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Complement activation in patients with primary antiphospholipid syndrome
  1. Kenji Oku (kenoku2005{at}yahoo.co.jp)
  1. Hokkido University Graduate School of Medicine, Japan
    1. Tatsuya Atsumi (at3tat{at}med.hokudai.ac.jp)
    1. Hokkaido University Graduate School of Medicine, Japan
      1. Miyuki Bohgaki
      1. Hokkaido University Graduate School of Medicine, Japan
        1. Olga Amengual
        1. Hokkaido University Graduate School of Medicine, Japan
          1. Hiroshi Kataoka
          1. Hokkaido University Graduate School of Medicine, Japan
            1. Tetsuya Horita (thorita{at}med.hokudai.ac.jp)
            1. Hokkaido University Graduate School of Medicine, Japan
              1. Shinsuke Yasuda (syasuda{at}med.hokudai.ac.jp)
              1. Hokkaido University Graduate School of Medicine, Japan
                1. Takao Koike (tkoike{at}med.hokudai.ac.jp)
                1. Hokkaido University Graduate School of Medicine, Japan

                  Abstract

                  Abstract Objective: To investigate the significance of complement activation in patients with primary antiphospholipid syndrome (APS). Methods: Thirty-six patients with primary APS, 42 control patients with non-SLE connective tissue diseases, and 36 healthy volunteers were analyzed retrospectively. Serum complement levels (C3, C4, CH50) and anaphylatoxins (C3a, C4a, C5a) were examined in all subjects, and serum complement regulatory factors (factor H and factor I) were measured in patients with primary APS. Plasma anticoagulant activity was determined in a mixing test using the activated partial thromboplastin time. Results: Serum complement levels were significantly lower in primary APS patients compared with patients with non-SLE connective tissue diseases (C3, 81.07ア17.86 vs. 109.8ア22.76 mg/dl, p=0.000005; C4, 13.04ア8.49 vs. 21.70ア6.96 mg/dl, p=0.0001; CH50, 31.32ア8.76 vs. 41.40ア7.70 mg/dl, p=0.000004) or healthy volunteers. No healthy subjects showed hypocomplementemia, except for two with low serum C4 levels, whereas most primary APS patients showed elevated serum C3a and C4a. No subjects showed elevated C5a. Primary APS patients with low serum C3 or C4 had significantly higher levels of C3a or C4a compared to healthy controls. No patients had low serum complement regulatory factors. Among patients with primary APS, hypocomplementemia was significantly more frequent in those with high anticoagulant activity compared with those with low or normal activity. Conclusion: Hypocomplementemia is frequent in patients with primary APS, reflecting complement activation and consumption, and was correlated with anticoagulant activity, suggesting that antiphospholipid antibodies may activate monocytes and macrophages via anaphylatoxins produced in complement activation.

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