Exploring necrotizing autoimmune myopathies with a novel immunoassay for anti-3-hydroxy-3-methyl-glutaryl-CoA reductase autoantibodies
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- 作者：Laurent Drouot (15)
Yves Allenbach (14)
Fabienne Jouen (15) (15)
Jean-Luc Charuel (14)
Jérémie Martinet (15) (15)
Alain Meyer (15)
Olivier Hinschberger (14)
Brigitte Bader-Meunier (14) (15)
Isabelle Kone-Paut (15)
Emmanuelle Campana-Salort (14)
Bruno Eymard (15)
Anne Tournadre (14)
Lucile Musset (14)
Jean Sibilia (15)
Isabelle Marie (15) (15)
Olivier Benveniste (14) (15)
Olivier Boyer (15) (15) - 刊名：Arthritis Research & Therapy
- 出版年：2014
- 出版时间：February 2014
- 年：2014
- 卷：16
- 期：1
- 全文大小：571 KB
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Yves Allenbach (14)
Fabienne Jouen (15) (15)
Jean-Luc Charuel (14)
Jérémie Martinet (15) (15)
Alain Meyer (15)
Olivier Hinschberger (14)
Brigitte Bader-Meunier (14) (15)
Isabelle Kone-Paut (15)
Emmanuelle Campana-Salort (14)
Bruno Eymard (15)
Anne Tournadre (14)
Lucile Musset (14)
Jean Sibilia (15)
Isabelle Marie (15) (15)
Olivier Benveniste (14) (15)
Olivier Boyer (15) (15)
15. Department of Internal Medicine, Rouen University Hospital, Rouen, France
14. Department of Rheumatology, Clermont-Ferrand University Hospital, Clermont-Ferrand, France - ISSN：1478-6354
文摘
Introduction Necrotizing autoimmune myopathies (NAM) have recently been defined as a distinct group of severe acquired myopathies, characterized by prominent myofiber necrosis without significant muscle inflammation. Because of the lack of appropriate biomarkers, these diseases have been long misdiagnosed as atypical forms of myositis. NAM may be associated to autoantibodies directed against signal recognition particle (SRP) or 3-hydroxy-3-methyl-glutaryl-CoA reductase (HMGCR). The objective of this work was to quantify anti-HMGCR autoantibodies in patients with suspicion of NAM through the development of a new addressable laser bead immunoassay (ALBIA). Methods Recombinant HMGCR C-domain was bound to fluorescent beads. After incubation with serum, autoantibodies were revealed using class- or subclass-specific anti-human immunoglobulin G (IgG) antibodies. Anti-HMGCR levels were assayed in 150 patients with suspicion of NAM, 142 controls with different inflammatory/autoimmune diseases and 100 healthy donors. Inhibition with free recombinant HMGCR and immunoprecipitation experiments confirmed test specificity. Reproducibility and repeatability were determined from sera with various levels of anti-HMGCR autoantibodies. A multiplex assay (ALBIA-NAM) was also developed to permit the simultaneous quantification of anti-HMGCR and anti-signal recognition particle autoantibodies. Results No controls scored positive. Of 150 patients with suspicion of NAM, 24% were positive for anti-HMGCR autoantibodies with levels ranging from 24 to 2,656?AU/mL. Anti-HMGCR positivity could be associated to a cytoplasmic pattern in immunofluorescence assay on HEp-2 cells. Anti-HMGCR-positive patients had high creatine kinase (CK) levels (mean 6,630?IU/L) and only 40% of them had been exposed to statins. Multiplex ALBIA-NAM was equally as effective as monoplex anti-HMGCR and anti-SRP ALBIA. Conclusions Both monoplex ALBIA-HMGCR and multiplex ALBIA-NAM reliably detect and quantify anti-HMGCR autoantibodies. A positive result allows ascribing patients with a necrotizing myopathy to an autoimmune form. Anti-HMGCR autoantibodies may be found in patients who have not taken statins.