Changes in serum complements and their regulators in generalized myasthenia gravis

Objective To investigate changes in serum complements and their regulators in the pathogenesis of myasthenia gravis (MG). Methods Forty‐four patients with acetylcholine receptor antibody‐positive MG, as well as 20 patients with non‐inflammatory neurological disorders were enrolled. Serum complements...

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Veröffentlicht in:European journal of neurology 2021-01, Vol.28 (1), p.314-322
Hauptverfasser: Ozawa, Y., Uzawa, A., Yasuda, M., Kojima, Y., Oda, F., Himuro, K., Kawaguchi, N., Kuwabara, S.
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Sprache:eng
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Zusammenfassung:Objective To investigate changes in serum complements and their regulators in the pathogenesis of myasthenia gravis (MG). Methods Forty‐four patients with acetylcholine receptor antibody‐positive MG, as well as 20 patients with non‐inflammatory neurological disorders were enrolled. Serum complements (C3, C4 and soluble C5b‐9) and complement regulators (vitronectin, clusterin and properdin) were extensively analysed by enzyme‐linked immunosorbent assay and their associations with clinical profiles of MG were examined. Results Serum C3, C4 and clusterin levels were not significantly different between patients with MG and controls. The patients with MG had higher soluble C5b‐9 (P = 0.09) and vitronectin (P = 0.001) levels than the controls; moreover, vitronectin levels decreased after treatment (P = 0.09). Serum properdin (P = 0.03) levels were lower in the patients with MG than in the controls, and negatively correlated with the MG Activities of Daily Living score (rs = −0.26, P = 0.09) and with the presence of bulbar palsy (P = 0.04). Conclusion Our results show that activation of complements and an altered complement network could contribute to the inflammatory pathogenesis of MG. Complements and their regulators changed in myasthenia gravis. Reflecting the classical pathway activation, sC5b‐9 and vitronectin levels were elevated and properdin levels were decreased in patients with myasthenia gravis.
ISSN:1351-5101
1468-1331
DOI:10.1111/ene.14500