4.7 Article

The target antigens of antineutrophil cytoplasmic antibodies (ANCA) induced by propylthiouracil

Journal

INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 7, Issue 1, Pages 55-60

Publisher

ELSEVIER SCIENCE BV
DOI: 10.1016/j.intimp.2006.07.033

Keywords

antineutrophil cytoplasmic antibodies; vasculitis; propylthiouracil; hyperthyroidism; target antigen

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Objective: Antineutrophil cytoplasmic antibody (ANCA) has been well documented in association with propylthiouracil (PTU), and some patients with PTU-induced ANCA also develop clinical vasculitis. The aim of the current study was to detect ANCA specificities in sera from patients with PTU-induced ANCA with and without clinical vasculitis. Methods: Sera from 65 patients with PTU-induced ANCA were collected, and 27 of these patients were diagnosed with PTU-induced ANCA associated systemic vasculitis (AASV). Indirect immunofluorescence assay and antigen-specific ELISAs were used to detect ANCA and their antigen specificities. The seven known target antigens included myeloperoxidase (MPO), protemase 3, human leukocyte elastase, lactoferrin, cathepsin G, azurocidin and bactericidal/pen-neability-increasing protein (BPI). Results: In IIF assay, P-ANCA was found in 58/65 (89.2%) sera, C-ANCA in two, both P-ANCA and C-ANCA in five, respectively. MPO (60%) and lactoferrin (63.1%) were the two most common target antigens detected in sera from all the patients. 25/27 sera from patients with PTU-induced AASV recognized multiple target antigens, which was significantly higher than those (13/38) from patients without (P < 0.001). Except anti-BPI antibodies, the prevalence of antibodies against the other six target antigens was significantly higher in patients with clinical vasculitis than that in patients without (P < 0.05, respectively). Conclusion: Antibodies against multiple ANCA specific antigens, especially the antigens rather than MPO and PR3, might be the characteristic of PTU-induced ANCA. Patients with antibodies against more ANCA specific antigens might be at increased risk of developing overt clinical vasculitis. The mechanism of ANCA production in PTU-induced cases was different from that in primary AASV (c) 2006 Elsevier B.V. All rights reserved.

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