have appeared or testing may not have been ordered until after the complement levels in serum have returned to normal.
Decreases
- systemic lupus erythematosus: C4 low, C3 sometimes low
- rheumatoid vasculitis : C3 low
- subacute bacterial endocarditis: both C3 & C4 low
- shunt nephritis: both C3 & C4 low
- post-streptococcal glomerulonephritis: C3 low, returns to normal in 3 months
- mesangio-capillary glomerulonephritis: C3 low, (persistent), C4 normal, factor B also found
- polymyalgia rheumatica: only C3 conversion product found
- mixed cryoglobulinemia: only C3 conversion product found
- gram-negative bacteremic shock (early diagnosis): C3 low, C4 normal, factor B low
- gram-positive bacteremia: both C3 & C4 low
- disseminated cytomegalovirus infection: C3 very low, C4 normal or increased
Specimen
No special patient preparations is required. 200 uL of serum, CSF or urine. Store sample in freezer at -15 to -25 C until ready for assay. Highly lipemic samples may result in inaccurate determination & should be redrawn on a fasting patient.
More general terms
Additional terms
Component of
References
- ↑ Beckman Array Protein System Operating Manual. W.B. Saunders, Co., Philadelphia, PA.
- ↑ Tietz, Norbert W. Textbook of Clinical Chemistry, 1986; pp. 575- 579.
- ↑ Panel of 4 tests Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0050119.jsp
- ↑ Mini Panel of 2 tests: Complement Component 3 . Complement Component 4 Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0050149.jsp
- ↑ Complement Component 3 Laboratory Test Directory ARUP: http://www.aruplab.com/guides/ug/tests/0050150.jsp