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. 2005 Jul 13;64(12):1698–1702. doi: 10.1136/ard.2005.035832

Anti-serum amyloid component P antibodies in patients with systemic lupus erythematosus correlate with disease activity

G Zandman-Goddard 1, M Blank 1, P Langevitz 1, L Slutsky 1, M Pras 1, Y Levy 1, O Shovman 1, T Witte 1, A Doria 1, J Rovensky 1, Y Shoenfeld 1
PMCID: PMC1755319  PMID: 16014675

Abstract

Objective: To determine the presence of raised titres of anti-serum amyloid P component (SAP) antibodies in patients with systemic lupus erythematosus (SLE) and to evaluate their correlation with clinical disease by the SLEDAI and clinical manifestations.

Methods: 452 samples were screened for raised anti-SAP antibody titres by an ELISA. Clinical measures and SLEDAI scores were independently reviewed from medical records. 21 serial samples from 7 patients with SLE were assessed for a change in anti-SAP antibody titres after treatment.

Results: Raised anti-SAP antibody titres were detected in 145/328 (44%) SLE samples. In 112 randomly selected samples, 69/112 (62%) patients had raised anti-SAP antibodies and anti-dsDNA antibody titres, whereas only 32/112 (28%) had raised anti-dsDNA antibody titres without raised anti-SAP antibody titres. The mean titre of anti-SAP antibodies in patients with active disease was higher than in patients with inactive disease and controls. SLEDAI scores, assessed in 54 patients, were raised in 26/31 (84%) patients with raised anti-SAP antibody titres. A SLEDAI score ⩾8 was found in 16/31 (52%) patients with raised anti-SAP antibody titres but in only 5/23 (22%) patients without raised titres. No specific pattern of disease was detected in patients with or without raised titres of anti-SAP antibodies. Serial sampling from patients with active SLE and raised anti-SAP antibody titres showed that anti-SAP antibody titres decreased after treatment and correlated with clinical improvement.

Conclusion: Raised anti-SAP antibody titres detected in patients with SLE correlate with disease activity and decrease with improvement of clinical disease, and thus may serve as an additional prognostic marker.

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Figure 1.

Figure 1

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 Titres of anti-SAP antibodies in 189 patients with SLE; 54 patients with SLE with clinically active disease (group I—Israel), 135 patients with SLE with clinically inactive disease (group II—Germany), and in 54 healthy controls.

Figure 2.

Figure 2

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 SAP dose dependent binding of protein G and dsDNA-cellulose affinity purified total IgG from four lupus patients positive for SAP (patients 1–4) and one lupus patient negative for SAP recognition (patient 5). The binding was assayed by ELISA. Data presented as OD at 405 nm, mean (SD) of three experiments.

Figure 3.

Figure 3

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 Inhibition of binding of affinity purified IgG from lupus patients to SAP by SAP. Total IgG affinity purified from five lupus patients incubated with different concentrations of SAP. Patients 1–4 had raised titres of anti-SAP antibodies. but patient 5 did not. The inhibition of the binding was calculated as the percentage inhibition of total IgG to SAP by SAP. The data are presented as mean (SD) of three experiments.

Figure 4.

Figure 4

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 SLEDAI scores for 54 patients with SLE, comparing the percentage of patients with and without raised anti-SAP antibody titres. Remission and mild disease: SLEDAI 0–4; moderate disease: SLEDAI 5–7; severe disease: SLEDAI ⩾8.

Figure 5.

Figure 5

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 Serial sampling of anti-SAP antibody titres in seven patients on 2–4 occasions. All patients had been recently diagnosed with SLE or had a flare. The first samples were taken before treatment. The OD for 3SD of the mean controls was 0.154.

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