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Acquired deficiencies of the complement system

M Kathryn Liszewski, PhD
John P Atkinson, MD
Section Editor
Peter H Schur, MD
Deputy Editor
Anna M Feldweg, MD


Deficiencies in complement proteins may be inherited or acquired (secondary). Secondary causes of complement deficiency will be presented in this topic review. Inherited disorders of the complement system as well as a description of the complement pathways and the clinical evaluation of complement are presented separately. (See "Inherited disorders of the complement system" and "Complement pathways" and "Overview and clinical assessment of the complement system".)


Acquired deficiencies in complement proteins are more common than inherited complement disorders. Reductions in complement secondary to acquired disease processes are usually only partial and affect several complement components at once. As an example, approximately 50 percent of patients with systemic lupus erythematosus (SLE) will have reductions in C4 and C3, reflecting classical pathway activation.

These acquired complement deficiencies are most commonly encountered in diseases featuring autoantibodies. In many diseases, such as milder forms of SLE, augmented hepatic synthesis of components may be sufficient to maintain the levels in the normal range. The management of most disorders of the complement system featuring excessive activation focuses on the treatment of the underlying disorders.


Acquired deficiencies in complement proteins may result from several mechanisms:

Accelerated consumption by immune complexes (common)


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Literature review current through: Sep 2016. | This topic last updated: Oct 1, 2015.
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