Changes in serum complements and their regulators in generalized myasthenia gravis
Autor: | Naoki Kawaguchi, Satoshi Kuwabara, Akiyuki Uzawa, Fumiko Oda, Keiichi Himuro, Manato Yasuda, Yukiko Ozawa, Yuta Kojima |
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Rok vydání: | 2020 |
Předmět: |
medicine.medical_specialty
Pathogenesis 03 medical and health sciences 0302 clinical medicine Internal medicine Activities of Daily Living Myasthenia Gravis Humans Medicine Receptors Cholinergic 030212 general & internal medicine Autoantibodies Bulbar palsy Acetylcholine receptor biology Clusterin business.industry COMPLEMENT REGULATORS Complement System Proteins medicine.disease Myasthenia gravis Endocrinology Neurology biology.protein Properdin Vitronectin Neurology (clinical) medicine.symptom business 030217 neurology & neurosurgery |
Zdroj: | European Journal of Neurology. 28:314-322 |
ISSN: | 1468-1331 1351-5101 |
Popis: | 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. |
Databáze: | OpenAIRE |
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