Rapid improvement of AA amyloidosis with humanised anti-interleukin 6 receptor antibody treatment
1 Department of Respiratory Medicine, Allergy and Rheumatic Diseases, Osaka University Graduate School of Medicine, Osaka, Japan
2 Centre for Advanced Science and Innovation, Osaka University, Osaka, Japan
3 Laboratory of Immune Regulation, Osaka University Graduate School of Frontier Biosciences, Osaka, Japan
Correspondence to:
Dr T Tanaka, Department of Respiratory Medicine, Allergy and Rheumatic Diseases, Osaka University Graduate School of Medicine, 2–2 Yamada-oka, Suita City, Osaka 565–0871, Japan; ttanak@imed3.med.osaka-u.ac.jp
Accepted 26 October 2008
| The first 150 words of the full text of this article appear below. |
AA amyloidosis is a serious complication of chronic inflammatory and infectious diseases.1 Amyloid fibril deposition causes progressive deterioration in various organs.
In October 2007, a 50-year-old woman was admitted to our hospital with severe diarrhoea and weight loss. She had had rheumatoid arthritis (RA) for 12 years. Despite vigorous treatment with prednisolone and disease-modifying anti-rheumatic drugs (DMARDs), including bucillamine, sulfasalazine, auranofin, leflunomide and methotrexate or tacrolimus, her disease remained active.
In January 2007, treatment was started with biological drugs. Subcutaneous injection of 25 mg of etanercept twice weekly for 2 months and, subsequently, intravenous injection of 3 mg/kg infliximab for 5 months combined with 20 mg of prednisolone failed to suppress disease activity as indicated by symptoms, C-reactive protein (CRP) levels of 2.4–3.9 mg/dl and serum amyloid A (SAA) levels of 13–2150 µg/ml. Colon biopsy showed marked deposits of amyloids in all three specimens from the terminal ileum and transverse
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