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Serum complement factor C5a in IgG4-related disease
  1. Shoichi Fukui1,2,
  2. Yuya Fujita1,
  3. Tomoki Origuchi1,3,
  4. Takahiro Maeda2,4,
  5. Atsushi Kawakami1
  1. 1 Department of Immunology and Rheumatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan
  2. 2 Department of Community Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan
  3. 3 Department of Rehabilitation Sciences, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan
  4. 4 Department of General Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan
  1. Correspondence to Dr Shoichi Fukui, Department of Community Medicine, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki 8528501, Japan; fukui-ngs{at}umin.ac.jp

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We read with great interest the correspondence by Umehara et al 1 which discussed the difficulties in the diagnosis of IgG4-related disease (IgG4-RD). They mention that increased IgG4 concentration is not a specific marker for IgG4-RD. Therefore, the markers for the diagnosis and the disease activity of IgG4-RD are demanded.

Approximately a quarter of patients with active IgG4-RD have hypocomplementaemia defined by the lower normal limit of C3 or C4 levels.2 Complement pathways consist of three pathways: classical, alternative and lectin pathways.3 Here, we focus on complement factors as makers of IgG4-RD and attempt to evaluate the entire complement system in IgG4-RD.

We enrolled 28 patients with active and untreated IgG4-RD, diagnosed based on the 2011 comprehensive diagnostic criteria4 and 28 sex-matched and age-matched healthy donors. We evaluated the characteristics of patients with IgG4-RD, the number of affected organs and the IgG4-RD Responder Index (IgG4-RD RI).5 None of the healthy donors had a history of inflammatory disease.

In the sera of the patients with …

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