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Anti-C1q antibodies: association with nephritis and disease activity in systemic lupus erythematosus

✍ Scribed by Carlos Geraldo Moura; Isabella Lima; Lúcio Barbosa; Daniel Athanazio; Eliana Reis; Mitermayer Reis; Rufus W. Burlingame; Mittermayer B. Santiago


Publisher
John Wiley and Sons
Year
2009
Tongue
English
Weight
92 KB
Volume
23
Category
Article
ISSN
0887-8013

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✦ Synopsis


Abstract

Background: Anti‐C1q antibodies have been described in systemic lupus erythematosus (SLE) as well as in other connective tissue diseases. They have been considered as a marker for disease activity and presence of nephritis.

Objective: The aim of this study was to determine the prevalence of anti‐C1q antibodies in Brazilian lupus patients as well as analyze their association with different clinical and serologic parameters.

Methods: Sera from 81 SLE patients, based on the American College of Rheumatology (ACR) criteria, were collected from a lupus referral outpatient clinic in Salvador, Brazil. Antibodies to C1q were detected by an enzyme‐linked immunoassay (ELISA) kit and antibodies to other cellular antigens identified by indirect immunofluorescence on HEp‐2 cell substrate (ANA), or Crithidia luciliae (dsDNA), and to nucleosome by ELISA. A cutoff of 20 U wasestablished for anti‐C1q and antinucleosome assays.

Results: Anti‐C1q antibodies were detected in 39.5% (32/81) of SLE sera. The presence of anti‐C1q antibodies was associated with proteinuria (P=0.028) but not with other laboratory or clinical features, such as antinucleosome or anti‐dsDNA antibodies, hematuria, urinary casts or renal failure, leukopenia, pericarditis, pleuritis, malar rash, seizures, and psychosis. There was a positive correlation between the titers of anti‐C1q antibodies and the systemic lupuis erythematosus disease activity index (SLEDAI) score (r=0.370; P=0.001).

Conclusion: This study in Brazilian SLE patients confirms previous findings of the association of anti‐C1q antibodies with nephritis and disease activity. J. Clin. Lab. Anal. 23:19–23, 2009. © 2009 Wiley‐Liss, Inc.


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