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Elevated anti-serum amyloid P component (SAP) antibodies in SLE patients
Arthritis Res Ther volume 5, Article number: 32 (2003)
Background
Serum amyloid P component (SAP) binds to DNA and chromatin and plays a role in the clearance of apoptotic debris. One postulated mechanism in the dysregulation of the immune system in systemic lupus erythematosus (SLE) is the aberrant clearance of apoptotic cells. We hypothesize that binding of SAP to anti-SAP antibody may alter SAP function.
Objective
The aim of the study was to determine the presence of anti-SAP antibodies in SLE patients and investigate the correlation with clinical disease.
Methods
Samples from 481 subjects (357 SLE patients, 124 normal controls) were screened for the presence of elevated anti-SAP antibody titers by the ELISA method (optical density 405 nm above 3 SD were considered elevated). Clinical parameters and SLEDAI scores were assessed from the review of files.
Results
Elevated anti-SAP antibody titers were detected in 47% of SLE samples, versus 2% of the control group. In a representative group (n = 112), 62% of patients had elevated anti-SAP antibodies and anti-dsDNA antibody titers. SLEDAI scores were assessed in 83 patients, of whom 54% had elevated anti-SAP antibody titers: 59% had a SLEDAI score of at least 8, an indication of severe disease. The distribution of 35 clinical manifestations in 34/135 patients with elevated anti-SAP antibody titers did not reveal a specific pattern. Serial sampling of two representative SLE patients revealed a decrease in anti-SAP antibody titers after treatment with IVIg that correlated with a decrease in anti-dsDNA antibody titers and with clinical improvement.
Conclusion
Elevated anti-SAP antibody titers were detected in SLE patients and correlated with disease activity. In SLE patients, elevated anti-SAP antibody titers may serve as an additional diagnostic and prognostic marker.
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Zandman-Goddard, G., Blank, M., Langevitz, P. et al. Elevated anti-serum amyloid P component (SAP) antibodies in SLE patients. Arthritis Res Ther 5 (Suppl 1), 32 (2003). https://doi.org/10.1186/ar662
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DOI: https://doi.org/10.1186/ar662