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Summary  Complement dysregulation is key in the pathogenesis of atypical  H aemolytic  U raemic  S yndrome (a HUS ), but no clear role for complement has been identified in  T hrombotic  T hrombocytopenic  P urpura ( TTP ). We aimed to assess complement activation and cytokine response in acute antibody‐mediated  TTP . Complement  C 3a and  C 5a and cytokines (interleukin ( IL )‐2,  IL ‐4,  IL ‐6,  IL ‐10, tumour necrosis factor, interferon‐γ and IL‐17a) were measured in 20 acute  TTP  patients and 49 remission cases. Anti‐ ADAMTS 13 immunoglobulin  G  ( I g G ) subtypes were measured in acute patients in order to study the association with complement activation. In acute  TTP , median  C 3a and  C 5a were significantly elevated compared to remission,  C 3a 63·9 ng/ml vs. 38·2 ng/ml ( P  < 0·001) and C5a 16·4 ng/ml vs. 9·29 ng/ml ( P  < 0·001), respectively. Median  IL ‐6 and  IL ‐10 levels were significantly higher in the acute vs. remission groups,  IL ‐6: 8 pg/ml vs. 2 pg/ml ( P  = 0·003), IL‐10: 6 pg/ml vs. 2 pg/ml ( P  < 0·001). C3a levels correlated with both anti‐ ADAMTS 13  I g G  ( r  s  = 0·604,  P  = 0·017) and IL‐10 ( r  s  = 0·692,  P  = 0·006). No anti‐ ADAMTS 13  I g G  subtype was associated with higher complement activation, but patients with the highest  C 3a levels had 3 or 4  I g G  subtypes present. These results suggest complement anaphylatoxin levels are higher in acute  TTP  cases than in remission, and the complement response seen acutely may relate to anti‐ ADAMTS 13  I g G  antibody and  IL ‐10 levels.

Complement and cytokine response in acute T hrombotic T hrombocytopenic P urpura