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Suppression of elevations in serum C reactive protein levels by anti-IL-6 autoantibodies in two patients with severe bacterial infections
  1. Toshihiro Nanki1,2,
  2. Ikumi Onoue1,3,
  3. Kenji Nagasaka4,
  4. Aiko Takayasu1,3,
  5. Masashi Ebisawa1,
  6. Tadashi Hosoya1,
  7. Toshizumi Shirai5,
  8. Takahiko Sugihara6,
  9. Shinya Hirata1,
  10. Tetsuo Kubota1,3,
  11. Masayoshi Harigai1,2,
  12. Nobuyuki Miyasaka1
  1. 1 Department of Medicine and Rheumatology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan
  2. 2 Department of Pharmacovigilance, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, Tokyo, Japan
  3. 3 Section of Microbiology and Immunology, Graduate School of Health Care Sciences, Tokyo Medical and Dental University, Tokyo, Japan
  4. 4 Department of Rheumatology, Ome Municipal General Hospital, Tokyo, Japan
  5. 5 Department of Cardio-Thoracic Surgery, Ome Municipal General Hospital, Tokyo, Japan
  6. 6 Department of Medicine and Rheumatology, Tokyo Metropolitan Geriatric Hospital, Tokyo, Japan
  1. Correspondence to Dr Toshihiro Nanki, Department of Medicine and Rheumatology, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8519 Japan; nanki.rheu{at}tmd.ac.jp

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Serum C reactive protein (CRP) is generally elevated by infection. We encountered two patients with severe bacterial infections without increases in CRP. Patient 1: A 67-year-old man developed thoracic empyema by Escherichia coli and Streptococcus intermedius. His body temperature was 36.6°C, his leukocyte count was elevated (9960/μl) and he was negative for CRP (0.01 mg/dl). Despite antibiotic treatment, he died of respiratory failure. Patient 2: A 56-year-old woman developed multiple subcutaneous abscesses by Staphylococcus aureus. She had rheumatoid arthritis (RA) for 30 years and was treated with sodium aurothiomalate. Her body temperature was 37.4°C, and leukocyte count (5600/μl) and CRP (0.05 mg/dl) were not elevated. She recovered with antibiotics. Neither patient had a past history of severe bacterial infection.

Since serum CRP is mainly controlled by interleukin (IL)-6,1 the lack of IL-6 function was suggested. Serum IL-6 was not detected by ELISA in either patient, although it is known to increase with severe infection.2 ,3 However, IL-6 production from peripheral blood monocytes with/without lipopolysaccharide stimulation was similar between Patient 1 and healthy controls (data not shown). Soluble IL-6 receptor (IL-6R) and IL-6 signal transducer (IL-6ST) serum levels were also …

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