 |
|
|
 |
Serum Amyloid P Component-DNA Complexes Are Decreased in Systemic Lupus Erythematosus. Inverse Association with Anti-dsDNA Antibodies ANNE VOSS, ELLEN HOLM NIELSEN, SVEN ERIK SVEHAG, and PETER JUNKER
ABSTRACT. Methods. The study population comprised 82 unselected patients of predominantly Scandinavian ancestry with SLE according to current classification criteria. Serum samples were collected at baseline and serially for up to 2 years. SAP component and SAP-DNA complexes were measured by ELISA. Associations between SAP-DNA and clinical manifestations or serological findings were analyzed. Ninety healthy, age-matched blood donors served as controls. Results. SLE patients had normal serum concentrations of SAP, whereas SAP-DNA complexes were decreased. Two-thirds of the SLE patients tested persistently SAP-DNA complex-negative. There was no relationship between the occurrence of SAP-DNA complexes and clinical manifestations. SAP-DNA-negative patients tended to have lower leukocyte counts and complement C3 levels, and higher erythrocyte sedimentation rates and C3d levels versus SAP-DNA-positive patients. There was an inverse association between the occurrence of anti-double-stranded DNA (anti-dsDNA) antibodies and SAP-DNA complexes. Co-occurrence of SAP-DNA complexes and anti-dsDNA antibodies was demonstrated in only one SLE patient, implying that 81/82 patients were discordant for the presence of anti-dsDNA antibodies and SAP-DNA complexes. Conclusion. The decreased level of SAP-DNA complexes in SLE patients and the inverse relationship between these complexes and anti-dsDNA antibody supports the concept that SAP component is implicated in the clearance of cell nuclear debris. (J Rheumatol First Release Feb 15 2008) Key Indexing Terms:
SYSTEMIC LUPUS ERYTHEMATOSUS
From the Department of Rheumatology, Odense University Hospital, and Department of Immunology and Microbiology, University of Southern Denmark, Odense, Denmark. Supported by the Danish Rheumatism Association, the Danish Medical Research Council, and A.J. Andersen and Wife's Foundation. A. Voss, MD, PhD, Department of Rheumatology, Odense University Hospital; E. Holm Nielsen, DMV, Department of Anatomy and Neurobiology; S-E. Svehag, DMV, Professor, Department of Immunology and Microbiology, University of Southern Denmark, Odense; P. Junker, MD, Professor, Department of Rheumatology, Odense University Hospital. Address reprint requests to Dr. A. Voss, Department of Rheumatology, Odense University Hospital, DK-5000 Odense C, Denmark. E-mail: anne.voss@OUH.regionsyddanmark.dk Accepted for publication November 8, 2007.
|
