Hypercomplementemia at relapse in patients with anti-aquaporin-4 antibody

H. Doi, T. Matsushita, N. Isobe, T. Matsuoka, M. Minohara, H. Ochi, Jun Ichi Kira

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Objective: Because Asian patients with opticospinal multiple sclerosis (OSMS) frequently have anti-aquaporin-4 (AQP4) antibody, complement-mediated disruption of astrocyte foot processes is proposed but not yet proven. We aimed to clarify whether complement consumption occurs at relapse in anti-AQP4 antibody-positive patients. Methods: We analyzed serum CH50, C3, C4, and C-reactive protein (CRP) levels and their relation to clinical phases in 118 MS patients with or without anti-AQP4 antibody. Serum CH50 levels were higher in 24 patients with anti-AQP4 antibody than in 39 OSMS and 54 conventional form of MS (CMS) patients without anti-AQP4 antibody at relapse Pcorr < 0.05) but not in remission. The frequency of hypercomplementemia at relapse was also higher in anti-AQP4 antibody-positive patients than in anti-AQP4 antibody-negative CMS patients (70.4% vs 29.0%, Pcorr < 0.05). C3 and C4 levels did not differ significantly among the three groups at relapse. In patients with anti-AQP4 antibody, the coexistence of hypercomplementemia and high CRP values was more common at relapse than in the remission phase (36.0% vs 10.5%, P < 0.05). In patients with extensive central nervous system lesions, hypercomplementemia was significantly more common in anti-AQP4 antibody-positive patients than anti-AQP4 antibody-negative ones (88.9% vs 16.7%, P < 0.01). We consider that hypercomplementemia in anti-AQP4 antibody-positive patients may reflect a systemic inflammatory reaction at relapse.

Original languageEnglish
Pages (from-to)304-310
Number of pages7
JournalMultiple Sclerosis
Volume15
Issue number3
DOIs
Publication statusPublished - Mar 13 2009

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Aquaporin 4
Recurrence
Antibodies
C-Reactive Protein
Serum
Astrocytes
Central Nervous System

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology

Cite this

Hypercomplementemia at relapse in patients with anti-aquaporin-4 antibody. / Doi, H.; Matsushita, T.; Isobe, N.; Matsuoka, T.; Minohara, M.; Ochi, H.; Kira, Jun Ichi.

In: Multiple Sclerosis, Vol. 15, No. 3, 13.03.2009, p. 304-310.

Research output: Contribution to journalArticle

Doi, H. ; Matsushita, T. ; Isobe, N. ; Matsuoka, T. ; Minohara, M. ; Ochi, H. ; Kira, Jun Ichi. / Hypercomplementemia at relapse in patients with anti-aquaporin-4 antibody. In: Multiple Sclerosis. 2009 ; Vol. 15, No. 3. pp. 304-310.
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AU - Kira, Jun Ichi

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N2 - Objective: Because Asian patients with opticospinal multiple sclerosis (OSMS) frequently have anti-aquaporin-4 (AQP4) antibody, complement-mediated disruption of astrocyte foot processes is proposed but not yet proven. We aimed to clarify whether complement consumption occurs at relapse in anti-AQP4 antibody-positive patients. Methods: We analyzed serum CH50, C3, C4, and C-reactive protein (CRP) levels and their relation to clinical phases in 118 MS patients with or without anti-AQP4 antibody. Serum CH50 levels were higher in 24 patients with anti-AQP4 antibody than in 39 OSMS and 54 conventional form of MS (CMS) patients without anti-AQP4 antibody at relapse Pcorr < 0.05) but not in remission. The frequency of hypercomplementemia at relapse was also higher in anti-AQP4 antibody-positive patients than in anti-AQP4 antibody-negative CMS patients (70.4% vs 29.0%, Pcorr < 0.05). C3 and C4 levels did not differ significantly among the three groups at relapse. In patients with anti-AQP4 antibody, the coexistence of hypercomplementemia and high CRP values was more common at relapse than in the remission phase (36.0% vs 10.5%, P < 0.05). In patients with extensive central nervous system lesions, hypercomplementemia was significantly more common in anti-AQP4 antibody-positive patients than anti-AQP4 antibody-negative ones (88.9% vs 16.7%, P < 0.01). We consider that hypercomplementemia in anti-AQP4 antibody-positive patients may reflect a systemic inflammatory reaction at relapse.

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